SNC’21 SINAPSA NEUROSCIENCE CONFERENCE ‘21 23-25 September, 2021 LJUBLJANA, SLOVENIA Sinapsa Neuroscience Conference ‘21 Ljubljana, 23–25 September 2021 Organised by SiNAPSA, Slovenian Neuroscience Association SNC’21 Programme Committee Maja Bresjanac (Chair), Lana Blinc, Matjaž Deželak, Blaž Koritnik, Matej Perovnik, Viktorija Radotič SNC’21 Organising Committee Viktorija Radotič (Chair), Maja Bresjanac, Lana Blinc, Matjaž Deželak, Blaž Koritnik, Andraž Matkovič, Matej Perovnik Conference was supported by International Brain Research Organisation (IBRO), Slovenian Research Agency (ARRS), Biogen, Pfizer, Roche, CogDec, Slovenian Society of Clinical Neurophysiology, Slovenian Neurological Society, Slovenian Psychiatric Association, University Medical Centre Ljubljana, Krka, Lek, Medis, Medistar, Novartis, Octapharma, Sanofi Genzyme, Wörwag Pharma Editors Andraž Matkovič, Maja Bresjanac Design Klemen Trupej, Damjan Osredkar, Grega Repovš Publisher SiNAPSA, Slovenian Neuroscience Association www.sinapsa.org Ljubljana, 2021 1st online edition Publication is available free of charge. URL: https://sinapsa.org/SNC21/media/files/SNC21_Book_of_ Abstracts.pdf CIP – Kataložni zapis o publikaciji Narodna in univerzitetna knjižnica, Ljubljana Kataložni zapis o publikaciji (CIP) pripravili v Narodni in univerzitetni knjižnici v Ljubljani COBISS.SI-ID 78313219 ISBN 978-961-95519-0-5 (PDF) SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 BOOK OF ABSTRACTS www.sinapsa.org/SNC21 Ljubljana, Slovenia 23—25 September 2021 Contents Programme at a Glance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 Scientific Programme . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 SiNAPSA Neuroscience Conference ‘21. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7 Educational Workshop on CNS protein misfolding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Clinical Neurophysiology Symposium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Abstracts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Plenary and Special Lectures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Thematic Symposia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Posters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Educational Workshop on CNS protein misfolding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Sponsors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 [4] Programme at a glance SiNAPSA Neuroscience Conference ‘21 Programme at a glance Thursday, September 23 Friday, September 24 Saturday, September 25 9:00 10:00 11:00 11:00–12:00 11:00–12:00 11:00–12:00 Biogen & Pfizer Satellite symposium Poster session I Poster session II 12:00 12:00–12:45 12:00–12:45 Dr. Janez Faganel Memorial lecture: Giuseppe Lauria Plenary talk: Eiko Fried 13:00 13:45–14:00 SNC’21 Opening 13:00–14:30 13:00–15:00 Symposium II: Deep Brain Symposium III: Music and Brain - 14:00 Stimulation for Movement Disorders Evidence Based Music Interventions in Medicine 14:00–16:00 13:00–18:00 15:00 Hot topic: SARS-CoV-2 and Brain Ljubljana Clinical Neurophysiology 15:00–15:45 15:00–17:00 Symposium EWPM I: Proteostasis & PM Disease Symposium IV: Brain Health Across 16:00 the Lifespan - Findings from the 16:00–18:00 15:45–17:45 Lifebrain Project Symposium I: Metabolic Brain EWPM II: Tauopathies, a- 17:00 Imaging in Neurodegenerative synucleinopathies, poly-Q, TDP43 17:00–17:45 Disorders Plenary talk: Tracy Bale 17:45–18:00 SNC’21 Closing 18:00 18:00–18:30 17:45–18:45 18:15–19:00 Roche Satellite symposium EWPM III: Prion diseases Plenary talk: Thilo van Eimeren 19:00 19:00–20:30 Prof. A.O. Župančič Memorial talk & Neuroscience and Society Dialogue 20:00 Sonia M. Vallabh 21:00 EWPM - Educational workshop on CNS protein misfolding SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 SiNAPSA Neuroscience Conference ‘21 Programme www.sinapsa.org/SNC21 Ljubljana, Slovenia 23—25 September 2021 SiNAPSA Neuroscience Conference ’21 Programme Thursday, 23 September 13:45—14:00 Opening of the SNC’21 14:00—16:00 Symposium SARS-CoV-2 and Brain Chairs: Maja Bresjanac Neuro-COVID - what it is and what it is not Raimund Helbok Neurological Associations of COVID-19 Vaccines Jennifer Frontera Learning during the pandemic: mapping potential educational inequalities across Europe Zsuzsa Blaskó Cognitive and Neurological Consequences of COVID-19 Adrian Owen 16:00—18:00 Symposium Metabolic Brain Imaging in Neurodegenerative Disorders Chair: Matej Perovnik and Maja Trošt Mechanisms of tau pathology spreading in Alzheimer’s disease and 4R tauopathies Nicolai Franzmeier Developing and Interpreting a Deep Learning Model for Alzheimer’s Disease Tracking Alison Deatsch Technical Factors Affecting Image Quality in PET Mauro Namías Cognition-related functional topographies in Parkinson’s disease: Localized loss of the ventral default mode network Katharina A Schindlbeck Metabolic correlates in PSP clinical subtypes Gloria Martí-Andrés Specific Metabolic Brain Patterns in Alzheimer’s dementia and dementia with Lewy bodies Matej Perovnik Correlations between brain metabolism and neuropathology in sporadic Creutzfeldt-Jakob disease Tomaž Rus [7] 18:15—19:00 Plenary talk Can brain imaging unravel the tangled web of neurodegeneration? Thilo van Eimeren Friday, 24 September 11:00—12:00 Short Oral Presentations Session I 12:00—12:45 Dr. Janez Faganel Memorial lecture Small fiber neuropathy Giuseppe Lauria 13:00—14:30 Symposium Deep Brain Stimulation for movement disorders – A neuroimaging perspective Chair: Maja Trošt and Dejan Georgiev Non-motor symptoms in Parkinson’s disease and Dystonia: Neuroimaging perspective Vladimira Vuletić The effect of Deep Brain Stimulation on Brain Metabolism in Movement Disorders Maja Trošt Parkinson’s disease as a network disorder: Lessons from connectivity studies Rok Berlot Frequency modulation in deep brain stimulation: Does it work and is there neuroimaging proof of its action? Dejan Georgiev Impulsivity in STN-DBS PD: More than a unitary phenomenon Tjaša Mlinarič Effects of subthalamic nucleus deep brain stimulation on language in advanced Parkinson’s disease Živa Drakulić 15:00—19:45 Workshop Educational Workshop on Proteostasis and Protein Misfolding in CNS Disorders 19:00—19:45 AOŽ Memorial lecture Genetic prion disorders and patient-scientist’s mandate Sonia M. Vallabh 19:45—20:30 Neuroscience and Society Dialogue: Conversation with Dr. Sonia M. Vallabh [8] Saturday, 25 September 11:00—12:00 Short Oral Presentations Session II 12:00—12:45 Plenary talk Systems all the way down: studying mental health problems as biopsychosocial systems Eiko Fried 13:00—15:00 Symposium Music and Brain: Evidence-based music interventions in medicine Chair: Igor M. Ravnik and Uroš Kovačič Neurology of Music and Brain Daniele Schoen Research towards evidence-based music interventions Stefan Koelsch The mother’s voice, singing and speaking, as a special tool for early interventions in the NICU Manuela Filippa Heart rate variability in relation to self-selected music or music genres preselected by the researchers Uroš Kovačič 15:00—17:00 Symposium Brain health across the lifespan – Findings from the Lifebrain project Chair: Isabelle Budin-Ljøsne Ageing and brain imaging in Lifebrain Klaus P. Ebmeier for Lifebrain Consortium What can blood biomarkers tell us about the brain? Christian A. Drevon What is brain health? Perceptions of respondents to the Global Brain Health Survey Isabelle Budin-Ljøsne for Lifebrain Consortium Brain asymmetry in aging and Alzheimer’s disease James M. Roe 17:00—17:45 Plenary talk Extracellular vesicles as stress signals: Identifying novel mechanisms of neurodevelopmental programming Tracy Bale 17:45—18:00 SNC’21 Closing [9] Poster sessions Friday, 24 September 11:00—12:00 Short Oral Presentations Session I Effect of repetitive transcranial magnetic stimulation on language performance in Alzheimer’s Disease: a Slovene- speaker case study Georgia Roumpea The Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog): standardisation of Slovenian version Janina Ulbl DNA methylation of candidate genes BDNF and COMT in Alzheimer’s disease Alja Videtić Paska Expression of Na+,K+-ATPase isoenzymes and myokines in cultured human myotubes innervated by rat spinal cord explants Vid Jan Saturday, 25 September 11:00—12:00 Short Oral Presentations Session II Role of PDGFRα - Integrin interactions in Anoikis resistance mediated glioblastoma progression Pampa Pain HMGB1 inhibition attenuates lipopolysaccharide (LPS)-induced neuroinflammation, cognitive dysfunction and sickness behavior Devlina Ghosh Educated vs. lay public view of neuroscience and science based brain health recommendations in Slovenia Matej Perovnik Physicians’ standpoints for the use of music-based interventions in Slovenian health care system Ana Kuder [10] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘17 Educational workshop on CNS protein misfolding www.sinapsa.org/SNC21/workshop Ljubljana, Slovenia 24 September 2021 Friday, 24 September 15:00—15:45 Proteostasis Collapse: A Basis for Aging and Neurodegenerative Diseases Richard I. Morimoto 15:45—16:15 An update on Tau-related diseases Gabor G. Kovacs 16:15—16:45 TDP-43 proteinopathies Boris Rogelj 16:45—17:15 Now it is time for research to crack Parkinson’s disease Patrik Brundin 17:15—17:45 Huntington’s disease Roger A. Barker 17:45—18:15 Transmissible Spongiform Encephalopathies Adriano Aguzzi 18:15—18:45 A structural biologist’s view of neuroscience Holger Wille 19:00—19:45 Genetic prion disorders and patient-scientist’s mandate Sonia M. Vallabh [12] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 Clinical Neurophysiology Symposium www.sinapsa.org/SNC21/simpozij Ljubljana, Slovenia 24 September 2021 Friday, 24 September 11:00—11:30 Biogen satellite symposium: Nusinersen treatment of spinal muscular atrophy Vladka Salapura 11:30—12:00 Pfizer satellite symposium: From transthyretin neuropathy to cardiomyopathy Janez Zidar, Gregor Zemljič 12:00—12:45 Dr. Janez Faganel Memorial lecture Small fiber neuropathy Giuseppe Lauria 13:00—18:00 Symposium Ljubljana Clinical Neurophysiology Symposium Chair: Blaž Koritnik Pattern recognition approach to neuropathy and neuronopathy Richard J. Barohn New 2021 EAN/PNS CIDP guideline Peter Van den Bergh Multifocal motor neuropathy Bruce V. Taylor Paraproteinemic neuropathies Elie Naddaf Inherited neuropathies Michaela Auer-Grumbach Small fiber neuropathy – Slovenian experience Mateja Baruca Grad Measurement of axonal excitability Mihai Moldovan Investigations of cardiovascular autonomic nervous system Ellen Merete Hagen Utility of ultrasonography in polyneuropathies Simon Podnar 18:00—18:45 Roche satellite symposium: SMA - new treatment options Damjan Osredkar, Lea Leonardis [14] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 Abstracts SNC’21 Plenary and Special Lectures www.sinapsa.org/SNC21 Ljubljana, Slovenia 23—25 September 2021 SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Thursday, September 23rd, 18:15 The clinical reliability of skin biopsy has been strengthened by the Can brain imaging unravel the tangled availability of normative values for both the immunohistochemistry techniques used and their comparison, and by side and short-term web of neurodegeneration? follow-up analyses. New studies expanded the panel on genes involved in small fibre neuropathy and opened new avenues for personalised therapies. Thilo van Eimeren, MD University Hospital Cologne, Multimodal Neuroimag- Friday, September 24th, 15:00 ing Group, Department of Nuclear Medicine, Cologne Proteostasis Collapse: A Basis for Ag- & Department of Neurology, University Hospital Co- logne, Cologne & German Center of Neurodegenera- ing and Neurodegenerative Diseases tive Disease (DZNE), Cologne, Germany Richard I. Morimoto, PhD Many generations after James Parkinson, Friedrich Lewy, Arnold Pick and Alois Alzheimer, neuroscientists are still facing a mystery Bill and Gayle Cook Professor of Biology, Rice Insti-about the origins and mechanisms of neurodegenerative diseases. tute of Biomedical Research, Northwestern University Every new generation holds even more sophisticated scientific tools Evanston, IL 60201 in their hands to chop away some parts of the obscurity enclosing this enigma. The investigation of histopathology and the identification of certain proteinaceous formations have paved the way to a deeper Aging is associated with the programmed decline of cell protective understanding of neurodegenerative processes. Yet, investigating stress responses and the loss of cellular proteostasis essential to the brain under the microscope after death is like seeing a still frame prevent the accumulation of misfolded and aggregated proteins com-of the end of a movie. In order to unveil the dynamic transformations mon to all neurodegenerative diseases. We have employed multiple leading up to protein pathologies, we would want to see “the whole biological systems and approaches to identify the composition of the movie”. Brain imaging, including PET imaging of molecular targets, proteostasis network (PN) that regulates protein synthesis, folding, is the ultimate and unique tool to investigate, track, and map meta-translocation and degradation, to demonstrate how the PN determines bolic, functional, molecular and structural changes over the course of the stability and function of the proteome in health and fails in aging disease development. A dynamic development that seems to start at a and diseases, and genetic and small molecule approaches to reset cross-road between various internal biological factors, live style deci-the PN and suppress aggregation and amyloid formation. sions and the exposition to external influences. Our current efforts are to identify the earliest events that predict pro-Brain imaging increasingly provides profound and novel insights in teostasis failure in neurons and other tissues. these dynamic processes from molecular changes to system failure. Cumulative evidence points to a triad of vulnerability, comprising the specific strain of misfolded protein, local cellular properties, and the Saturday, September 25th, 12:00 way brain areas are functionally and structurally connected (‘connec-Systems all the way down: studying tomics’). We may now, for the first time, truly be able to untangle the web of neurodegenerative diseases and ultimately trace the pathways mental health problems as biopsycho-back to their origins. social systems Friday, September 24th, 12:00 Eiko Fried, PhD Small fiber neuropathy Associate Professor at Leiden University, The Nether- lands Giuseppe Lauria, MD We’re not doing so well in mental health research. Despite global Università di Milano - Fondazione I.R.C.C.S., Istituto research efforts and increasing political and funding priorities, our Neurologico Carlo Besta · Clinical Neurosciences understanding of mental health problems, and our ability to treat them, Milan, Italy remain disappointing. In this talk, I sketch three reasons for the lack of progress. The first is diagnostic literalism: we may be looking at In the last five years, knowledge on small fibre neuropathy has been the wrong phenotypes. The second is reductionism: unreasonable widened by new preclinical and clinical leading to a more compre-simplifications—ranging from the Freudian unconscious to the idea hensive approach to patients in clinical practice and research. The that mental illness can be fully understood by investigating the brain— spectrum of clinical features has been widened from the classical hinder progress. The third barrier is lack of theory building and testing: presentation of burning feet as length-dependent small fibre neuropa-research efforts are largely exploratory, and few overarching, formal thy to that of small fibre dysfunction and/or degeneration associated theories or models exist. I will suggest that conceptualizing and study-with focal, diffuse and episodic neuropathic pain syndromes. The ing mental health problems as complex, biopsychosocial systems involvement of small nerve fibres in neurodegenerative diseases has offers unique opportunities, and conclude by reviewing current efforts been further defined, challenging the relationship between neuropathic to do so. pain symptoms and small fibre loss. [16] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Saturday, September 25th, 17:00 Extracellular vesicles as stress sig- nals: Identifying novel mechanisms of neurodevelopmental programming Tracy Bale Center for Epigenetic Research in Child Health & Brain Development, University of Maryland School of Medicine, Baltimore, MD, USA Extracellular vesicles (EVs) are a novel signaling mechanism involved in numerous developmental processes including the transmission of parental life experiences across generations. The protein and sncRNA content of EVs is dramatically altered by stress in mice and trauma in humans, and these changes can impact the course and rate of embryo and fetal brain development, altering adult brain function. [17] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 Abstracts SNC’21 Thematic Symposia www.sinapsa.org/SNC21 Ljubljana, Slovenia 23—25 September 2021 SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Thursday, September 23rd, 14:00 [Symposium: SARS-CoV-2 and Brain] Thursday, September 23rd, 14:00 [Symposium: SARS-CoV-2 and Brain ] Neuro-COVID - what it is and what it is Learning during the pandemic: map-not ping potential educational inequalities across Europe Raimund Helbok Medical University of Innsbruck, Department of Zsuzsa Blaskó Neurology, Neurocritical Care Unit, Anichstr.35, 6020 Joint Research Centre, European Commission Innsbruck, Austria, Europe Since the beginning of the Covid-19 pandemic there has been little Since the recognition of SARS-CoV-2 outbreak in 2019, several neu-doubt that physical school closures would lead to a substantial learn-rological manifestations have been reported. Prevalence rates largely ing loss among school children. It was also clear that the size of this vary (6-84%) and range from mild (headache, hyposmia, myalgia) to loss will vary across student groups, with the most vulnerable ones severe (encephalopathy, strokes, seizures). Recently, “Long-COVID” falling further behind. These predictions followed from our pre-existing has been recognized as novel entity and long-term neurological knowledge on how (other types of) disruptions of education can affect consequences or novel manifestations after COVID-19 have been learning progress. Over a year after the pandemic started we still reported. have only limited evidence on the actual learning consequences of the school closures. The evidence we have however is very worrying, as This talk will cover pathophysiologic aspects of “Neuro-COVID” clinical it seems to fully justify early concerns. In my presentation I will give course and longterm outcomes. an overview of existing research on the size of the Covid-19 related learning losses in Europe and the socioeconomic differences in it. Relying on our research study I will show how (in a situation of severe Thursday, September 23rd, 14:00 [Symposium: SARS-CoV-2 and Brain] data-lack) pre-Covid educational data can help to assess the relative Neurological Associations of COV-size of learning losses and the related social inequalities across the various countries of Europe. Our analyses help to identify countries ID-19 Vaccines with the biggest risk of experiencing an educational crisis due to the pandemic and call for interventions to mitigate the damage. Jennifer Frontera You can download the full paper here: https://www.iza.org/publica-tions/dp/14298/learning-loss-and-educational-inequalities-in-europe-NYU Langone Health, NY, USA mapping-the-potential-consequences-of-the-covid-19-crisis Despite widespread availability of extremely effective SARS-CoV-2 vaccines in the U.S., hesitancy related to concerns over vaccine Thursday, September 23rd, 14:00 [Symposium: SARS-CoV-2 and Brain] safety have hampered efforts to quell the COVID-19 outbreak, leading Cognitive and Neurological Conse-to a pandemic of the unvaccinated. Vaccine safety data as reported by drug companies, the FDA and the CDC illuminate the safety of quences of COVID-19 the vaccine, particularly compared to the high risks of morbidity and mortality related to COVID-19 illness itself. However, incidence rates of neurological complications from SARS-CoV-2 vaccinations have not Adrian Owen been reported. The CDC Vaccine Adverse Event Reporting System (VAERS) contains clinician and patient self-reported complications of There are now more than 160 million people in the world with COV-a variety of vaccines available in the U.S. including Pfizer, Moderna, ID-19 and 1.3 million in Canada alone. As people recover, more and and J & J SARS-CoV-2 vaccines. more are reporting cognitive challenges like problems with memory, concentrating and problem solving. These problems could be caused In this talk, we explore the incidence of neurological adverse events by many aspects of COVID-19 - from direct viral effects on the brain following SARS-CoV-2 vaccination. itself, to indirect effects due to inflammation, blood clots, low oxygen levels, sedation and spending time on a ventilator. In June 2020, we launched a global, online longitudinal study of the short and long-term cognitive sequelae of COVID-19 infection (covidbrainstudy.com). In this talk, I will present the first results from this study, which address the following questions: i) If COVID-19 infection does result in significant cognitive impairment, what cognitive domains are specifically affected? ii) Is the burden of cognitive impairment greater in those with more severe infection (i.e., those who require ICU stay or hospitalisation outside the ICU) iii) Are there interactions with sex, age and medical risk factors that result in greater impact in some populations? [19] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neuro-this purpose. However, models employing 18F FDG PET images and degenerative Disorders] longitudinal data are underdeveloped, despite potential advantages in Mechanisms of tau pathology spread- performance improvement and early detection. Our goal is to develop ing in Alzheimer’s disease and 4R a deep learning model to distinguish brain images of patients with AD from normal controls, and to interpret this model by (1) examining the tauopathies influence of longitudinal data, disease duration, and imaging modality on performance and (2) identifying regions of the brain which are most influential to the network’s decision. Nicolai Franzmeier We develop a convolutional neural network (CNN) with a cascaded recurrent neural network (RNN) for binary classification. Attention Institute for Stroke and Dementia Research, Klinikum heatmaps are output to visualize the CNN decision-making. Two sets der Universität München, Ludwig-Maximilians-Univer-of brain images and clinical data from ADNI were used for training sität LMU, Munich, Germany and testing: (1) 560 FDG PET scans from 422 patients, of which 122 have multiple timepoints with 1-2 year gaps, (2) 418 T1-weighted MRI The progressive spread of tau pathology throughout the brain is a key from 193 patients, of which 130 have multiple timepoints. We validate driver of neurodegeneration and cognitive decline across a variety of the model with an independent dataset of 104 FDG PET scans. neurodegenerative diseases including Alzheimer’s disease (AD) and ROC analysis revealed a maximum area under the curve (AUC) 4-repeat (4R) tauopathies. Thus, understanding tau spreading mecha- of 0.87±0.06. Model comparison showed that adding longitudinal nisms may be critical in order to develop tau targeting interventions. information improves classification performance over single timepoint Pre-clinical studies have emphasized that tau spreads across inter-analysis and that the PET-trained network outperforms MRI. CNN connected neurons in an activity-dependent manner, suggesting that heatmaps illuminate imaging patterns indicative of AD and move this tau spreading is an active process routed by the brains’ connectome. work toward identification of a quantitative imaging biomarker for AD Thus, we aimed to translate this concept of connectivity-mediated tau diagnosis. spreading to AD and 4R tauopathy patient data. To this end, we com-bine tau-PET imaging (i.e. Flortaucipir tau-PET in AD vs. PI2620 tau-PET in 4R tauopathies) and regional post-mortem tau-assessments Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neurodegenerative Disorders] (in 4R tauopathies) with resting-state functional MRI-based connectivity data. Across both AD and 4R tauopathies, we observe that i) func-Technical Factors Affecting Image tionally connected brain regions show correlated tau-PET levels and that ii) tau-PET deposition patterns follow the seed-based connectivity Quality in PET pattern of regions with earliest tau pathology (i.e. tau epicenters). A congruent result pattern can be detected using post-mortem tau data in 4R tauopathy patients, where functionally connected brain regions Mauro Namías(1) and Robert Jeraj(2,3) show correlated post-mortem tau levels. Using longitudinal tau-PET data in AD patients, we show further that tau spreads successively 1: Medical physics department, Fundación Centro from circumscribed tau epicenters across closely connected brain Diagnóstico Nuclear, Buenos Aires, Argentina regions, which can be used for patient-centered prediction of future 2: Department of Medical Physics, University of Wis-tau spreading. Together, our findings support a close link between consin – Madison, United States of America functional brain networks and tau spreading in AD and 4R tauopa-3: Faculty of Mathematics and Physics, University of thies, supporting the concept of connectivity-mediated tau spreading in neurodegenerative tauopathies. Ljubljana, Ljubljana, Slovenia Image quality, quantitative accuracy and reproducibility in PET imag- Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neuro-ing can be affected by different factors, such as scanner design, ac-degenerative Disorders] quisition protocols and reconstruction settings, among others. Spatial Developing and Interpreting a Deep resolution can be modeled by the modulation transfer function (MTF) of the system, while noise can be modeled by the noise power spec-Learning Model for Alzheimer’s Dis- trum (NPS). We present an image formation model based on the MTF ease Tracking and the NPS of the reconstructed images, which includes a correlated and signal-dependent noise term. A simplified and automated method-ology to estimate the MTF and NPS from cylindrical phantom scans is Alison Deatsch(1), Matej Perovnik(2,3), Rob- presented, based on previously developed quantitative harmonization techniques. The MTF is estimated from the edges of the cylindrical ert Jeraj(1,3) phantom, while the NPS is estimated from uniform regions inside 1 University of Wisconsin – Madison, Madison, WI it. In addition, a framework to simulate realistic images for complex objects like the brain, based on the resolution and noise measure-2 University Medical Centre Ljubljana, Ljubljana, ments, is also presented. The concepts of signal to noise ratio and Slovenia noise equivalent quanta will be introduced as tools to model signal 3 University of Ljubljana, Ljubljana, Slovenia detectability by an ideal observer. The impact of different reconstruction settings (voxel size, iterations, filters, etc.) and acquisition times Despite a clear clinical need, there is a lack of a comprehensive, will be presented and we will briefly discuss optimization strategies to generalizable tool for reliable diagnosis of Alzheimer’s disease (AD). improve image quality. Significant work has been done to develop deep learning networks for [20] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neuro-Conclusions degenerative Disorders] The findings show that the PDCP is a reproducible cognition-related Cognition-related functional topogra-network that is topographically distinct from the DMN. The utility of the phies in Parkinson’s disease: Local-PDCP as a network biomarker of cognitive dysfunction in PD is further highlighted by its independence of imaging platform and treatment ized loss of the ventral default mode condition. network Katharina A Schindlbeck(1), An Vo(1), Paul J Mattis(1,2), Kersten Villringer(3), Frank Mar- zinzik(4), Jochen B Fiebach(3), and David Eidelberg(1) 1 Center for Neurosciences, The Feinstein Institutes for Medical Research, Manhasset, NY 2 Department of Neurology, Northwell Health, Manhas- set, NY 3 Center for Stroke Research, Charité – Universitäts- medizin Berlin, Hindenburgdamm 30, 12200 Berlin, Germany 4 Department of Neurology, Charité – Universitäts- medizin Berlin, Hindenburgdamm 30, 12200 Berlin, Germany Background Cognitive decline, a common symptom in patients with Parkinson’s disease (PD), has been associated with stereotyped changes in normal resting state networks and cognition related networks evolving over time. We sought to determine whether functional network abnormalities seen in patients with Parkinson’s disease (PD) and cognitive decline reflect the loss of the default mode network (DMN), the gain of an abnormal network topography, or a combination of both. Methods We first analyzed 18F-FDG PET metabolic images to evaluate network expression levels in a large PD sample (n=153) with varying cognitive performance at NorthShore (NS). We then used independent component analysis to identify PD cognition-related pattern (PDCP) and DMN topographies in resting-state fMRI (rs-fMRI) data from an independent population in Berlin (n=23). The spatial relationship of the two topographies was determined at the subnetwork level. The topographies were further compared to previously described PDCP networks from NS to evaluate their consistency across cohorts, imaging platforms, and medication state. Results Cognitive impairment in PD is associated with increases in metabolic PDCP expression and reflects partial loss of DMN activity. We identified a fPDCP topography in an independent cohort scanned with rs-fMRI in the on-medication state. fPDCP_BERLIN expression correlated with verbal memory performance and was elevated in PD patients with MCI compared to their counterparts without cognitive deficits. This topography resembled the previously described PDCP_NS patterns from FDG PET and rs-fMRI data scanned in the off-medication state. The rs-MRI analysis uncovered that PDCP selectively involves the ventral DMN subnetwork (precuneus and PCC), while the anterior and posterior subcircuits of the DMN are not affected. Importantly, the PDCP goes beyond the DMN topography with activity changes in dorsolateral prefrontal and medio-temporal areas that are unrelated to the DMN space. [21] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neuro- Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neurodegenerative Disorders] degenerative Disorders] Metabolic correlates in PSP clinical Specific Metabolic Brain Patterns in subtypes Alzheimer’s dementia and dementia with Lewy bodies Gloria Martí-Andrés(1), Liza Van Bom- mel(2), Elena Prieto(1), Rafael Valentí(1), Matej Perovnik(1,2), Petra Tomše(3), Luka Laura Armengou-García(1), Mario Riverol(1), Ležaić(1,3), Maja Trošt(1,2,3) Sanne Meles(2), Rosalie Kogan(2), Remco Renken(2), Vita Gurvits(2), Teus Van Laar(2), 1 Medical Faculty, University of Ljubljana, Ljubljana, Marco Pagani(3), M Rosario Luquin(1), Slovenia Klaus Leenders(2), Javier Arbizu(1) 2 Department of Neurology, University Medical Center Ljubljana, Ljubljana, Slovenia 1 Clínica Universidad de Navarra, Pamplona, Spain. 3 Department of Nuclear Medicine, University Medical 2 University Medical Center Groningen, Groningen, Center Ljubljana, Ljubljana, Slovenia Netherlands. 3 Institute of Cognitive Sciences and Technologies, Rome, Italy. Aims: To identify dementia with Lewy bodies related pattern (DLBRP) and to investigate its relationship with previously identified Alzheimer’s Objective: To evaluate brain glucose metabolic abnormalities in dementia related pattern (ADRP). patients with a clinical diagnosis of PSP variants. Methodology: We applied a network analysis (scaled subprofile model/ Methodology: We performed a retrospective, multicenter cohort study principal component analysis - SSM/PCA) on FDG PET scans from on 73 PSP patients who were referred for a FDG-PET scan: PSP-RS 20 DLB1 and 20 normal controls (NC1) for DLBRP identification. The n=46; PSP-P n=19; and PSP-PGF n=8. We included 55 HC and 58 procedure was first performed on the unmodified subjects’ scans and PD patients as reference groups. We analyzed the regional differenc-then also on scans from which ADRP was removed by an orthogonali-es in metabolism between the groups using two analytical approaches zation. Furthermore, we removed DLBRP from ADRP. Expressions (SPM and SSM/PCA). Additionally, we obtained a PSP related pattern of newly identified DLBRP, DLBRP-orthoADRP, ADRP and ADRP- (PSPRP) and then cross-validated in independent populations at the orthoDLBRP were calculated on a validation group of 60 DLB2, 21 individual level. NC2 and 63 biomarker-confirmed AD patients. Results: Compared to HC, analyses showed relative hypometabolism Results: Expression of ADRP, characterized by reduced metabolism in the midbrain, basal ganglia, thalamus and frontoinsular cortices, in temporoparietal cortices, thalami and precuneus with relative and relative hypermetabolism in the cerebellum, sensorimotor and increases in the cerebellum and pons, was elevated in AD and DLB posterior insula cortices associated with PSP. Compared to PD, the patients. DLBRP expression, characterized by reduced metabolism in metabolic abnormalities in PSP were similar but involved more severe parietal and occipital cortices and precuneus with relative increases hypometabolism in the putamen and globus pallidus, and hypermetab- in the cerebellum and pons was significantly higher in DLB patients olism in the occipital cortices. The PSPRP obtained showed optimal compared to NC and to AD patients. DLBRP could only modestly diagnostic accuracy to distinguish between PSP and HC and between distinguish between the two dementias (AUC = 0.71). Based on the PSP and PD. Moreover, PSP-RS and PSP-P patients showed signifi-expression of DLBR-orthoADRP, characterized by reduced metabolic cantly more PSPRPs expression than PD and HC. activity in the occipital cortices and preserved metabolic activity in Conclusions: The glucose metabolism assessed by FDG-PET is a temporal cortices and posterior cingulum, we could accurately distin-useful and reproducible supportive diagnostic tool for PSP in different guish between the two groups (AUC = 0.89). Based on the expression populations and PSP variants. of ADRP-orthoDLBRP, characterized by reduced metabolic activity in temporal, parietal and frontal cortices and preserved metabolism in occipital corticies and anterior cingulate cortex we could moderately distinguish the two groups (AUC = 0.77). Conclusions: DLBRP-orthoADRP can best distinguish between AD and DLB among the studied metabolic patterns. It may reflect the metabolic pattern related to core DLB pathology, after AD related pattern was removed. [22] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Thursday, September 23rd, 16:00 [Symposium: Metabolic Brain Imaging in Neuro-more variability found in PrPsc load and activated microglia (slight degenerative Disorders] consistency). Metabolic changes significantly correlated with vacuoli-Correlations between brain metabo- zation but not with PrPsc load and activated microglia n group level. lism and neuropathology in sporadic However, multivariate mixed model analysis showed significant linear relationship between brain metabolism and vacuolization (p<0.0001), Creutzfeldt-Jakob disease activated microglia (p=0.004) and nonsignificant relationship with PrPsc load (p=0.07). Conclussion: Our study confirms robust changes in brain metabolism in CJD largely independent of special distribu-Tomaž Rus (1,2), Jernej Mlakar (3), Mara tion of pathological changes. These findings indicate an existence of Popović (3), Luka Ležaić (4), Milica Kram-robust metabolic brain network specific for CJD despite pathological berger (1,2), Zvezdan Pirtošek (1,2), Maja and clinical variability consistent with previous reserch. Trošt (1,2,4) Friday, September 24th, 13:00 [Symposium: Deep Brain Stimulation for movement 1 Medical Faculty, University of Ljubljana, Ljubljana, disorders – A neuroimaging perspective] Slovenia Non-motor symptoms in Parkinson’s 2 Department of Neurology, University Medical Center Ljubljana, Ljubljana, Slovenia disease and Dystonia: Neuroimaging 3 Institute of Pathology, Medical Faculty, University of perspective Ljubljana, Ljubljana, Slovenia 4 Department of Nuclear Medicine, University Medical Vladimira Vuletić Center Ljubljana, Ljubljana, Slovenia Clinical Department of Neurology, University Hospital Backgrounds: Sporadic Creutzfeldt-Jakob’s disease (CJD) is a Rijeka, Rijeka, Croatia progressive neurodegenerative disorder characterized by rapidly progressing dementia with additional neurological signs. Final diagnosis Our aim was to see the effect of Deep brain stimulation (DBS) on is possible only by pathohistological examination of brain tissue which nonmotor symptoms in patients with dystonia and Parkinson’s disease is obligated by law in case of any clinical suspicion. Due to short dis- (PD). ease duration and availability of final pathological diagnosis CJD may We conducted investigation with anamnesis and treatments’ data, be considered an in vivo model of neurodegeneration. The aim of our Pittsburgh Sleep Quality Index (PSQI), ), PD Questionnaire-39, Par-study was to correlate brain metabolism measured by FDG-PET in a kinson’s disease sleep scale (PDSS), Visual Analogue Scale, McGill living CJD patient with histopathological changes post mortem. Meth-questionnaire and Hospital Anxiety and Depression Scale (HADS), ods: 16 CJD patients and 16 normal controls (NC) underwent brain Montreal Cognitive Assessment (MoCA) and Mini Mental State FDG-PET imaging. Images were spatially normalized and smoothed Examination (MMSE), 36-Item Short Form Health Survey (SF-36), in SPM5 software and region-of-interest analysis was performed using Functional Independence Measure (FIM) instrument, Unified Parkin-MarsBar toolbox for SPM. Twelve strategic regions (on the left side) son Disease Rating Scale (especially motor score and activities of were chosen based on previous research. Each region was indepen-daily living) (UPDRS), Burke-Marsden-Fahn Dystonia Scale (BMFDS). dently standardized (z-scored) according to NC. In all 16 CJD patients The study involved 30 patients with dystonia and 100 patients with final diagnosis was confirmed at pathohistological examination. At PD treated by DBS. We did the basal testing before treatment and autopsy brain samples were obtained from the same twelve strategic another investigation after 6 months. regions, paraffin embedded and histologically (hematoxylin-eosin; HE) or immunohistochemically processed (IHC; using anti-PrP12F10 After DBS in dystonia patients we observed significant decrease in antibody against PrPsc protein and anti-HLA-DR antibody to detect frequency concerning sleep problems (from 80% to 10% of patients), activated microglia). All the HE samples (16 x 12) were examined for anxiety (from 50% to 30%), depression (from 56% to 25%) and pain vacuolization and subjectively scored by three independent examin- (from 90% to 25%) (p< 0.05). The cognition was without any change ers according to the number of vacuoles (estimated 0-3). All the IHC in all patients (16% vrs 17%). samples (16 x 12 samples treated with anti-PrP12F10 antibody and 16 In PD patients we found a significant reduction in frequency concern-x 12 samples treated with anti-HLA-DR antibody) were assessed for ing pain (from 70% to 45%, p<0.05)), sleep problems (from 60% PrPsc load and activated microglia by three independent examiners to 35%, p<0.05) and anxiety (from 75% to 45%, p<0.05) but in (estimated 0-3) and with automated machine-learning-based analy-cognition (from 30% to 27%) and depression (45% to 35%) was not sis of high-resolution scans of IHC samples using QuPath software significant after DBS. (University of Edinburg). Agreement among the three examiners was evaluated using single score intraclass correlation method using irr DBS helps in relieving of the pain, sleep and mood problems in package run in R software. We investigated consistency of metabolic dystonia and PD patients what improved their quality of life. Further and pathologic changes in CJD patients (single score intraclass cor-randomized studies are needed to confirm these findings. relation analysis), correlated brain metabolism with pathohistological changes on group level and built multivariate mixed linear models to investigate relationship between brain metabolism and pathological changes on a single subject level. Results: Examiners achieved good agreement for HE, PrP12F10 and HLA-DR analysis. While there was a substantial consistence in brain metabolism in selected brain regions among CJD patents, vacuolization (HE changes) was more variable (fair consistency in vacuolization of regions) and there was even [23] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Friday, September 24th, 13:00 [Symposium: Deep Brain Stimulation for movement with motor symptoms of PD. Less is known about the mechanisms disorders – A neuroimaging perspective] underlying non-motor and cognitive manifestations of the disease, The effect of Deep Brain Stimulation which might depend on structural decline of distinct grey matter areas on Brain Metabolism in Movement as well as functional alterations of distributed brain networks. In this presentation, we will discuss some neuroimaging correlates and pre-Disorders dictors of PD symptoms with an emphasis on brain network measures. Further, we will examine cases where focal lesions in various brain locations lead to parkinsonism to establish a role of a distributed brain Maja Trošt network in parkinsonism. Next, we will turn to treatment with deep-brain stimulation which - through affecting a single network node – Department for Neurology and Department for Nuclear impacts the whole-brain network. Finally, we will discuss how network Medicine UMC Ljubljana imaging approaches can be utilised to guide treatment with deep-brain Medical Faculty, University of Ljubljana stimulation. Deep brain stimulation (DBS) is a neuromodulation therapy routinely used as a non-pharmacological treatment of patients with a variety of Friday, September 24th, 13:00 [Symposium: Deep Brain Stimulation for movement disorders – A neuroimaging perspective] neurological and psychiatric disorders. Frequency modulation in deep brain Brain glucose metabolism is a proxy of synaptic activity and can be stimulation: Does it work and is there evaluated with FDG PET, which enables clinicians to improve early differential diagnosis, monitor disease progression, assess treatment neuroimaging proof of its action? effects, and predict functional recovery of novel experimental therapies. FDG PET can also provide neuroimaging correlates of clinical response to DBS and offer an insight on mechanisms of action of DBS Dejan Georgiev treatment. Department of Neurology, University Medical Centre Movement disorders represent a variety of neurodegenerative Ljubljana, Ljubljana, Slovenia diseases with progressive motor and cognitive dysfunction involving cortico-striato-pallido-thalamocortical (CSPTC) circuits. A disease Deep brain stimulation (DBS) of the subthalamic nucleus (STN-DBS) specific metabolic brain patterns have been identified by the network and globus pallidus pars interna (GPi-DBS) are now well-established analysis of FDG PET images. For example, Parkinson’s Disease Re-treatment options for movement disorders, including Parkinson’s lated Pattern (PDRP), which was associated with motor features and disease (PD) and dystonia. Even though there is no doubt in the long-Parkinson’s Disease Tremor Pattern (PDTP) associated with tremor in term clinical benefits of the STN-DBS in PD patients and GPi-DBS in PD. Both patterns reflect widely distributed network abnormality in the dystonia there are certain side effects of DBS, such as gait abnor-CSPTC and cerebello-thalamo-cortical pathways respectively. Studies malities, postural instability, falls, dysarthria in PD and parkinsonian have shown that DBS of STN and GPi suppresses the expression of symptoms in dystonia. PDRP. Further, PDRP expression was reduced with STN DBS but not with Vim DBS. On the other hand, PDTP network activity declined in Frequency of stimulation (FS), in addition to other parameters (ampli-both Vim and STN DBS groups, however greater PDTP modulation tude, pulse width, contact configuration), has been shown to have an was achieved with Vim DBS. important impact on certain clinical aspects of PD and dystonia. FS, unlike the other parameters, has a more specific mechanism of action. These are only few examples of how FDG PET and the applied Namely, while high frequency stimulation (HFS, > 100 Hz) is usually network analytical approaches evaluate DBS related changes in brain effective in controlling the appendicular symptoms of the disease metabolism. (bradykinesia, tremor, rigidity), it can often worsen axial symptoms (gait, postural instability, dysarthria). Low frequency stimulation (LFS, < 100 Hz) might be beneficial for the treatment of these symptoms. Friday, September 24th, 13:00 [Symposium: Deep Brain Stimulation for movement Only few studies have explored the effect of LFS in dystonia patients, disorders – A neuroimaging perspective] which suggest that LFS might be beneficial in the treatment of the Parkinson’s disease as a network main symptoms in dystonia. However, the results of the studies in disorder: Lessons from connectivity both, PD and dystonia are inconsistent, the methodologies used differ, and the mechanisms of LFS action are not clear. In addition to making studies an overview of the clinical aspects of the use of LFS in DBS for movement disorders, in this presentation we will also focus on the possible mechanisms of of LFS with an emphasis of the use of imaging in the Rok Berlot study of LFS mode of action. Department of Neurology, University Medical Centre Ljubljana The link between the cardinal motor symptoms of Parkinson’s disease (PD) and progressive degeneration of dopaminergic neurons in the nigrostriatal pathway has been firmly established. However, neuroimaging studies suggest that activity in multiple brain regions correlates [24] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Friday, September 24th, 13:00 [Symposium: Deep Brain Stimulation for movement treatment on language skills. To reach this goal, various language disorders – A neuroimaging perspective] tasks in Slovenian language as well as structural and functional brain Impulsivity in STN-DBS PD: More than imaging will be applied to PD patients treated with standard treatment a unitary phenomenon and STN DBS. Liu Y, Li W, Tan C, et al. Meta-analysis comparing deep brain stimulation of the globus pallidus and subthalamic nucleus to treat advanced Tjaša Mlinarič, Dejan Georgiev Parkinson disease. J Neurosurg. 2014; 121 (3): 709–18. Lozano AM, Lipsman N, Bergman H, et al. Deep brain stimulation: Department of Neurology, University Medical Centre current challenges and future directions. Nat Rev Neurol. 2019; 15: Ljubljana, Ljubljana, Slovenia 148–160. Cernera S, Okun MS, Gunduz A. a review of cognitive outcomes Along with the obvious motor problems, patients with Parkinson’s across movement disorder patients undergoing deep brain stimulation. disease (PD) develop a number of non-motor deficits, which challenge Front Neurol. 2019; 10: 419. their daily activities. Impulsive behaviors are common non-motor com-Smith KM, Caplan DN. Communication impairment in Parkinson’s plications in PD patients, and they are usually attributed to the treat-disease: Impact of motor and cognitive symptoms on speech and ment of PD. Both dopaminergic medication and deep brain stimulation language. Brain Lang. 2018; 185: 38–46. of the subthalamic nucleus (STN-DBS) have been previously shown to Silveri MC, Ciccarelli N, Baldonero E, et al. Effects of stimulation of affect impulsivity in several domains. the subthalamic nucleus on naming and reading nouns and verbs in Parkinson’s disease. Neuropsychologia. 2012; 50 (8): 1980–9. The aim of our study was to establish how three impulsivity domains Phillips L, Litcofsky KA, Pelster M, et al. Subthalamic nucleus deep are affected in patients with PD relative to dopaminergic medication brain stimulation impacts language in early Parkinson’s disease. PLoS and STN-DBS treatments. To answer this question, we assessed One. 2012; 7 (8): e42829. patients with PD and healthy controls on different impulsivity measures in several conditions. With our research, we hoped to disentangle between different effects of medication and STN-DBS treatment on Saturday, September 25th, 13:00 [Symposium: Music and Brain: Evidence-based impulsivity and to contribute to the understanding of the post-treat-music interventions in medicine] ment functioning of PD patients in their daily living. Neurology of Music and Brain Friday, September 24th, 13:00 [Symposium: Deep Brain Stimulation for movement disorders – A neuroimaging perspective] Daniele Schoen, PhD Effects of subthalamic nucleus deep Aix-Marseille University, France brain stimulation on language in ad- vanced Parkinson’s disease How does the brain work? No one knows. What is certain is that it allows us to interact with the world. A dynamical system perspective, with complex oscillatory dynamics visible in the cerebral rhythms, Živa Drakulić1, Christina Manouilidou2, Maja may allow to explain how the brain quickly adapts to the external ever-changing context. Nevertheless, the brain does not process Trošt1 the entire sensory experience, but rather the difference between the input and an internal model of the world. Our priors about the world 1 Department for Neurology, UMC Ljubljana, Slovenia become very important. Changing priors will change our perception 2 Department of Comparative and General Linguistics, of the world. Music is a good model to address the coupling between Faculty of Arts, University of Ljubljana, Slovenia brain activity and the surrounding world. It is temporally and spectrally structured and it requires to anticipate with precision in time (rhythm) Deep brain stimulation of subthalamic nuclei (STN DBS) is an and in content (harmony) as well as to flexibility and quickly adapt to established surgical treatment for motor symptoms in advanced changes. In this perspective, music making, by modifying the oscilla-Parkinson’s disease (PD). The improvement of motor function as tory properties of complex neural networks, may improve the ability to measured by Unified Parkinson’s disease rating scale (UPDRS) has anticipate, which in turn will affect other cognitive nonmusical skills. been consistently determined after STN DBS (1). However, the effects of STN DBS on cognitive and other non-motor functions are less studied and its mechanisms of action are still poorly understood (2). PD and STN DBS treatment can both impair language (3, 4). Various language domains seem to be altered in PD: speech, processing of syntax and grammar, production, fluency, action words, pausing and non-verbal communication (4). On the other hand, STN DBS might cause cognitive adverse events such as worsened verbal fluency, executive dysfunction and decreased attention. These may all impair language processing and production in PD patients (3). Other studies have shown that STN DBS improves language processing, such as performance in lexical decision and naming tasks for action related words (5–7). We plan to determine specific domains of language dysfunction in PD patients, its mechanism, and the effect of STN DBS [25] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Saturday, September 25th, 13:00 [Symposium: Music and Brain: Evidence-based different genres (classical music, baroque music, Gregorian chants music interventions in medicine] and ambiental music), 2) participant self-selected music and 3) silent The mother’s voice, singing and control. Music chosen by the participants varied greatly compared speaking, as a special tool for early to preselected music chosen by the researchers in terms of tempo, genre and elicited arousal. Participants reported self-selected music interventions in the NICU to be more pleasant than music chosen by the researchers. Listening to music (reactivity phase) showed a trend in decreasing activity of the parasympathetic (vagal) ANS function when compared to baseline Manuela Filippa, PhD conditions (resting HRV) or when compared to control protocol (silence). Notably, HRV parameters, indicating higher parasympathetic University of Geneva, Switzerland (vagal) tonus in the recovery phase after music listening, increased significantly when compared to the reactivity phase during music It is now clearly established that the environment and the sensory listening. Music listening has future perspectives as a simple non-stimuli, particularly during the perinatal period, have an impact on pharmacological method to modulate the listener’s ANS function in a infant’s development. During the last trimester of gestation, activity-clinical setting. dependent plasticity shapes the fetal brain, and prematurity has been shown to alter the typical developmental trajectories. In this delicate period, preventive actions aiming at modulating these developmen- Saturday, September 25th, 15:00 [Symposium: Brain health across the lifespan – Findings from the Lifebrain project] tal trajectories through activity-inducing interventions are currently underway to be tested. Our purpose is to describe the potentialities Ageing and brain imaging in Lifebrain of early vocal contact and music for supporting the preterm infant’s development, and their potential beneficial effect for example on pain protection. Klaus P. Ebmeier for Lifebrain Consortium Scientific evidence supports a behavioral orientation of the newborn Department of Psychiatry, University of Oxford, UK to organized sounds, such as those of voice and music, and recent neuroimaging studies further confirm full cerebral processing of music While classical mechanisms underlying Alzheimer pathology have not as multisensory stimuli. However, the impact of long-term effects of been generating effective interventions, a more broad-based approach music exposure and early vocal contact on preterm infants’ long-term to biological markers of cognitive deterioration is of interest. Similarly, neurodevelopment needs be further investigated. Research projects relatively non-specific exposures, such as to risk factors for vascu-are currently on the way to fill this gap in knowledge. lar disease and metabolic syndrome or diabetes appear to predict development of degenerative dementia. The Lifebrain Consortium consists of European Cohort Studies, including approximately 8000 Saturday, September 25th, 13:00 [Symposium: Music and Brain: Evidence-based MRI scans in 5000 participants [1]. Brain measurements have been music interventions in medicine] used to predict chronological age, using the residual of the regres-Heart rate variability in relation to self- sion to define a “brain age gap”, defining the individual brain as either selected music or music genres pre-biologically older or younger than its chronological age. “Brain age” suggests a dynamic process, capturing the speed of aging. However, selected by the researchers Lifebrain data have shown that brain age relates to early life factors, such, as birth weight and polygenic scores, but not to accelerated brain aging [2]. Similarly, educational attainment which is often related Uroš Kovačič, MD, PhD, and Maja Derlink, to cognitive or “brain reserve”, appears not to influence brain ageing PhD [3]. In contrast, education was positively related to intracranial (ICV) and total brain grey matter (GM) volume in US and European cohorts, Institute of Pathophysiology, University of Ljubljana, while socioeconomic stratum or income was more strongly related to Faculty of Medicine, Zaloška 4, Ljubljana, Slovenia brain and cognition in US than European cohorts [4]. 1. Walhovd KB, Fjell AM, Westerhausen R, et al. Healthy minds Listening to music is a complex phenomenon, involving psychological, 0-100 years: Optimising the use of European brain imaging co-emotional and physiological responses, such as heart contractility, horts ("Lifebrain"). Eur Psychiatry 2018;50:47-56. DOI: heart rate, heart rate variability (HRV), blood pressure and respiratory 10.1016/j.eurpsy.2017.12.006. rate. HRV, variation in interbeat intervals, is a measure of autonomic 2. Vidal-Piñeiro D, Wang Y, Krogsrud S, et al. “Brain age” relates to nervous system (ANS) activity. Some HRV parameters can be used early life factors but not to accelerated brain aging. BioRxiv 2021. as an index of cardiac vagal tone. Previous studies of physiological 3. Nyberg L, Magnussen F, Lundquist A, et al. Educational attainment effects elicited by different music genres show that tempo affects the does not influence brain aging. Proceedings of the National Academy arousal, whereas major/minor mode affects mood. Nevertheless, of Sciences of USA (in press) 2021. due to application of very heterogeneous musical stimuli in different 4. Walhovd KB, Fjell AM, Wang Y, et al. Education and income show studies, there is inconsistency when the effects of specific musi-heterogeneous relationships to lifespan brain and cognitive differences cal stimuli on ANS are being determined along with corresponding across European and US cohorts. bioRxiv 2020:2020.10.12.335687. cardiovascular changes. Our aim was to measure the effects of music DOI: 10.1101/2020.10.12.335687. listening on the modulation of ANS via measurement of HRV. Healthy adult volunteers were exposed to music listening via headphones in a supine position. Each person participated in three recording sessions, with distinct protocols: 1) preselected music comprised of four Saturday, September 25th, 15:00 [Symposium: Brain health across the lifespan – Findings from the Lifebrain project] [26] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 What can blood biomarkers tell us Saturday, September 25th, 15:00 [Symposium: Brain health across the lifespan – Findings from the Lifebrain project] about the brain? Brain asymmetry in aging and Alzhei- mer’s disease Christian A. Drevon & Thomas E. Gundersen Vitas Ltd. Oslo Science Park, Gaustadalléen 21, 0349 James M. Roe Oslo, Norway Department of Psychology, University of Oslo, Norway Several hundred markers of diet, inflammation, and some risk factors of disease are analyzed by Vitas Ltd – a Norwegian contract labora-Aging and Alzheimer’s Disease (AD) are accompanied by large-scale tory, which is member of the Lifebrain consortium. Vitas has exten-alterations in brain organization, and brain changes accelerated in sive experience with most types of biological material also collected AD may occur gradually over the lifespan – suggesting dimensionality on dried blood spots (DBS) making sampling much cheaper, more between aging and AD. Although structural asymmetry is an organ-convenient and applicable in the field. Combining biomarkers from izing feature of the cerebral cortex, it is not known whether or how blood, brain imaging and cognitive tests may provide new approaches continuous age- and AD-related cortical degradation alters cortical to brain biology. asymmetry. Thus, the foundational question of whether and where the cerebral hemispheres atrophy at different rates in aging and AD It is not surprising that several well-known markers of cardiac health remains open. also seem to be relevant for brain health. Thus, blood lipids like essential fatty acids, cholesterol and triacylglycerols, and glucose Applying novel analyses in Lifebrain’s longitudinal adult lifespan and vitamin D3, are associated with anatomical as well as functional cohorts, we uncover a new principle of brain aging, and find evidence aspects of the brain. From some preliminary data it seems to be a link to suggest that brain changes in normal aging and AD may at least between a certain class of lipids named diacylglycerols and sleep, partly exist on a continuum – highlighting the importance of lifespan although it turns out to be much more complicated than expected from perspectives for understanding the pathophysiology of AD. a few previously published studies. Saturday, September 25th, 15:00 [Symposium: Brain health across the lifespan – Findings from the Lifebrain project] What is brain health? Perceptions of respondents to the Global Brain Health Survey Isabelle Budin-Ljøsne for Lifebrain Consor- tium Department of Genetics and Bioinformatics, Norwe- gian Institute of Public Health, Oslo, Norway Brain health has recently been launched as a concept encompass-ing brain integrity, mental health and cognitive health. Maintaining a healthy brain is essential for individual well-being and functioning. The Global Brain Health Survey collected data about people’s perceptions of brain health, and willingness to take care of their brain by adopting new lifestyles [1]. The survey was conducted online and translated into 14 languages and collected 27,590 responses from 81 countries. In this talk, survey results on how respondents perceived the concept of brain health will be presented, with particular focus on results relating to: (1) factors respondents believed to influence brain health, (2) life periods considered important to look after one’s brain, and (3) diseases and disorders associated with the brain. Differences between demographic groups will be investigated and implications for health policy raised. Preliminary insights into which actions respondents are willing to undertake to maintain a healthy brain will also be presented. [1] Budin-Ljøsne I, Friedman BB, Suri S, et al. The Global Brain Health Survey: Development of a Multi-Language Survey of Public Views on Brain Health. Front Public Health. 2020 Aug 14;8:387. doi: 10.3389/ fpubh.2020.00387. [27] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 Abstracts SNC’21 Posters www.sinapsa.org/SNC21 Ljubljana, Slovenia 24—25 September 2021 SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Friday, September 24th, 11:00 [Poster section: Short Oral Presentations Session I] Friday, September 24th, 11:00 [Poster section: Short Oral Presentations Session I] Effect of repetitive transcranial mag- The Alzheimer’s Disease Assessment netic stimulation on language per- Scale–Cognitive Subscale (ADAS- formance in Alzheimer’s Disease: a Cog): standardisation of Slovenian Slovene-speaker case study version Georgia Roumpea (a), Katarina Marjanovič Janina Ulbl, Martin Rakusa (a), Tjaša Mlinarič (b), Zvezdan Pirtošek (b), Jure Bon (c), Christina Manouilidou (a) Department of Neurology, University Medical Centre Maribor, Slovenia (a) Department of Comparative and General Linguis- tics, University of Ljubljana, Ljubljana, Slovenia. (b) Introduction: number of patients with Alzheimer’s disease rapidly Department of Neurology, University Medical Centre, increases worldwide. ADAS-Cog is an eleven-task screening tool Ljubljana, Slovenia. (c) Psychiatric Clinic, Ljubljana, developed for detecting early cognitive changes due to Alzheimer’s disease. A higher total score correlates with more significant cogni-Slovenia. tive impairment. Our study aim was to standardise ADAS-Cog for the Slovenian population. We investigated the effect of repetitive transcranial magnetic stimula-Methods: we included 84 cognitively unimpaired people who were tion (rTMS) on production of simple and derived words, and lexical tested with the Slovenian version of ADAS-Cog. Descriptive statistics decision in a Slovene-speaker with AD. rTMS has been found to have for demographic data, score on each ADAS-Cog task, and total score positive effects on naming in AD, but while previous studies have fo-were calculated. Mean values for each task and total score were com-cused on the dissociation between objects and verbs, deverbal forms pared between sexes and people younger or older than 65 years. In (agent bralec ‘reader’ and process branje ‘reading’ nominalizations) the end, we create a linear model between the ADAS-Cog total score have not been examined. Moreover, to our knowledge, the effect of and sex, age, and years of education. rTMS on accuracy and reaction time (RT) on lexical decision task, as Results: mean age was 67.3 (SD 11.1) years, mean years of educa-well as accuracy in derivation task, is addressed for the first time in tion 12.5 (SD 2.8) years, and mean total score 7.4 (SD 2.3) points. the rTMS in AD literature. Intervention: high-frequency rTMS over the There were no differences between sexes in demographic data or DLPFC bilaterally for 3 weeks (5/week). Method: naming, derivation ADAS-Cog score at a single task or in total. A significant difference by definition, online and offline lexical decision tasks. Participant: one was found in the total score between younger and older participants female diagnosed with mild AD. Results: Participant’s average ac- (5.9; SD 1.6 vs 8.2 SD 2.3). With linear regression, we found that the curacy was slightly increased at the post-treatment evaluation on both total score was significantly influenced by age (B=0.138, p<0.001) naming (80% vs. 90%) and offline LDT (93% vs. 96%) tasks. Regard-and years of education (B=-0.236, p=0.018). ing the naming conditions, a high increase in the accuracy was mainly Conclusion: we standardised ADAS-Cog for the Slovenian population. observed in the categories of agent and process nominalizations (75% The total score for cognitively unimpaired people is relatively low and vs. 95%; 60% vs. 90%, respectively). On the derivation task, a slight is following similar studies. However, older people with lower educa-decrease was observed in participant’s performance post-treatment tion may achieve lower scores than the rest of the population. (97 % vs. 91%). Participant’s accuracy in the online LDT was highly increased post-treatment (73% vs. 95%) and her average RT was im-Keywords: Alzheimer’s disease, cognitive impairment, cognitive tests proved (2281ms vs. 1445ms). Discussion: rTMS appears to improve accuracy in naming and LDT tasks. It also positively influenced LDT latency by speeding RT. Further research is needed for more accurate results. Keywords: rTMS, Alzheimer’s disease, naming, derivation, lexical decision [29] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Friday, September 24th, 11:00 [Poster section: Short Oral Presentations Session I] Friday, September 24th, 11:00 [Poster section: Short Oral Presentations Session I] DNA methylation of candidate genes Expression of Na+,K+-ATPase isoen- BDNF and COMT in Alzheimer’s dis- zymes and myokines in cultured hu- ease man myotubes innervated by rat spi- nal cord explants Matea Nikolac Perković1, Katarina Kouter2, Dubravka Švob Štrac1, Mojca Katrašnik2, Vid Jan1, Katarina Miš1, Natasa Nikolic2, Suzana Uzun3,4, Oliver Kozumplik3,4, Ni- Klemen Dolinar1, Metka Petrič1, Andraž noslav Mimica3,5, Nela Pivac1, Alja Videtič Bone1, G. Hege Thoresen2,3, Arild C. Paska2 Rustan2, Tomaž Marš1, Alexander V. Chiba- 1 Laboratory for Molecular Neuropsychiatry, Division lin4,5, Sergej Pirkmajer1,* of Molecular Medicine, Ruder Boskovic Institute, HR- 1: Institute of Pathophysiology, Faculty of Medicine, 10000 Zagreb, Croatia. University of Ljubljana, Ljubljana, Slovenia 2: Section 2 Medical Center for Molecular Biology, Institute of for Pharmacology and Pharmaceutical Biosciences, Biochemistry and Molecular Genetics, Faculty of Department of Pharmacy, University of Oslo, Oslo, Medicine, University of Ljubljana, SI-1000 Ljubljana, Norway 3: Department of Pharmacology, Institute of Slovenia. Clinical Medicine, University of Oslo, Oslo, Norway 3 University Psychiatric Hospital Vrapce, HR-10090 4: National Research Tomsk State University, Tomsk, Zagreb, Croatia Russia 5: Department of Molecular Medicine and 4 School of Medicine, Josip Juraj Strossmayer Univer- Surgery, Integrative Physiology, Karolinska Institutet, sity of Osijek, HR-31000 Osijek, Croatia Stockholm, Sweden *Presenting/corresponding author 5 University of Zagreb Medical School, HR-10000 Zagreb, Croatia Na+,K+-ATPase (NKA), a heterodimeric (α/β) ion pump and P-type ATPase, maintains transmembrane ion gradients and is essential For diagnosis of Alzheimer’s disease (AD) there are currently no for skeletal muscle excitability and contractility. Denervation reduces validated biomarkers which can be used to accurately diagnose or to the NKA content in skeletal muscle, while reinnervation increases distinguish it from other dementia-causing neuropathologies. Tests it. Primary human myotubes, a widely used model to study human based on molecular-genetic biology analysis are only entering the skeletal muscle in vitro, are most commonly cultured without the routine clinical practice, but are as are other clinical tests, relevant presence of neurons and typically do not contract spontaneously. We only after the disease has already made considerable progress. Epi-have recently examined1 whether the myotubes innervated by motor genetic alterations, like DNA methylation, have been implicated in the neurons from the embryonic rat spinal cord explants expressed higher pathogenesis of different human diseases, including AD. levels and/or a different pattern of NKA subunits (α and β) compared In our study we applied contemporary methods (next generation with the aneurally cultured myotubes. The auxiliary (regulatory) sequencing, droplet digital PCR) and determined methylation status subunits of NKA (FXYD1 and FXYD5) as well as myokines, which are of AD candidate genes, COMT and BDNF, in white blood cells and regulated by contractions, were also assessed. Myotubes innervated circulating cell-free DNA (cfDNA) from plasma in clinically well-defined by rat spinal cords started to contract within 7-10 days, and had higher AD patients and subjects with mild cognitive impairment (MCI). mRNA levels of myokines, such as IL-6, IL-7, IL-8, and IL-15, after Using PCR-amplicon library preparation approach, we sequenced 9 10-11 days of co-culture. The mRNA expression of NKA, FXYDs, amplicons residing in BDNF gene and 3 amplicons residing in COMT and myokines, such as musclin, cathepsin B, meteorin-like protein, gene, covering 169 and 62 CpG sites, respectively. Changes were or SPARC, remained similar between the innervated and aneural observed for both genes. Biggest change was observed in two BDNF cultures. In 21-day-old co-cultures the protein abundance of NKAα1, amplicons (BDNF_3 and BDNF_9), located at the CpG islands in the NKAα2, FXYD1, and phospho-FXYD1(Ser68) was increased, while promoter region and in the first intron of the BDNF gene. On average, the mRNA levels of NKA subunits and myokines were similar to those we observed lower levels of methylation in both BDNF amplicons in in the aneural cultures. Suppression of the neuromuscular transmis-patients with AD compared to subjects with MCI. sion with α-bungarotoxin or tubocurarine did not alter the NKA or Our results suggest that further search for epigenetic marks of AD not FXYD mRNA expression. Collectively, our results show that gene only in the central nervous system, but also on the periphery, could expression of NKA isoenzymes in cultured human myotubes does not provide some more information on molecular-genetic background of depend on innervation. this complex disorder. 1:Jan et al. PLoS One. 2021;16(2):e0247377. Keywords: Alzheimer’s disease, epigenetics, DNA methylation, BDNF, COMT Keywords: Na+,K+-ATPase, FXYD, cultured human myotubes, in vitro innervation, myokines [30] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Saturday, September 25th, 11:00 [Poster section: Short Oral Presentations Session Saturday, September 25th, 11:00 [Poster section: Short Oral Presentations Session II] II] Role of PDGFRα - Integrin interac- HMGB1 inhibition attenuates lipopol- tions in Anoikis resistance mediated ysaccharide (LPS)-induced neuroin- glioblastoma progression flammation, cognitive dysfunction and sickness behavior Pampa Pain, Dr Prakash P. Pillai Division of Neurobiology Devlina Ghosh1, Aditi Singh1, Alok Kumar3, Department of Zoology Neeraj Sinha2 Faculty of Science 1Amity Institute of Biotechnology, Amity University The Maharaja Sayajirao University of Baroda Uttar Pradesh, Lucknow Campus, Gomti Nagar Exten- Vadodara, Gujarat - 390002 India sion, Lucknow 226028, India 2 Centre of Biomedical Research, SGPGIMS-Campus, Glioblastoma Multiforme (GBM) is a highly aggressive and invasive Raibareli Road, Lucknow 226014, India. solid tumor which occurs in the cerebral hemispheres of the Human brain. GBM tumor has a unique property of metastasizing to distant re- 3 Department of Molecular Medicine and Biotechnol-gions in the brain itself through anchorage independent growth, which ogy, Sanjay Gandhi Postgraduate Institute of Medical induces anoikis resistance phenomena. Anchorage in cells is facili-Sciences (SGPGIMS), Lucknow, India. tated by many cell-cell and cell-ECM interacting proteins and one such family of proteins are Integrins, which are upregulated in many solid Glycyrrhizin (GL), a natural component extracted from licorice (Glycyr-tumors. Interestingly, Integrins are found to be upregulated in GBM rhiza glabra) root/rhizomes, is an antagonist of HMGB1. Chemically a cells as well, and specifically involved in maintaining cell-cell interac-triterpene glycol, GL has been administered in traditional clinical prac-tion even in anchorage independent condition leading to cell survival tices as an anti-inflammatory/antiviral since ages to treat chronic hep-and proliferation. Moreover, Integrins also interact with Growth Factor atitis cases. Recent studies have shown that GL binds directly to box receptors, majorly receptors which belong to Tyrosine kinase family A and box B of HMGB1 while inhibiting its chemotactic and mitogenic in regulating cell survival and proliferative pathways in solid tumors activity. It has been found that GL reduces the level of oxidative stress including GBM. RTK proteins such as PDGFR-α, a type of PDGFR by increasing the level of antioxidants and reducing the oxidation in (Platelet Derived Growth Factor Receptor), is overexpressed in most case of focal cerebral ischemia. However that partly answers the anti-aggressive and invasive subtypes of GBM i.e., Proneural and Mesen-inflammatory property associated with GL, in our study we found that chymal and leads to upregulation of the cell survival and proliferative that GL attenuates the adverse effects of neuroinflammation/sickness pathways. In GBM, there is an upregulation of cholesterol synthesis, behavior and improves the functional outcome. We demonstrate that which leads to the increase in formation of transient membrane rafts in vitro and in vivo LPS stimulated subjects show extensive release of known as lipid rafts. These rafts structures, sequesters Integrins and nitrite, an inflammatory signal, while the same subjects when treated RTKs and elevate the expression of proteins involved in downstream with GL, show significant reduction in nitrite release indicating neuroin-signaling of cell survival and proliferative pathways. However, it is not flammatory regulation. In accordance, the secretion of reactive oxygen quite well understood how these lipid rafts are playing an important species is also dropped when LPS induced cells are exposed to GL. role in Anchorage independent induced Anoikis resistance regulated Furthermore, the release of proinflammatory cytokines in LPS induced by PDGFR-α-Integrin interaction in inducing cell survival mechanism. BV2 cells as well as mice model, takes a plunge in presence GL thus regulating the microglia proinflammatory response. Our behavioral study support the fact that GL treatment improves the cognitive func-Keywords: Anoikis resistance, PDGFR-AA, Integrins and Glioblas-tion while reducing anxiety/ depressive symptoms in LPS induced toma Multiforme neuroinflammatory mouse model. Thus targeting HMGB1 using GL, presents a promising therapeutic possibility for regulating neuroinflammatory response and improving the outcome in neurobehavioral dysfunction. Keywords: Glycyrrhizin, neuroinflammatory response, proinflammatory cytokines [31] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Saturday, September 25th, 11:00 [Poster section: Short Oral Presentations Ses- Saturday, September 25th, 11:00 [Poster section: Short Oral Presentations Session II] sion II] Educated vs. lay public view of neu- Physicians’ standpoints for the use of roscience and science based brain music-based interventions in Slove- health recommendations in Slovenia nian health care system Matej Perovnik (1,2,3), Nastja Tomat (1, 4), Ana Kuder, Manca Kok, Saška Rakef, Igor Gaj Vidmar (3, 5, 6), Vesna Van Midden (1, 2), Mihael Ravnik Sara Fabjan (1, 7), Hana Hawlina (1), Dolores Trol (1), Alina Holnthaner (1), Sebastijan Kra- B-AIR (all authors) jnc (1), Maruša Grešak (1), Liza Žerdin (1), University of Primorska (Ana Kuder) Judita Vidmar (8) and Mara Bresjanac (1, 3) Leiden University (Manca Kok) 1 SiNAPSA, Slovenian Neuroscience Association, As a part of the interdisciplinary project B-AIR (Creative Europe, in-Slovenia tended to create sound, voice and music programmes for babies and 2 Department of Neurology, University Medical Centre, vulnerable groups of any age), a plan was developed to sensitize the medical community and general public to consider music as a relevant Ljubljana, Slovenia agent in health care. A study was designed with the main goal of find-3 Faculty of Medicine, University of Ljubljana, Slove- ing out the interest and motivation to introduce the use of music in the nia health care system among Slovenian physicians. The pilot version of 4 Institute for the Deaf and Hard of Hearing (Ljubljana), the questionnaire has already been administered to a smaller group Slovenia of Slovenian physicians, known for their active interest in music. The preliminary results show a moderate interest and knowledge about 5 University Rehabilitation Institute (Slovenia), Slove-the benefits of using music in Slovenian health care and limited cur-nia rent use of music by the respondents. Many respondents expressed 6 Department of Psychology, Faculty of Mathemat-the beneficial use of music in neurorehabilitation and chronic pain ics, Natural Sciences and Information Technologies, syndromes. Some of the respondents expressed willingness to work University of Primorska, Slovenia in a task force expected to be created as one of the results of the study and help with further development of the domain. A modified 7 Faculty of Health Sciences, University of Primorska, questionnaire will survey a larger medical population sample, and Slovenia 8 UMNI Institute, Ljubljana, Slovenia other professions allied to medicine, focusing specifically on the use of music in clinical practice and in research in neurology and psychiatry, The aim of our study was to gain insight into Slovenian public view in order to further explore the preliminary findings. The aim of the on science based recommendations for brain health and neurosci-study is to get a more realistic picture of the knowledge and potential ence. Within the project “Z možgani za možgane” (Aim for the brain) implementation of music in diverse settings. The results may be used we have conducted a survey that was filled out in part or completely for devising the most feasible future implementations. by 2568 participants. The responders were divided into two separate subgroups based on their brain-related education (current or former). Keywords: music-based interventions, Slovenian health care, inter-Responders, n = 1012, that were not nor had they ever been engaged disciplinary project in formal education about the brain nor they professionally relied on knowledge about the brain were considered to represent the lay public and key findings were recently reported (1). The remaining responders, n = 1438, were considered to represent a specifically educated group. Here we will present the views of neuroscience and science based brain health recommendations of this, specifically educated, subgroup and draw comparisons with lay public view. We will analyse similarities and differences between self-declared lay and educated responders to test the hypothesis that knowledge gap underlies possible differences in behaviour aimed at maintaining brain health . Keywords: Health Literacy, Public Engagement, Brain Disorders, Brain health [32] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 Abstracts Educational workshop on CNS protein misfolding www.sinapsa.org/SNC21/workshop Ljubljana, Slovenia 24 September 2021 SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Friday, September 24th, 15:00 overwhelming majority (95%) of ALS and over 60% of FTD cases, are Proteostasis Collapse: A Basis for Ag- cytoplasmic aggregation and nuclear clearance of otherwise nuclear TDP-43 protein defining them as TDP-43 proteinopathies. TDP-43 ing and Neurodegenerative Diseases positive cytoplasmic inclusions have also been described in 57% of Alzheimer disease cases, 20% of Dementia with Lewy bodies and in a variety of other neurodegenerative conditions. Conversely, the TDP-Richard I. Morimoto, PhD 43-negative pathology is defined mainly by aggregations of proteins FUS (ALS and FTD) or SOD1 (ALS) or tau (FTD). However, mutations Bill and Gayle Cook Professor of Biology Rice Insti-in TDP-43 and FUS are uncommon in ALS and account for only up to tute of Biomedical Research Northwestern University 5% of familial and 1-5% of sporadic ALS cases and are very rare in Evanston, IL 60201 www.morimotolab.org FTD. In light of this, one of the most important questions in this field is what makes wildtype TDP-43 (or FUS) mislocalize and aggregate. The answer lies in the age and disease related changes of their de Aging is associated with the programmed decline of cell protective novo expression, modification, localization and/or degradation. These stress responses and the loss of cellular proteostasis essential to changes may also arise from disease-causing mutations in other prevent the accumulation of misfolded and aggregated proteins com-genes, principal among which is the TDP-43 proteinopathy associated mon to all neurodegenerative diseases. We have employed multiple GGGGCC ((G4C2)n) hexanucleotide repeat expansion (HRE) muta-biological systems and approaches to identify the composition of the proteostasis network (PN) that regulates protein synthesis, folding, tion in C9ORF72. translocation and degradation, to demonstrate how the PN determines the stability and function of the proteome in health and fails in aging and diseases, and genetic and small molecule approaches to reset Friday, September 24th, 16:45 the PN and suppress aggregation and amyloid formation. Now it is time for research to crack Our current efforts are to identify the earliest events that predict pro-Parkinson’s disease teostasis failure in neurons and other tissues. Patrik Brundin, M.D. Ph.D. Friday, September 24th, 15:45 Deputy Chief Scientific Officer, Van Andel Institute An update on Tau-related diseases Director, Parkinson’s Disease Center, Department of Neurodegenerative Science, Van Andel Institute, Gabor G. Kovacs, MD, PhD, FRCPC Grand Rapids, MI, USA https://patrikbrundinlab.vai. org/overview/ University of Toronto, Department of Laboratory Medi- cine and Pathobiology and Tanz Centre for Research Parkinson’s disease research has reached a very exciting time where in Neurodegenerative Disease (CRND) Consultant we know more about the molecular underpinnings of the disease than Neuropathologist/Neurologist,University Health Net-ever before. The accumulation of aggregated proteins, the loss of work (UHN) https://neuropath-ggkovacs.com https:// mitochondrial function and the development of neuroinflammation all seem to play a role. By targeting these processes we hope that novel www.tanz.med.utoronto.ca therapies can slow the rate of disease progression. Filamentous deposits of known composition in brain cells define most human neurodegenerative conditions. Assemblies of the microtubule- Friday, September 24th, 17:15 associated protein Tau comprise the most frequent neurodegenerative proteinopathies. Diseases with filamentous Tau pathology can be Huntington’s disease divided into three groups, based on the isoforms in the filaments. In these diseases, be they sporadic or inherited, Tau is extensively modified post-translationally. The purpose of this presentation is to present Roger A. Barker, BA, MBBS, MRCP, PhD a neuropathology-based approach to tau-related conditions and to highlight current hot topics of the field. Wellcome - MRC Cambridge Stem Cell Institute and Department of Neurology, University of Cambridge, UK http://www.thebarkerwilliamsgraylab.co.uk Friday, September 24th, 16:15 TDP-43 proteinopathies History, diagnosis, clinical features, pathogenesis and current and future treatment of Huntington’s disease will be presented. Boris Rogelj Work funded by the HDA; NIHR; ABN; EU; CHDI; Rosetrees trust and and Evelyn Trust Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two ends of a phenotypic spectrum of disabling, relentlessly progressive and ultimately fatal neurodegenerative diseases. There is no cure for either of the diseases. Pathological hallmarks of the [34] SiNAPSA Neuroscience Conference ‘21, Ljubljana, 23—25 September 2021 Friday, September 24th, 17:45 Transmissible Spongiform Encepha- lopathies Adriano Aguzzi, MD, PhD, DVM, hc FRCPath MD, PhD, DVM, hc FRCPath, Institute of Neuropa- thology, University Hospital of Zürich Schmelzberg- strasse 12, CH-8091 Zürich, Switzerland https://new. usz.ch/fachbereich/neuropathologie/ Transmissible spongiform encephalopathies (TSEs) are neurodegenerative diseases of humans and many animal species caused by prions. The main constituent of prions is PrPSc, an aggregated moiety of the host-derived membrane glycolipoprotein PrPC. Prions were found to encipher many phenotypic, genetically stable TSE variants. The latter is very surprising, since PrPC is encoded by the host genome and all prion strains share the same amino acid sequence. Here I will review what is known about the infectivity, the neurotoxicity, and the neuroinvasiveness of prions. Also, I will explain why I regard the prion strain question as a fascinating challenge – with implications that go well beyond prion science. Finally, I will report some recent results obtained in my laboratory, which is attempting to address the strain question and some other basic issues of prion biology with a “systems” approach that utilizes organic chemistry, photophysics, proteomics, and mouse transgenesis. Friday, September 24th, 18:15 A structural biologist’s view of neuro- science Holger Wille, PhD Associate Professor, University of Alberta, Depart- ment of Biochemistry & Centre for Prions and Protein Folding Diseases & Neuroscience and Mental Health Institute Alberta, Canada https://www.ualberta.ca/biochemistry/people/faculty/ holger-wille.html https://www.ualberta.ca/prion-centre/faculty-and-staff/ holger-wille.html The infectious prion protein is characterized by a distinct, three-dimensional conformation, which results in the surface exposure of disease-specific epitopes. We have used insights into the structure of the infectious prion protein to create a structure-based prion vaccine that specifically mimics the surface of the infectious conformer. Efficacy trials in a genetic prion disease mouse model demonstrated a significant extension in the health-span of immunized mice versus unimmunized controls. [35] SNC’21 SiNAPSA NEUROSCIENCE CONFERENCE ‘21 Sponsors www.sinapsa.org/SNC21/sponsors Ljubljana, Slovenia 23—25 September 2021 Conference sponsors Principal sponsors & SiNAPSA supporters for 2021 The organizers thank the following sponsors for supporting the SiNAPSA Neuroscience Conference ‘21: International Brain Research Organisation, IBRO SiNAPSA is a proud recipient of the IBRO-PERC National Neuroscience Societies Partnership Program Award for the events accompanying the SNC’21 core programme: SARS-CoV-2 and Brain Workshop, Educational Workshop on Protein Misfolding in CNS Disorders, and the Neuroscience & Society Dialogue special event, open to general public. SiNAPSA also received the IBRO Global Engagement Seed Grant for 2021, which has supported neuroscience-promotional activities related to the SNC’21. Slovenian Research Agency awarded SiNAPSA a grant for science promotion in 2021 (grant agreement No. 1000-21-2115). Biogen Pfizer Roche Supporting sponsors & SiNAPSA supporters for 2021 SNC’21 also acknowledges support by: European Union’s Horizon 2020 research and innovation programme CogDec (grant agreement No. 857375). This support reflects only the organizer’s view. The Research Executive Agency is not responsible for any use that may be made of the information SNC’21 contains. Slovenian Society of Clinical Neurophysiology Slovenian Neurological Society Slovenian Psychiatric Association University Medical Centre Ljubljana Krka Lek Medis Medistar Novartis Octapharma Sanofi Genzyme Wörwag Pharma [37] [39] COGDEC.Twinning Quantifying Ageing Related Cognitive Decline and Mild Cognitive Impairment This project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 857375. This website reflects only the Author's view. The Research Executive Agency is not responsible for any use that may be made of the information this website contains. [40]