Speaker Profile

Executive Summary：
Dr. Hatano entered the Graduate School of Juntendo University in 2003. He graduated with his PhD in 2007 and was appointed Assistant Professor of Neurology at Juntendo University School of Medicine in the same year. In 2011, he was appointed Associate Professor. Since 2023, Dr. Hatano has been a Senior Associate Professor of Neurology at Juntendo University School of Medicine.
His main research interests include the pathogenesis of Parkinson’s disease. In 2010, he received a silver medal for a case presentation at a Video Olympic event at the 14th International Congress of Parkinson’s Disease and Movement Disorders in Buenos Aires. He was elected to join the leadership program (LEAP) of the International Movement Disorder Society (MDS)-Asia-Oceania section (AOS) in 2016. In addition, He received the Juntendo Academic Encouragement Award in 2020, a grant from the Uehara Memorial Foundation in 2023, and a Japanese Society of Neurology 2023 Award in 2024. He is a Treasurer-elect of the MDS-AOS

Lecture Abstract：
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons and the presence of Lewy bodies. α-Synuclein (AS), a major component of Lewy bodies and glial cytoplasmic inclusions, is pivotal in the pathogenesis of PD and multiple system atrophy (MSA), respectively. Mutations and multiplications of the AS gene are implicated in familial forms of PD, confirming the critical role of AS in synucleinopathies. AS is an amphipathic protein that interacts with lipid membranes, and its altered membrane binding due to mutations or overexpression in familial PD leads to enhanced aggregation. AS oligomers are crucial in PD pathogenesis, as they disrupt normal membrane interactions and promote aggregation in organelles such as mitochondria, lysosomes, synaptic vesicles, and autophagosomes. These oligomers can act as seeds for further aggregation, and their detection may offer valuable insights into PD diagnosis and the mechanisms underlying synucleinopathies. Recent advances in synuclein amplification assays, such as real-time quaking-induced conversion combined with immunoprecipitation (IP/RT-QuIC) and Protein Misfolding Cyclic Amplification (PMCA), have enabled the detection of AS oligomers in body fluids and tissue samples. These techniques exploit the seeding properties of AS oligomers to amplify trace amounts. Our use of IP/RT-QuIC allowed the detection of AS seeds in the serum of patients with synucleinopathies, suggesting its potential as a diagnostic biomarker. Moreover, the aggregation and propagation characteristics, along with the microstructures of fibrils obtained from IP/RT-QuIC, revealed distinct variations among different synucleinopathies.

Executive Summary：
Dr. Chin-Hsien Lin graduated from College of Medicine, National Taiwan University, and received her neurological residency training in National Taiwan University Hospital (NTUH). She received her PhD training from Institute of Molecular Biology, Academia Sinica, and investigated the molecular mechanisms of LRRK2 mutations in neurons by using a Drosophila model system. She received post-doctoral fellowship training in the Center for University of British Columbia, Canada (Dr. Matthew Farrer’s laboratory).

Dr. Lin is now a professor in Department of Neurology, National Taiwan University Hospital. Her main academic interests include genetic and molecular biology studies of Parkinson’s disease and related neurodegenerative disorders. She investigated the molecular mechanisms of mutations of Parkinson’s disease or dystonia causative genes in neuronal degeneration by using cellular and animal model systems. She was elected to join the leadership program (LEAP) of international Movement Disorder Society (MDS)-AOS section in 2015. Dr. Lin is now the President of Taiwan Movement Disorders Society and is also joining several committees of MDS, including executive committee of the MDS-AOS section, evidence-based medicine (EBM) and basic neuroscience committees of MDS.

Lecture Abstract：
Neuropathology studies have shown that the pathognomonic feature of Parkinson’s disease (PD), one of the most common neurodegenerative disorders, may start from the gut enteric nervous system and then spread to the central dopaminergic neurons through the gut-brain axis. With the advent of metagenomic sequencing and metabolomic analysis, a plethora of evidence has revealed different gut microbiomes and gut metabolites in patients with PD compared with unaffected controls. Currently, although dopaminergic treatments and deep brain stimulation can provide some symptomatic benefits for motor symptoms of the disease, their long-term use is problematic. A mechanism-targeted therapy to halt the neurodegeneration
is lacking. The recently observed gut microenvironmental changes in the early stages of
the disease play a vital role in the PD pathogenesis. Patients whose disease begins in the gut may benefit most from interventions that target the gut microenvironments. In this talk, we will summarize the current studies demonstrating multifunctional roles of gut microbiota in the gut-brain axis of PD and the currently available evidence for targeting the gut microbiota as a novel approach to potential disease-modifying therapy in PD.N/A.

Executive Summary：
Dr. Lorraine Kalia is a clinician-scientist at the University of Toronto whose clinical practice and research program focus on Parkinson’s disease. She received her MD/PhD and neurology residency training at the University of Toronto. She conducted a postdoctoral research fellowship at Massachusetts General Hospital and a movement disorders fellowship at Toronto Western Hospital. Currently, she is an associate professor in the Division of Neurology at the University of Toronto and a senior scientist in the Krembil Brain Institute at University Health Network. She is also a movement disorders neurologist in the Edmond J. Safra Program in Parkinson’s Disease and
Morton and Gloria Shulman Movement Disorders Centre at Toronto Western Hospital. She holds the Wolfond-Krembil Chair in Parkinson’s Disease Research.

Her research program aims to understand the key molecular mechanisms responsible for neurodegeneration in Parkinson’s disease and to identify therapeutic agents that can modulate these molecular mediators of neurodegeneration. Her group uses a comprehensive approach involving molecular biology and biochemical techniques, cellular models, and in vivo invertebrate and vertebrate systems. Dr. Kalia is the treasurer of the Canadian Movement Disorders Society and co-chair of the Scientific Issues Committee and the Basic Science Special Interest Group of the International Parkinson and Movement Disorder Society. She is co-editor-in-chief of the Journal of Parkinson’s Disease.

Lecture Abstract：
Parkinson’s disease is a multifaceted neurodegenerative disorder characterized by a broad range of symptoms and an expanding array of underlying pathobiological mechanisms. Advances in understanding these molecular pathways have identified novel targets for potential disease-modifying therapies. The primary learning objective of this plenary session is to review and summarize emerging therapeutic targets and strategies aimed at altering the course of the disease. Recently completed and ongoing clinical trials, with a focus on phase 2 and 3 studies, will be discussed, highlighting their relevance to clinical practice in the near future.

Executive Summary：
Prof. Tiago Outeiro graduated in Biochemistry at the University of Porto and was an Erasmus student at the University of Leeds in the UK. Prof. Outeiro did his PhD thesis at the Whitehead Institute for Biomedical research – MIT and worked at FoldRx Pharmaceuticals as a Research Scientist and Consultant. Prof. Outeiro was a Postdoctoral Research Fellow in the Department of Neurology of the Massachusetts General Hospital – Harvard Medical School where he focused on the study of Neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease. Prof. Outeiro directed the Cell and Molecular Neuroscience Unit at IMM, Lisbon, from 2007 to 2014, and is currently Full Professor and the Director of the Department of Experimental Neurodegeneration at the University Medical Center Goettingen, in Germany. Prof. Outeiro holds a joint Professor position at Newcastle University in the UK, and is an invited Professor at the University of the Algarve. Prof. Outeiro has authored >300 research articles in international journals and participates in various international boards and in collaborative projects with the aim of identifying the molecular basis of neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease. He has been awarded multiple prizes and grants in Germany, from the European Union, and from other international funding agencies.

Lecture Abstract：
Soluble and insoluble aggregated forms of alpha-synuclein have been considered neurotoxic species with a central role in the pathogenesis of Parkinson's disease and related disorders. Therefore, strategies aimed at reducing and clearing such species from the brain have been explored, in the hope of obtaining therapeutic benefit. Antibody-based therapies have been widely studied in animal models, with positive results. Several clinical trials have now been performed, and the initial results were disappointing. However, based on the example of Alzheimer’s disease, there is still hope that new antibodies directed against more relevant alpha-synuclein species may be successful. In this lecture, I will discuss the rationale for using antibody-based therapies and recent findings.The accumulation of proteinaceous inclusions rich in alpha-synuclein in the brain is a common feature in Parkinson's disease (PD), and dementia with Lewy bodies (DLB). Interestingly, these inclusions are enriched not only in α-synuclein (aSyn), but also in lipid species, organelles, membranes, and even nucleic acids. Furthermore, several genetic risk factors for PD are mutations in genes involved in lipid metabolism, such as GBA1, VSP35, or PINK1. Thus, it is not surprising that mechanisms that have been implicated in PD, such as inflammation, altered intracellular and vesicular trafficking, mitochondrial dysfunction, and alterations in the protein degradation systems, may be also directly or indirectly connected through lipid homeostasis. Therefore, lipid biology may constitute an important driver of PD, and requires renovated attention. Lipids may bear implication in the accumulation of aSyn and in the spreading of aSyn pathology, in mitochondrial dysfunction, and in ER stress. Together, this suggests we should broaden the view of PD not only as a proteinopathy but also as a lipidopathy.