[S-36-3] How does exogenous alpha-synuclein get access to the endogenous alpha-synuclein proteins?
Multisystem atrophy (MSA) is a multi-system neurodegenerative disease of the cerebellum, pyramidal and extrapyramidal tract, and autonomic nervous system, which is characterized by the α-synuclein deposition in oligodendrocytes. There are still many unsolved issues about the pathological mechanism, and there is an urgent need to develop new therapeutic agents. Researches on MSA mainly cover the pathogenesis of α-synuclein, and includes disease-causing factors in DNA polymorphisms and microRNAs, and the dysfunction of neural networks by fMRI. It is important to confirm and discuss about the latest knowledge to develop further researches on MSA. Therefore, in this symposium, the latest research results on MSA in Japan will be presented, aiming discussion between speakers and participants to establish a new research goal on MSA.
Dr. Hasegawa received his M.D. in 1995 and Ph.D. in 2000 from Tohoku University, Sendai Japan. In 2006, he received Alexander von Humboldt fellowship and joined Dr. Philipp J. Kahle's Lab as a post doc in Hertie-Institute, Tübingen, Germany. In 2008, he went back to Japan and currently he serves as the PI of Parkinson study group in Department of Neurology, Tohoku University School of Medicine. His primary research interest is the functional roles of membrane trafficking in the pathogenesis of Parkinson’s disease (PD) and other neurodegenerative disorders. In addition, Dr. Hasegawa’s group are devoted to establish novel surrogate markers including amyloid PET imaging in synucleinopathy and tauopathy.
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