[HT-05-4] Endo-lysosomal trafficking defect as a unifying concept of neurodegenerative diseases
Autophagy sequesters cytoplasmic material and organelles to lysosomes for degradation. The magnitude of autophagy depends on starvation, oxidative stress, or other noxious conditions, which thereby exerts quality control function that contributes to neurodegeneration and aging. The lysosome was once thought of as a waste bag, a dead-end destination where cellular debris was sent for disposal. However, recent studies have challenged this simple view and found that Lysosomes are not just a sack of digestive enzymes, but rather a signaling/sorting hub related to all of the materials used in the cell. In this symposium, we will invite four speakers with known expertise to share the recently discovered properties of the autophagy-lysosome system in neurological conditions and offer helpful hints on how to develop therapeutic strategies to combat these devastating diseases.
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 to elucidate how membrane trafficking machinery contribute to the initiation and progression of neurodegenerative disorders such as Parkinson's disease. 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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