[S-25] Symposium 25
The Implication of Autophagy in Alzheimer's disease and Dementia

[S-25-1] Degradation of amyloid ß protein and tau in Autophagy

^○Tadanori Hamano (Department of Neurology, University of Fukui, Japan)

The deposition of abnormally misfolded proteins, amyloid β protein (Aβ), and tau protein is pathogenic mechanisms of Alzheimer’s disease (AD). Aβ forms senile plaques, and tau aggregates forms neurofibrillary tangles. Misfolded α-synuclein is observed in dementia with lewy bodies (DLB), and aggregated α-synuclein forms Lewy bodies. Autophagy is the main conserved pathway for the degeneration of aggregated proteins, Aβ, tau, and dysfunctional organelles in the cell. α-synuclein is also degraded in autophagy. Many animal model studies have demonstrated that autophagy normally functions as the protective factor against AD, and DLB. So, the upregulation of autophagy can be favorable in AD, or DLB treatment. The cellular and molecular machineries of autophagy, their function in the pathogenesis of AD and DLB, and current drug discovery strategies will be discussed.

Fukui Medical School, Japan M.D. 1990 Medicine
Fukui Medical University, Japan Ph.D. 1997 Biochemistry

2013- Associate Professor, 2nd Dept. of Internal Medicine, University of Fukui,
Japan
Neurologist in Chief, University of Fukui Hospital, Japan
2006-Senior Assistant professor, 2nd Dept. of Internal Medicine,University of Fukui,
Japan
2004-2006 Visiting Scientist in Mayo Clinic Jacksonville, FL, USA. Supervisor Prof Yen
2000- Assistant Professor, 2nd Dept. of Internal Medicine, University of Fukui, Japan
1993-1997 Graduate Student, 2nd Dept. of Internal Medicine, University of Fukui,
Japan. Supervisor Prof. Kuriyama, Fukui Medical School, and Prof.
Ihara, Dept of Neuropathology, University of Tokyo, Japan
1992 Resident in the Dept. of Neurology, Meitetsu Hospital, Japan
1990 Resident in 2nd Dept. of Internal Medicine, Fukui Medical School, Japan