Mechanisms of the inclusion body formation in the brain: Association of an inclusion body and the neuronal cell death

2015 Fiscal Year Final Research Report

• Project Area: Brain Environment
• Project/Area Number: 23111003
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Juntendo University
• Principal Investigator: Hattori Nobutaka 順天堂大学, 医学(系)研究科(研究院), 教授 (80218510)
• Co-Investigator(Renkei-kenkyūsha): SATO Shigeto 順天堂大学, 医学部, 准教授 (00445537)
• Project Period (FY): 2011-04-01 – 2016-03-31
• Keywords: パーキンソン病 / 封入体 / タンパク分解 / オートファジー / ドーパミン細胞 / 神経細胞死

Outline of Final Research Achievements

Parkinson’s disease (PD) may be caused by mitochondrial and autophagy lysosome pathway dysfunction, which are probably affected by both genetic predisposition and environmental factors. The discovery of gene including CHCHD2 and the function of PINK1 and Parkin, which associated with the mitochondria, also enhanced the understanding of cellular functions. Kufor-Rakeb syndrome (KRS) was originally described in association with an autosomal recessive form of early-onset parkinsonism. The causative gene for KRS has been identified as ATP13A2, which encodes a lysosomal type 5 P-type ATPase whose physiological function in mammalian cells remains unknown. We recently showed that KRS/PARK9-linked mutations lead to several lysosomal alterations, including reduced proteolytic processing of a lysosomal enzyme.

Free Research Field

パーキンソン病