2010 Fiscal Year Final Research Report

Research on molecular function of ATP13A2 and neuronal cell death causing altered localization of ATP13A2

Research Project

Project/Area Number	21790852
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Neurology
Research Institution	Hoshi University (2010) Juntendo University (2009)
Principal Investigator	SATO Fumiaki Hoshi University, 薬学部, 助教 (10468580)
Project Period (FY)	2009 – 2010
Keywords	神経分子病態学
Research Abstract	ATP13A2, identified as one of the causative gene product for familial parkinson's disease (PARK9), localized at lysosomal membrane. The suppression of ATP13A2 expression led to apoptosis in SH-SY5Y cells. The defective expression also was increased an enzyme activity of cathepsins, especially cathepsin D. Moreover, electron microscopy showed the accumulation of high density large structure, which was immunoreacted with antibodies against lamp2 and cathepsin D, in SH-SY5Y cells. These data suggests that PARK9 caused by loss-of-function of ATP13A2 is associated with lysosomal dysfunction, resulting in cell death.

(4 results)