J-GLOBAL ID:200904081637975349  Research Project code:0150001892 Update date:Jan. 06, 2005

Impairment of intracellular transport for alzheimer amyloid precursor protein

Study period:2000 - 2003
Organization (1):
Investigating Researcher (1):
Research overview:
Although recent studies on the relation of PS1 and APP report that PS1 is a gamma secretion enzyme itself necessary for formation of A beta from APPC fragments (APPCTF) or co-factor for gamma secretion enzyme to have activity, it has not been perfectly confirmed. The authors suggested that PS1 was present in cerebral axon and the possibility of relation with transportation of protein by observing accumulation of APPCTF in cultured cell expressing PS1. Considering with the results of analysis of PS1 defective mouse or PS1 antisense introduced culture cell, the possibility is suggested that PS1 regulates the intraceller transport of protein and A beta generation may be increased by its impairment. The mechanism is considered that in AD APPCTF transport capacity is decreased by some reason and APPCTF is accumulated on the site of gamma secretion enzyme, resulting in an increase in A beta production. In this study, relation of impairment of protein transport in the metabolic process where A beta is produced from APP with A beta production is-chemically analyzed using cultured cell proving the occurrence of the same phenomenon in AD brain.
Keywords (6):
Alzheimer's disease ,  amyloid ,  amyloid precursor protein ,  presenilin ,  PC12D cells ,  processing
Project Organization (1):
  • (J184000000)
Research program: Ordinary Research

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