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Twenty-nine missense mutations linked with familial Alzheimer's disease alter the processing of presenilin 1.

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By Murayama O, Murayama M, Honda T, Sun X, Nihonmatsu • • July 1, 1999

Full-length form of human presenilin 1 (PS1) is processed and an N-terminal fragment (28 KD) and C-terminal fragment (19 KD) are generated. To elucidate the possible role of presenilin mutations in Alzheimer's disease (AD), the authors analyze the effects of AD-linked mutations on PS1 processing in cultured cells.

Complementary DNAs encoding genes for human PS1 harboring twenty-nine missense mutations linked with familial Alzheimer's disease (FAD) were introduced into PC12 cells. Human PS1 exogenously expressed in the cells was detected by immunoblotting using a monoclonal antibody that recognized the N-terminal region of human PS1. The amounts of full-length form (48 KD) and N-terminal fragment (28 KD) of PS1 was quantified by densitometrical analysis.

The ratio of the N-terminal fragment to total PS1 was reduced by twenty-nine mutations. The specific effects on PS1 processing varied according to mutation.

These results suggest that AD-linked missense mutations of PS1 are involved in neurodegeneration via inhibition of PS1 processing.

Source: Prog Neuropsychopharmacol Biol Psychiatry 1999 Jul;23(5):905-13
PMID: 10509383, UI: 99438799

(Laboratory for Alzheimer's Disease, Brain Science Institute, RIKEN, Saitama, Japan. )

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