Mitochondrial abnormalities in neuroectodermal cells stably expressing human amyloid precursor protein (hAPP751).

Abstract:

:Metabolic hypofunction is a common finding in a number of neurodegenerative diseases, including Alzheimer's disease (AD). The strong linkage between the amyloid precursor protein (APP) and AD led us to examine whether over-expression of this protein in CNS-type cells had an effect on mitochondria. We found abnormal morphology in mitochondria of the neuroectodermal progeny of P19 cells stably transfected with human APP751. In addition, the mitochondria of APP-transfected clones had a decreased mitochondrial membrane potential. These changes were independent of Abeta toxicity and distinct from complex I inhibition. Our results have important implications for the earliest events in the pathophysiology of AD and, by extrapolation, for intervention therapies.

journal_name

Neuroreport

journal_title

Neuroreport

authors

Grant SM,Shankar SL,Chalmers-Redman RM,Tatton WG,Szyf M,Cuello AC

doi

10.1097/00001756-199901180-00008

subject

Has Abstract

pub_date

1999-01-18 00:00:00

pages

41-6

issue

1

eissn

0959-4965

issn

1473-558X

journal_volume

10

pub_type

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