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
Neuroreportjournal_title
Neuroreportauthors
Grant SM,Shankar SL,Chalmers-Redman RM,Tatton WG,Szyf M,Cuello ACdoi
10.1097/00001756-199901180-00008subject
Has Abstractpub_date
1999-01-18 00:00:00pages
41-6issue
1eissn
0959-4965issn
1473-558Xjournal_volume
10pub_type
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