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

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 mitochondr...

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Bibliographic Details
Published inNeuroreport Vol. 10; no. 1; p. 41
Main Authors Grant, S M, Shankar, S L, Chalmers-Redman, R M, Tatton, W G, Szyf, M, Cuello, A C
Format Journal Article
LanguageEnglish
Published England 18.01.1999
Subjects
Amyloid beta-Protein Precursor - biosynthesis
Animals
Humans
Membrane Potentials - physiology
Mice
Microscopy, Electron
Mitochondria - metabolism
Mitochondria - pathology
Neuroectodermal Tumors - metabolism
Neuroectodermal Tumors - pathology
Oxidation-Reduction
Tumor Cells, Cultured
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Summary: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.
ISSN:0959-4965
DOI:10.1097/00001756-199901180-00008