Jan 22, 2019

C99 selectively accumulates in vulnerable neurons in Alzheimer's disease.

BioRxiv : the Preprint Server for Biology
Maria PulinaVictor Bustos

Abstract

Amyloid Precursor Protein (APP) and its cleavage product beta-amyloid are widely believed to be key players in the development of Alzheimer's disease (AD). However, the distribution of amyloid deposits in the brain does not correlate well with disease progression. Therefore, it seemed possible that APP metabolites other than beta-amyloid might make a strong contribution to AD pathology. We developed a sensitive assay adapted to the detection of C99, an intermediate in the conversion of APP to beta-amyloid. Brain tissue sections were obtained from patients suffering from sporadic AD and non-demented controls. Our results demonstrate that C99 levels correlate with the degree of vulnerability to neurodegeneration and cognitive impairment in patients suffering from AD.

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Mentioned in this Paper

Neurons
Brain
Cessation of Life
Nerve Degeneration
Alzheimer's Disease
Amyloid beta-protein precursor C-terminal fragment beta, human
Amyloid
APP
Impaired Cognition
Pathology

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