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C99 selectively accumulates in vulnerable neurons in Alzheimer’s disease
Preprint — published as 10.1016/j.jalz.2019.09.002
Abstract
Introduction: The levels and distribution of amyloid deposits in the brain does not correlate well with Alzheimer’s disease (AD) progression. Therefore, it is likely that Amyloid-precursor-protein proteolytic fragments other than beta-amyloid contribute to the onset of AD. Methods: We developed a sensitive assay adapted to the detection of C99, the direct precursor of beta-amyloid. Three postmortem groups were studied: control with normal and stable cognition; subjects with moderate AD, and individuals with severe AD. The amount of C99 and beta-amyloid was quantified and correlated with the severity of AD. Results: C99 accumulates in vulnerable neurons, and its levels correlate with the degree of cognitive impairment in patients suffering from AD. In contrast, beta-amyloid levels are increased in both vulnerable and resistant brain areas. Discussion: These results raise the possibility that C99, rather than beta-amyloid plaques, is responsible for the death of nerve cells in Alzheimer’s disease.
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C99 shows a better correlation than Aβ with the degree of vulnerability to neurodegeneration.
“and shows a better correlation than Aβ with the degree of vulnerability to neurodegeneration (Pulina et al., 2019)”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Pulina et al., 2019
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García-González, L., Pilat, D., Baranger, K., & Rivera, S. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00244 · Cited by 88
Metadata
- Authors
- Pulina, M. V., Hopkins, M., Haroutunian, V., Greengard, P., & Bustos, V.
- Publisher
- openRxiv
- Published
- 2019-01-22
- Cited by
- 9
- References
- 1
- Type
- Preprint
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