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C99 selectively accumulates in vulnerable neurons in Alzheimer’s disease

Maria V. Pulina, Maya Hopkins, Vahram Haroutunian, Paul Greengard, Victor Bustos
doi: https://doi.org/10.1101/527572
Maria V. Pulina
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY.
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Maya Hopkins
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY.
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Vahram Haroutunian
Icahn School of Medicine at Mount Sinai, New York, NY.JJ Peters VA Medical Center, Bronx, New York, NY.
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Paul Greengard
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY.
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Victor Bustos
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY.
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  • For correspondence: vbustos@rockefeller.edu
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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.

Footnotes

  • Figure 4C shows C99 increases in neurons with high Tau levels, a marker of neurodegeneration.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted August 21, 2019.
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C99 selectively accumulates in vulnerable neurons in Alzheimer’s disease
Maria V. Pulina, Maya Hopkins, Vahram Haroutunian, Paul Greengard, Victor Bustos
bioRxiv 527572; doi: https://doi.org/10.1101/527572
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C99 selectively accumulates in vulnerable neurons in Alzheimer’s disease
Maria V. Pulina, Maya Hopkins, Vahram Haroutunian, Paul Greengard, Victor Bustos
bioRxiv 527572; doi: https://doi.org/10.1101/527572

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