Investigating neural stem cell function in an Alzheimer's disease model

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Abstract/Contents

Abstract
Alzheimer's disease is a progressive neurodegenerative disease characterized by dementia and amyloid plaques. In a mouse model of Alzheimer's disease harboring mutant amyloid precursor protein, we show elevated expression of Cdkn2a, a gene linked to brain aging, apoptosis, and neural precursor cell long-term proliferation defects. Genetic reduction of USP16, a critical up-regulator of Cdkn2a, led to decreased astrogliosis and neuronal apoptosis, reduced neural precursor cell proliferation defects, and improved memory. In combination with agents targeting classical Alzheimer's disease pathologies, we identify USP16 as a potential therapeutic target that may help to ameliorate the cognitive deficits in some cases of Alzheimer's disease.

Description

Type of resource text
Form electronic resource; remote; computer; online resource
Extent 1 online resource.
Place California
Place [Stanford, California]
Publisher [Stanford University]
Copyright date 2019; ©2019
Publication date 2019; 2019
Issuance monographic
Language English

Creators/Contributors

Author Reinitz, Felicia Sarah
Degree supervisor Clarke, Michael F
Thesis advisor Clarke, Michael F
Thesis advisor Heller, H. Craig
Thesis advisor Monje-Deisseroth, Michelle
Degree committee member Heller, H. Craig
Degree committee member Monje-Deisseroth, Michelle
Associated with Stanford University, Department of Stem Cell Biology and Regenerative Medicine.

Subjects

Genre Theses
Genre Text

Bibliographic information

Statement of responsibility Felicia Sarah Reinitz.
Note Submitted to the Department of Stem Cell Biology and Regenerative Medicine.
Thesis Thesis Ph.D. Stanford University 2019.
Location electronic resource

Access conditions

Copyright
© 2019 by Felicia Sarah Reinitz

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