Investigating neural stem cell function in an Alzheimer's disease model
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 |
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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 |
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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 |
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Genre | Text |
Bibliographic information
Statement of responsibility | Felicia Sarah Reinitz. |
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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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