Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 44, Issue 2, Pages 379-383Publisher
IOS PRESS
DOI: 10.3233/JAD-141755
Keywords
Alzheimer's disease; cerebrospinal fluid; choroid plexus; selenium; selenoprotein P; selenoproteins; Sepp1
Categories
Funding
- Hawaii Community Foundation Ingeborg v.F. McKee Fund [08PR-43031]
- NIH [P20RR016467, U01AG019349, G12MD007601]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016467, G12RR003061] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [U01AG019349] Funding Source: NIH RePORTER
- National Institute on Minority Health and Health Disparities [U54MD008149, G12MD007601] Funding Source: NIH RePORTER
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Subjects with Alzheimer's disease (AD) have elevated brain levels of the selenium transporter selenoprotein P (Sepp1). We investigated if this elevation results from increased release of Sepp1 from the choroid plexus (CP). Sepp1 is significantly increased in CP from AD brains in comparison to non-AD brains. Sepp1 localizes to the trans-Golgi network within CP epithelia, where it is processed for secretion. The cerebrospinal fluid from AD subjects also contains increased levels Sepp1 in comparison to non-AD subjects. These findings suggest that AD pathology induces increased levels of Sepp1 within CP epithelia for release into the cerebrospinal fluid to ultimately increase brain selenium.
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