期刊
NEUROBIOLOGY OF DISEASE
卷 32, 期 1, 页码 37-49出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2008.06.012
关键词
gamma-secretase; presenilin; Alzheimer's disease; kainic acid; COPI
资金
- NIH [AG021495, AG019070]
- ATP [NS055223]
- KSV [IIRG-06-26148, NIRG-05-14427]
- Canadian Institutes of Health Research
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS055223] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG019070, R01AG021495] Funding Source: NIH RePORTER
Sequential processing of amyloid precursor protein by beta- and gamma-secretases generates Alzheimer's disease (AD)-associated beta-amyloid peptides. Recently it was reported that the transmembrane protein p23/TMP21 associates with gamma-secretase, and negatively regulates beta-amyloid production. Despite the link between p23 function and AD pathogenesis, the expression of p23 has not been examined in the brain. Here, we describe the detailed immunohistochemical characterization of p23 expression in rodent and human brain. We report that p23 is co-expressed with gamma-secretase subunits in select neuronal cell populations in rodent brain. Interestingly, the steady-state level of p23 in the brain is high during embryonic development and then declines after birth. Furthermore, the steady-state p23 level is a rereduced in the brains of individuals with AD. We conclude that p23 is expressed in neurons throughout the brain and the decline in p23 expression during postnatal development may significantly contribute to enhanced beta-amyloid production it) the adult brain. (C) 2008 Elsevier Inc. All rights reserved.
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