Journal
NEUROBIOLOGY OF AGING
Volume 24, Issue 1, Pages 77-84Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0197-4580(02)00043-X
Keywords
Alzheimer's disease; telomeres; T cells; immune system
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Funding
- NCRR NIH HHS [RR00865] Funding Source: Medline
- NIA NIH HHS [AG10415, AG16570] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000865] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P60AG010415, P50AG016570] Funding Source: NIH RePORTER
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Telomeres, the repeated sequences that cap chromosome ends, undergo shortening with each cell division, and therefore serve as markers of a cell's replicative history. In vivo, clonal expansion of T cells during immune responses to both foreign and autoantigens is associated with telomere shortening. To investigate possible immune alterations in Alzheimer's disease (AD) that might impact current vaccine-based therapeutic strategies, we analyzed telomere lengths in immune cell populations from AD patients. Our data show a significant telomere shortening in PBMC from AD versus controls (P = 0.04). Importantly, telomere length of T cells, but not of B cells or monocytes, correlated with AD disease status, measured by Mini Mental Status Exam (MMSE) scores (P = 0.025). T cell telomere length also inversely correlated with serum levels of the proinflammatory cytokine TNFalpha (a clinical marker of disease status), with the proportion of CD8+ T cells lacking expression of the CD28 costimulatory molecule, and with apoptosis. These findings suggest an immune involvement in AD pathogenesis. (C) 2002 Elsevier Science Inc. All rights reserved.
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