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Impaired platelet mitochondrial activity in Alzheimer's disease and mild cognitive impairment
被引:143
作者:
Valla, Jon
Schneider, Lonnie
Niedzielko, Tracy
Coon, Keith D.
Caselli, Richard
Sabbaah, Marwan N.
Ahern, Geoffrey L.
Baxter, Leslie
Alexander, Gene
Walker, Douglas G.
Reiman, Eric M.
机构:
[1] St Josephs Hosp, Barrow Neurol Inst, Arizona Alzheimers Dis Consortium, Phoenix, AZ 85013 USA
[2] Translat Genom Res Inst, Phoenix, AZ USA
[3] Mayo Clin Arizona, Dept Neurol, Scottsdale, AZ USA
[4] Arizona Alzheimers Dis Consortium, Scottsdale, AZ USA
[5] Arizona Alzheimers Dis Consortium, Sun City, AZ USA
[6] Cleo Roberts Ctr Clin Res, Sun Hlth Res Inst, Sun City, AZ USA
[7] Arizona Alzheimers Dis Consortium, Tucson, AZ USA
[8] Univ Arizona, Hlth Sci Ctr, Tucson, AZ USA
[9] Arizona Alzheimers Dis Consortium, Tempe, AZ USA
[10] Arizona State Univ, Dept Psychol, Tempe, AZ 85287 USA
[11] Univ Arizona, Banner Alzheimers Inst, Translat Genom Res Inst, Phoenix, AZ USA
关键词:
cytochrome oxidase;
cytochrome reductase;
electron transport chain;
Alzheimer's disease;
mild cognitive impairment;
at-risk population;
D O I:
10.1016/j.mito.2006.10.004
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Mitochondrial abnormalities are found in Alzheimer's disease (AD), but previous reports have not examined at-risk groups. In subjects with AD, mild cognitive impairment (MCI), and non-demented aged controls, platelet and lymphocyte mitochondria were isolated and analyzed for Complexes I, III and IV of the electron transport chain. Western blots Were used to control for differential enrichment of samples. Results demonstrated significant declines in Complexes III and IV in AD, and a significant decline in Complex IV in MCI. This report confirms mitochondrial deficiencies in AD, extends them to MCI, and suggests they are present at the earliest symptomatic stages of disease. (c) 2006 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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页码:323 / 330
页数:8
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