Mitochondria and Alzheimer's disease

被引：29

作者：

Piaceri, Irene ^{[1
]}

Rinnoci, Valentina ^{[1
]}

Bagnoli, Silvia ^{[1
]}

Failli, Ylenia ^{[1
]}

Sorbi, Sandro ^{[1
]}

机构：

[1] Univ Florence, Dept Neurol & Psychiat Sci, DENOTHE Excellence Ctr, I-50134 Florence, Italy

来源：

JOURNAL OF THE NEUROLOGICAL SCIENCES | 2012年 / 322卷 / 1-2期

关键词：

Alzheimer's disease; Mitochondria; Beta-amyloid; Mitochondrial DNA; Neurodegeneration; Oxidative stress; Dementia; AMYLOID PRECURSOR PROTEIN; A-BETA; NEURODEGENERATIVE DISEASES; OXIDATIVE DAMAGE; MATERNAL HISTORY; FREE-RADICALS; ATP SYNTHASE; DNA; CELLS; BRAIN;

D O I：

10.1016/j.jns.2012.05.033

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Reductions in cerebral metabolism sufficient to impair cognition in normal individuals also occur in Alzheimer's disease (AD). FDG PET studies have shown that decreased glucose metabolism in AD precedes clinical diagnosis and the degree of clinical disability in AD correlates closely to the magnitude of the reduction in brain metabolism. This suggests that the clinical deterioration and metabolic impairment in AD are related closely. Diminished metabolism can lead to the hyperphosphorylation of tau and increased production of amyloid beta peptide, hallmarks of AD. These observations suggest also that early mitochondrially therapeutic interventions may be an important target in delaying AD progression in elderly individuals and in treating AD patients. (C) 2012 Published by Elsevier B.V.

引用

收藏

页码：31 / 34

页数：4

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