Oxidatively modified, mitochondria-relevant brain proteins in subjects with Alzheimer disease and mild cognitive impairment

被引:90
作者
Sultana, Rukhsana [1 ,2 ,3 ]
Butterfield, D. Allan [1 ,2 ,3 ]
机构
[1] Univ Kentucky, Dept Chem, Lexington, KY 40506 USA
[2] Univ Kentucky, Ctr Membrane Sci, Lexington, KY 40506 USA
[3] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40506 USA
关键词
Oxidative stress; Alzheimer's disease; Mitochondria; MCI; LIPID-PEROXIDATION PRODUCT; AMYLOID PRECURSOR PROTEIN; DEPENDENT ANION CHANNEL; CYTOCHROME-C-OXIDASE; CREATINE-KINASE BB; BETA-PEPTIDE; 1-42; A-BETA; PROTEOMIC IDENTIFICATION; ATP-SYNTHASE; CELL-DEATH;
D O I
10.1007/s10863-009-9241-7
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Alzheimer disease (AD) is an age-related neurodegenerative disorder, characterized histopathologically by the presence of senile plaques (SP), neurofibrillary tangles and synapse loss in selected brain regions. Positron emission tomography (PET) studies of glucose metabolism revealed decreased energetics in brain of subjects with AD and arguably its earliest form, mild cognitive impairment (MCI), and this decrease correlated with brain structural studies using MRI. The main component of senile plaques is amyloid beta-peptide (A beta), a 40-42 amino acid peptide that as oligomers is capable of inducing oxidative stress under both in vitro and in vivo conditions and is neurotoxic. In the mitochondria isolated from AD brain, A beta oligomers that correlated with the reported increased oxidative stress markers in AD have been reported. The markers of oxidative stress have been localized in the brain regions of AD and MCI that show pathological hallmarks of this disease, suggesting the possible role of A beta in the initiation of the free-radical mediated process and consequently to the build up oxidative stress and AD pathogenesis. Using redox proteomics our laboratory found a number of oxidatively modified brain proteins that are directly in or are associated with the mitochondrial proteome, consistent with a possible involvement of the mitochondrial targeted oxidatively modified proteins in AD progression or pathogenesis. The precise mechanistic link between mitochondrial oxidative damage and role of oligomeric A beta has not been explicated. In this review, we discuss the role of the oxidation of mitochondria-relevant brain proteins to the pathogenesis and progression of AD.
引用
收藏
页码:441 / 446
页数:6
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