Indices of metabolic dysfunction and oxidative stress

被引:21
作者
Casadesus, Gemma
Moreira, Paula I.
Nunomura, Akihiko
Siedlak, Sandra L.
Bligh-Glover, William
Balraj, Elizabeth
Petot, Grace
Smith, Mark A.
Perry, George
机构
[1] Univ Texas, Coll Sci, San Antonio, TX 78249 USA
[2] Case Western Reserve Univ, Dept Neurosci, Cleveland, OH 44106 USA
[3] Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal
[4] Asahikawa Med Coll, Dept Psychiat & Neurol, Asahikawa, Hokkaido 078, Japan
[5] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA
[6] Cuyahoga Cty Coroners Off, Cleveland, OH USA
[7] Case Western Reserve Univ, Dept Nutr, Cleveland, OH 44106 USA
基金
美国国家卫生研究院;
关键词
Alzheimer disease; apolipoprotein E; diet; metabolism; neuronal size;
D O I
10.1007/s11064-007-9296-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Metabolic alterations are a key player involved in the onset of Alzheimer disease pathophysiology and, in this review, we focus on diet, metabolic rate, and neuronal size differences that have all been shown to play etiological and pathological roles in Alzheimer disease. Specifically, one of the earliest manifestations of brain metabolic depression in these patients is a sustained high caloric intake meaning that general diet is an important factor to take in account. Moreover, atrophy in the vasculature and a reduced glucose transporter activity for the vessels is also a common feature in Alzheimer disease. Finally, the overall size of neurons is larger in cases of Alzheimer disease than that of age-matched controls and, in individuals with Alzheimer disease, neuronal size inversely correlates with disease duration and positively associates with oxidative stress. Overall, clarifying cellular and molecular manifestations involved in metabolic alterations may contribute to a better understanding of early Alzheimer disease pathophysiology.
引用
收藏
页码:717 / 722
页数:6
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