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The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's disease
被引:0
|作者:
Aliev, G
Smith, MA
Seyidova, D
Neal, ML
Lamb, BT
Nunomura, A
Gasimov, EK
Vinters, HV
Perry, G
LaManna, JC
Friedland, RP
机构:
[1] Case Western Reserve Univ, Sch Med, Ctr Electron Microscopy, Cleveland, OH 44106 USA
[2] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
[3] Case Western Reserve Univ, Dept Anat, Cleveland, OH 44106 USA
[4] Case Western Reserve Univ, Dept Neurol, Cleveland, OH 44106 USA
[5] Case Western Reserve Univ, Dept Genet, Cleveland, OH 44106 USA
[6] Asahikawa Med Coll, Dept Psychiat & Neurol, Asahikawa, Hokkaido 078, Japan
[7] Baku Med Univ, Dept Histol & Embryol, Baku, Azerbaijan
[8] Univ Calif Los Angeles, Med Ctr, Dept Pathol & Lab Med, Sect Neuropathol, Los Angeles, CA 90024 USA
[9] Univ Calif Los Angeles, Med Ctr, Inst Brain Res, Los Angeles, CA 90024 USA
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D O I:
暂无
中图分类号:
R74 [神经病学与精神病学];
学科分类号:
摘要:
Alzheimer's disease (AD) and stroke are two leading causes of age-associated dementia. A rapidly growing body of evidence Indicates that increased oxidative stress from reactive oxygen radicals is associated with the aging process and age-related degenerative disorders such as atherosclerosis, Ischemia/reperfusion, arthritis, stroke, and neurodegenerative diseases. New evidence has also indicated that vascular lesions are a key factor in the development of AD. This Idea is based on a positive correlation between AD and cardiovascular and cerebrovascular diseases such as arterio- and atherosclerosis and ischemia/reperfusion injury. In this review we consider recent evidence supporting the existence of an intimate relationship between oxidative stress and vascular lesions in the pathobiology of AD. We also consider the opportunities for therapeutic interventions based on the molecular pathways involved with these causal relationships.
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页码:21 / 35
页数:15
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