期刊
JOURNAL OF NEUROSCIENCE RESEARCH
卷 94, 期 12, 页码 1588-1603出版社
WILEY
DOI: 10.1002/jnr.23925
关键词
vascular dementia; neurovasculature; neuroinflammation; oxidative stress; inflammasome; cell stress response; hormesis; vitagenes
资金
- Children's Hospital and Clinics Foundation
- William H. and Ruth Crane Schaefer Endowment
Vascular dementia (VaD), considered the second most common cause of cognitive impairment after Alzheimer disease in the elderly, involves the impairment of memory and cognitive function as a consequence of cerebrovascular disease. Chronic cerebral hypoperfusion is a common pathophysiological condition frequently occurring in VaD. It is generally associated with neurovascular degeneration, in which neuronal damage and blood-brain barrier alterations coexist and evoke beta-amyloid-induced oxidative and nitrosative stress, mitochondrial dysfunction, and inflammasome- promoted neuroinflammation, which contribute to and exacerbate the course of disease. Vascular cognitive impairment comprises a heterogeneous group of cognitive disorders of various severity and types that share a presumed vascular etiology. The present study reviews major pathogenic factors involved in VaD, highlighting the relevance of cerebrocellular stress and hormetic responses to neurovascular insult, and addresses these mechanisms as potentially viable and valuable as foci of novel neuroprotective methods to mitigate or prevent VaD. (C) 2016 Wiley Periodicals, Inc.
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