期刊
EXPERIMENTAL NEUROLOGY
卷 336, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2020.113541
关键词
Stroke; Comorbidity; Hyperhomocysteinemia; Homocysteine; GluN2A-NMDA receptors; ERK MAPK
资金
- National Institutes of Health [RO1 NS083914]
Hyperhomocysteinemia, a common metabolic disorder, is considered a risk factor for ischemic stroke, but it is unclear whether predisposition to this disorder affects the severity of stroke outcome. Current research focuses on the advantages and limitations of rodent models, the impact of mild hyperhomocysteinemia on ischemic brain damage, and the mechanisms of homocysteine-induced neurotoxicity. These findings provide insight into hyperhomocysteinemia as a comorbidity for ischemic stroke and its implications for potential therapeutic agents.
Hyperhomocysteinemia or systemic elevation of the amino acid homocysteine is a common metabolic disorder that is considered to be a risk factor for ischemic stroke. However, it is still unclear whether predisposition to hyperhomocysteinemia could contribute to the severity of stroke outcome. This review highlights the advantages and limitations of the current rodent models of hyperhomocysteinemia, describes the consequence of mild hyperhomocysteinemia on the severity of ischemic brain damage in preclinical studies and summarizes the mechanisms involved in homocysteine induced neurotoxicity. The findings provide the premise for establishing hyperhomocysteinemia as a comorbidity for ischemic stroke and should be taken into consideration while developing potential therapeutic agents for stroke treatment.
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