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Hyperhomocysteinemia is an emerging comorbidity in ischemic stroke
1Department of Neurology, University of New Mexico Health Sciences Center, 1 University of New Mexico, Albuquerque, NM 87131, USA.
Insights
Mild hyperhomocysteinemia, an elevation of homocysteine, may worsen ischemic stroke outcomes. This review examines rodent models and mechanisms, suggesting hyperhomocysteinemia as a stroke comorbidity for therapeutic development.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Stroke Research
Background:
- Hyperhomocysteinemia (elevated homocysteine) is a known risk factor for ischemic stroke.
- The impact of hyperhomocysteinemia predisposition on stroke severity remains unclear.
- Understanding this link is crucial for developing effective stroke treatments.
Purpose of the Study:
- To review rodent models of hyperhomocysteinemia.
- To assess the effect of mild hyperhomocysteinemia on ischemic brain damage.
- To summarize homocysteine-induced neurotoxicity mechanisms.
Main Methods:
- Analysis of existing literature on rodent models of hyperhomocysteinemia.
- Evaluation of preclinical studies on mild hyperhomocysteinemia and ischemic brain damage.
- Synthesis of research on neurotoxic mechanisms of homocysteine.
Main Results:
- Rodent models offer insights but have limitations for studying hyperhomocysteinemia.
- Mild hyperhomocysteinemia exacerbates ischemic brain damage in preclinical models.
- Homocysteine exerts neurotoxicity through various identified mechanisms.
Conclusions:
- Hyperhomocysteinemia may be a significant comorbidity influencing ischemic stroke severity.
- Findings support considering hyperhomocysteinemia in stroke therapeutic strategies.
- Further research is warranted to translate these findings into clinical practice.
Abstract:
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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