Hyperhomocysteinemia is an emerging comorbidity in ischemic stroke

Ranjana Poddar1

  • 1Department of Neurology, University of New Mexico Health Sciences Center, 1 University of New Mexico, Albuquerque, NM 87131, USA.

Experimental Neurology
|December 5, 2020
PubMed

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.

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