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Hyperhomocysteinemia as a Risk Factor for Vascular Contributions to Cognitive Impairment and Dementia

Brittani R Price1, Donna M Wilcock1, Erica M Weekman1

  • 1Department of Physiology, Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, United States.

Frontiers in Aging Neuroscience
|November 16, 2018
PubMed

Insights

Hyperhomocysteinemia (HHcy), a risk factor for vascular contributions to cognitive impairment and dementia (VCID), is linked to B vitamin deficiency. Lowering homocysteine via B vitamin supplementation shows conflicting results in clinical trials for treating HHcy-induced VCID.

Area of Science:

  • Neurology
  • Gerontology
  • Biochemistry

Background:

  • Vascular contributions to cognitive impairment and dementia (VCID) is the second leading cause of dementia, impacting 10-40% of patients.
  • Hyperhomocysteinemia (HHcy), elevated plasma homocysteine levels, is an underrecognized major risk factor for VCID.
  • B vitamin deficiency, a common cause of HHcy, is prevalent in the elderly population.

Purpose of the Study:

  • To review HHcy as a significant risk factor for VCID.
  • To explore proposed mechanisms underlying homocysteine-induced cognitive decline.
  • To examine clinical trials investigating the efficacy of lowering plasma homocysteine for VCID.

Main Methods:

  • Review of preclinical studies (cell culture, animal models) on homocysteine's mechanisms.
  • Analysis of clinical trial data on B vitamin supplementation for lowering homocysteine.
  • Focus on study design challenges and conflicting results in therapeutic interventions.

Main Results:

  • Conflicting results from clinical trials on B vitamin supplementation for reducing homocysteine and improving cognitive function.
  • Proposed mechanisms in preclinical studies suggest various pathways for homocysteine-induced neurotoxicity.
  • Challenges in study design have impacted the interpretation of therapeutic benefits.

Conclusions:

  • Despite B vitamin supplementation's safety and low cost, its effectiveness in treating HHcy-induced VCID remains uncertain due to conflicting clinical trial outcomes.
  • Understanding the diverse mechanisms of homocysteine's neurotoxicity is crucial for developing targeted therapies.
  • Further research with optimized study designs is needed to clarify the role of homocysteine lowering in VCID prevention and treatment.

Keywords:
B vitaminsdementiahomocysteinehyperhomocysteinemiavascular cognitive impairment and dementia

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