Critical levels of brain atrophy associated with homocysteine and cognitive decline

Abstract Few B-vitamin trials to lower homocysteine (Hcy) have reported evidence of beneficial effects on cognition in older adults with cognitive impairment or Alzheimer's disease. This article reviews the role of Hcy in cognitive decline. It also considers some reasons why meta-analyses have...

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Bibliographic Details
Published in:Neurobiology of aging 2014-09, Vol.35, p.S35-S39
Main Author: de Jager, Celeste A
Format: Article
Language:English
Subjects:
Alzheimer's disease
Atrophy
B vitamins
B12 deficiency
Brain - pathology
Cognition
Cognition Disorders - drug therapy
Cognition Disorders - etiology
Cognition Disorders - metabolism
Cognition Disorders - pathology
Folic acid
Folic Acid - therapeutic use
Homocysteine
Homocysteine - blood
Humans
Internal Medicine
Mild cognitive impairment
Neurology
Vitamin B 12 Deficiency - complications
Vitamin B Complex - therapeutic use
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Summary:Abstract Few B-vitamin trials to lower homocysteine (Hcy) have reported evidence of beneficial effects on cognition in older adults with cognitive impairment or Alzheimer's disease. This article reviews the role of Hcy in cognitive decline. It also considers some reasons why meta-analyses have failed to find effects of B-vitamin treatment. Findings from the successful VITACOG trial are examined from a new perspective of critical levels of Hcy and brain atrophy that may impact on the efficacy of B-vitamin treatment. It appears that there is a critical level of brain shrinkage, possibly mediated by elevated Hcy, which when reached, results in cognitive decline, especially in episodic memory performance. Supplements, food sources, and effects of folic acid fortification are discussed in relation to B12 deficiency.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2014.03.040