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Homocysteine and Alzheimer's disease.
Lancet Neurol. 2003 Jul; 2(7):425-8.LN

Abstract

BACKGROUND

A high circulating concentration of the amino acid homocysteine is an independent risk factor for stroke. Alzheimer's disease (AD) commonly co-occurs with stroke. Epidemiological studies found associations between hyperhomocysteinaemia and both histologically confirmed AD and disease progression and revealed that dementia in AD was associated with evidence of brain infarcts on autopsy. Thus, hyperhomocysteinaemia and AD could be linked by stroke or microvascular disease. However, given known relations between B-group-vitamin deficiency and both hyperhomocysteinaemia and neurological dysfunction, direct causal mechanisms are also plausible.

RECENT DEVELOPMENTS

A recent prospective study (S Seshadri and colleagues N Engl J Med; 2002 346: 476-83) showed hyperhomocysteinaemia to be a strong, independent risk factor for dementia and AD. The researchers found a graded increase in risk of both outcomes with rising plasma concentration of homocysteine after multivariate control for putative risk factors for AD. In conjunction with demonstration of a fall in homocysteine concentrations in response to increasing B-group-vitamin status, these findings give hope that mental decline, or AD itself, could be prevented by dietary modification or food fortification. WHERE NEXT? 25% of dementia cases are attributed to stroke. The possibility that some of the other 75% might be prevented by the lowering of homocysteine concentrations greatly increases the hope of maintaining self-sufficiency into old age. If homocysteine lowering can reduce the incidence of dementia or AD, decreased incidence of these disorders may be seen in Canada and the USA, where government-mandated folate-fortification programmes are in effect. Future research should focus on early detection of AD and on the possibility that the disease itself, or its primary symptom, could be prevented by folate supplementation.

Authors+Show Affiliations

Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA. martha.morris@tufts.edu <martha.morris@tufts.edu>

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

12849121

Citation

Morris, Martha Savaria. "Homocysteine and Alzheimer's Disease." The Lancet. Neurology, vol. 2, no. 7, 2003, pp. 425-8.
Morris MS. Homocysteine and Alzheimer's disease. Lancet Neurol. 2003;2(7):425-8.
Morris, M. S. (2003). Homocysteine and Alzheimer's disease. The Lancet. Neurology, 2(7), 425-8.
Morris MS. Homocysteine and Alzheimer's Disease. Lancet Neurol. 2003;2(7):425-8. PubMed PMID: 12849121.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Homocysteine and Alzheimer's disease. A1 - Morris,Martha Savaria, PY - 2003/7/10/pubmed PY - 2003/9/4/medline PY - 2003/7/10/entrez SP - 425 EP - 8 JF - The Lancet. Neurology JO - Lancet Neurol VL - 2 IS - 7 N2 - BACKGROUND: A high circulating concentration of the amino acid homocysteine is an independent risk factor for stroke. Alzheimer's disease (AD) commonly co-occurs with stroke. Epidemiological studies found associations between hyperhomocysteinaemia and both histologically confirmed AD and disease progression and revealed that dementia in AD was associated with evidence of brain infarcts on autopsy. Thus, hyperhomocysteinaemia and AD could be linked by stroke or microvascular disease. However, given known relations between B-group-vitamin deficiency and both hyperhomocysteinaemia and neurological dysfunction, direct causal mechanisms are also plausible. RECENT DEVELOPMENTS: A recent prospective study (S Seshadri and colleagues N Engl J Med; 2002 346: 476-83) showed hyperhomocysteinaemia to be a strong, independent risk factor for dementia and AD. The researchers found a graded increase in risk of both outcomes with rising plasma concentration of homocysteine after multivariate control for putative risk factors for AD. In conjunction with demonstration of a fall in homocysteine concentrations in response to increasing B-group-vitamin status, these findings give hope that mental decline, or AD itself, could be prevented by dietary modification or food fortification. WHERE NEXT? 25% of dementia cases are attributed to stroke. The possibility that some of the other 75% might be prevented by the lowering of homocysteine concentrations greatly increases the hope of maintaining self-sufficiency into old age. If homocysteine lowering can reduce the incidence of dementia or AD, decreased incidence of these disorders may be seen in Canada and the USA, where government-mandated folate-fortification programmes are in effect. Future research should focus on early detection of AD and on the possibility that the disease itself, or its primary symptom, could be prevented by folate supplementation. SN - 1474-4422 UR - https://www.unboundmedicine.com/medline/citation/12849121/Homocysteine_and_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1474442203004381 DB - PRIME DP - Unbound Medicine ER -
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