Tags

Type your tag names separated by a space and hit enter

The methionine-homocysteine cycle and its effects on cognitive diseases.
Altern Med Rev 2003; 8(1):7-19AM

Abstract

Homocysteine, a sulfur-containing amino acid, is a metabolite of the essential amino acid methionine, and exists at a critical biochemical intersection in the methionine cycle - between S-adenosylmethionine, the indispensable ubiquitous methyl donor, and vitamins B12 and folic acid. High blood levels of homocysteine signal a breakdown in this vital process, resulting in far-reaching biochemical and life consequences. The link between homocysteine and cardiovascular disease is well established, and decreasing plasma total homocysteine by providing nutritional cofactors for its metabolism has been shown to reduce the risk of cardiovascular events. Information has been emerging regarding a connection between homocysteine metabolism and cognitive function, from mild cognitive decline (age-related memory loss) to vascular dementia and Alzheimer's disease. Significant deficiencies in the homocysteine re-methylation cofactors cobalamin (B12) and folate, as well as the trans-sulfuration cofactor vitamin B6, are commonly seen in the elderly population, with a resultant increase in homocysteine with advancing age. Hyperhomocysteinemia has been shown to be an independent risk factor for cognitive dysfunction. Indirect and direct vascular damage can be caused by homocysteine, which has been implicated in vascular dementia, with an increased risk of multiple brain infarcts and dementia as homocysteine levels rise. A significant correlation has been found between risk of Alzheimer's disease and high plasma levels of homocysteine, as well as low levels of folic acid, and vitamins B6 and B12. All of these disease associations are thought to be interrelated via increased homocysteine and S-adenosylhomocysteine and subsequent hypomethylation of numerous substances, including DNA and proteins, that render vascular structures and neurons more susceptible to damage and apoptosis. Providing the nutritional cofactors for proper functioning of the methionine cycle may improve methylation and protect the brain from damage. Further studies need to be performed to assess whether this will also reduce the risk of cognitive diseases and/or improve cognitive functioning.

Authors+Show Affiliations

Thorne Research, P.O. Box 25, Dover, ID 83825. alan@thorne.com

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12611557

Citation

Miller, Alan L.. "The Methionine-homocysteine Cycle and Its Effects On Cognitive Diseases." Alternative Medicine Review : a Journal of Clinical Therapeutic, vol. 8, no. 1, 2003, pp. 7-19.
Miller AL. The methionine-homocysteine cycle and its effects on cognitive diseases. Altern Med Rev. 2003;8(1):7-19.
Miller, A. L. (2003). The methionine-homocysteine cycle and its effects on cognitive diseases. Alternative Medicine Review : a Journal of Clinical Therapeutic, 8(1), pp. 7-19.
Miller AL. The Methionine-homocysteine Cycle and Its Effects On Cognitive Diseases. Altern Med Rev. 2003;8(1):7-19. PubMed PMID: 12611557.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The methionine-homocysteine cycle and its effects on cognitive diseases. A1 - Miller,Alan L, PY - 2003/3/4/pubmed PY - 2003/4/22/medline PY - 2003/3/4/entrez SP - 7 EP - 19 JF - Alternative medicine review : a journal of clinical therapeutic JO - Altern Med Rev VL - 8 IS - 1 N2 - Homocysteine, a sulfur-containing amino acid, is a metabolite of the essential amino acid methionine, and exists at a critical biochemical intersection in the methionine cycle - between S-adenosylmethionine, the indispensable ubiquitous methyl donor, and vitamins B12 and folic acid. High blood levels of homocysteine signal a breakdown in this vital process, resulting in far-reaching biochemical and life consequences. The link between homocysteine and cardiovascular disease is well established, and decreasing plasma total homocysteine by providing nutritional cofactors for its metabolism has been shown to reduce the risk of cardiovascular events. Information has been emerging regarding a connection between homocysteine metabolism and cognitive function, from mild cognitive decline (age-related memory loss) to vascular dementia and Alzheimer's disease. Significant deficiencies in the homocysteine re-methylation cofactors cobalamin (B12) and folate, as well as the trans-sulfuration cofactor vitamin B6, are commonly seen in the elderly population, with a resultant increase in homocysteine with advancing age. Hyperhomocysteinemia has been shown to be an independent risk factor for cognitive dysfunction. Indirect and direct vascular damage can be caused by homocysteine, which has been implicated in vascular dementia, with an increased risk of multiple brain infarcts and dementia as homocysteine levels rise. A significant correlation has been found between risk of Alzheimer's disease and high plasma levels of homocysteine, as well as low levels of folic acid, and vitamins B6 and B12. All of these disease associations are thought to be interrelated via increased homocysteine and S-adenosylhomocysteine and subsequent hypomethylation of numerous substances, including DNA and proteins, that render vascular structures and neurons more susceptible to damage and apoptosis. Providing the nutritional cofactors for proper functioning of the methionine cycle may improve methylation and protect the brain from damage. Further studies need to be performed to assess whether this will also reduce the risk of cognitive diseases and/or improve cognitive functioning. SN - 1089-5159 UR - https://www.unboundmedicine.com/medline/citation/12611557/The_methionine_homocysteine_cycle_and_its_effects_on_cognitive_diseases_ L2 - http://archive.foundationalmedicinereview.com/publications/8/1/7.pdf DB - PRIME DP - Unbound Medicine ER -