Abstract

HOMOCYSTEINE AND METABOLIC SYNDROME: FROM CLUSTERING TO ADDITIONAL UTILITY IN PREDICTION OF COGNITIVE DECLINE

V. Sreedevi*, Dr. P. R. Anand Vijaya Kumar, G. Neelamma, Treesa P. Varghes

ABSTRACT

Homocysteine (Hcy) is a sulfur-containing amino acid that is generated during methionine metabolism. It has a physiologic role in DNA metabolism via methylation, a process governed by the presentation of folate, and vitamins B6 and B12. Physiologic Hcy levels are determined primarily by dietary intake and vitamin status. Elevated plasma levels of Hcy (eHcy) can be caused by deficiency of either vitamin B12 or folate, or a combination thereof. Certain genetic factors also cause eHcy, such as C667T substitution of the gene encoding methylenetetrahydrofolate reductase. eHcy has been observed in several medical conditions, such as cardiovascular disorders, atherosclerosis, myocardial infarction, stroke, dementia, Parkinson's disease, multiple sclerosis, epilepsy, and eclampsia. Moreover an elevated blood level of homocysteine is a risk factor for cognitive impairment and dementia. Homocysteine can be lowered by folate and/or vitamin B12 supplementation; antioxidants might also be required for optimal reduction in neurovascular tissue. This report presents clinical and radiological findings from administering the antioxidant N-acetylcysteine together with B vitamins to cognitively impaired patients with hyperhomocysteinaemia. There is evidence from laboratory and clinical studies that Hcy, and especially eHcy, exerts direct toxic effects on both the vascular and nervous systems. This article provides a review of the current literature on the possible roles of eHcy relevant to various neurologic disorders.

Keywords: Gene encoding, Multiple sclerosis, Cognitive impairment, antioxidants, Hyperhomocysteinaemia etc.