Question

Mechanisms of homocysteine-induced multiples sclerosis

Answer 1

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Deficiencies in vitamin B6, vitamin B12, or folate are associated with elevated plasma levels of homocysteine. In the search for a possible relationship between vitamin B12 deficiency and multiple sclerosis (MS), two studies found elevated plasma homocysteine levels in patients with MS.1,2 The frequency of biologically relevant vitamin B12 deficiency in MS is low,2,3 and it is uncertain whether this provides a satisfactory explanation for the raised plasma homocysteine concentrations. A recent report studying oxidative stress found elevated plasma homocysteine levels in patients with secondary progressive MS compared with healthy controls,4 but another group reported no significant difference in plasma homocysteine concentrations between patients with MS and controls.5

The nervous system may be particularly sensitive to extracellular homocysteine, as it promotes excitotoxicity via stimulation of N‐methyl‐D‐asparate receptors, and damages neuronal DNA, thereby triggering apoptosis.6,7 Increased levels of homocysteine may play a role in the pathogenesis of Alzheimer's disease, through both vascular and degenerative mechanisms, and hasten the onset and progression of Parkinson's disease.8,9 High homocysteine resulting from poor reconversion to methionine is related to low methionine availability. Methionine is an important methyl group donor in many biochemical processes. Hypomethylation of myelin basic protein (MBP)‐arginine decreases the hydrophobicity of MBP and could give rise to less stable myelin structures and enhance degeneration of the myelin sheath.10