Homocysteine Level and Mechanisms of Injury in Parkinson’s Disease as Related to MTHFR, MTR, and MTHFD1 Genes Polymorphisms and L-Dopa Treatment
This review article by Rozycka et al (2014) discusses hyperhomocysteinemia (HHcy) and its effect on Alzheimer’s and Parkinson’s Disease. This is due HHcy being found to have a neurotoxic effect that participates in neuro-degeneration via excititoxicity, oxidative stress calcium accumulation and apoptosis.
HHcy has been thought to interact with dopaminergic receptors and neurons, with several studies linking a higher concentration of Hcy in PD relating to the long term administration of levodopa.
HHcy can also reflect nutritional deficiencies involved in the remethylation of Hcy into Methionine (B12& folate_ and the transulfuration to cysteine (B6). Genetic polymorphisms involved in folate metabolism (such as MTHFR C677T, A1298C. C1793A, MTR A2756G and MTHFD1 A1958A) have been found to be generally increased in patients with Parkinson’s Disease, as well as reduced concentrations of B vitamins. Increased levels of Hcy in Parkinson’s disease could potentially lead to dementia, depression and progression of the disease.
While this article highlights the effect of Hcy on brain function, it also highlights the importance of sufficient nutrition to allow our methylation cycles to function sufficiently. This ensures our brain tissue is not damaged by high homocysteine.