Hyperhomocysteinemia for Alzheimer’s Disease: Risk Factor, Biomarker or Both?

Background: Alzheimer’s disease (AD) is the most common display ofneurodegeneration. It is a multifactorial disease both at earlyand late-onset. A number of studies have found that H-Hcycan be significantly correlated with increased risk of AD in the late onset form only. Methods and Results: Several evidences shown that H-Hcy may promote AD by more than one mechanism including impair lipoprotein E genotype, involved in lipid transport and neuronal repair and synaptogenesis. But, endothelial dysfunction; neurotoxicity; apoptosis; Ca++dysregulation; neuronal DNA damage and homocysteic acid (N-methyl-D-aspartate agonist) production are also responsible of AD. Some of these have a causal connection with AD. Others act a simple marker of different conditions, such as DNA hypometilation consequent to H-Hcy. Both these mechanisms can induce AD, acting such as risk factor or marker at the same time. Conclusions: Conclusively, H-Hcy can act such as risk factor, marker, or both for AD pathogenesis by unknown mechanisms.