Figure 1.

Mechanisms of homocysteine-induced neurotoxicity. The figure depicts the various mechanisms involved in the neurotoxic effects of elevated homocysteine levels. Multiple factors, including nutritive folate deficiency, diseases, aging, and MTHFR C677T polymorphism, can contribute to hyperhomocysteinemia. Elevated homocysteine levels disrupt the delicate balance of key biochemical processes within the central nervous system. The cascade of events triggered by hyperhomocysteinemia includes a decrease in S-adenosylmethionine (SAMe) levels and an increase in S-adenosylhomocysteine (SAH) levels. This imbalance leads to heightened oxidative stress due to elevated reactive oxygen species (ROS) production. The resulting oxidative stress and endothelial dysfunction contribute to neurotoxicity. The neurotoxic effects of elevated homocysteine levels are implicated in the development of depressive illness. The disrupted biochemical pathways and increased oxidative stress ultimately contribute to the pathogenesis of depressive symptoms. The figure has been modified based on [78].