Cellular and Molecular Neurobiology · 7 authors, 8 centres
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This narrative review discusses how hyperhomocysteinemia, often caused by vitamin deficiencies and L-dopa therapy in Parkinson's disease patients, may contribute to disease development and progression through mechanisms like oxidative stress and neuroinflammation.
This is a narrative review that synthesizes existing literature on the potential link between hyperhomocysteinemia and Parkinson's disease (PD). The authors discuss how PD patients frequently develop deficiencies in folate, vitamin B6, and B12 due to lifestyle changes and prolonged L-dopa therapy, which can lead to elevated homocysteine levels. The review proposes that hyperhomocysteinemia may contribute to PD neuropathology through several biological mechanisms, including the induction of oxidative stress, mitochondrial dysfunction, apoptosis, endothelial dysfunction, and the activation of inflammatory signaling pathways such as NF-κB and NLRP3 inflammasome. The central argument is that hyperhomocysteinemia could be a separate risk factor that directly degenerates dopaminergic neurons or indirectly exacerbates neuroinflammation in PD. The implications suggest a need for further preclinical and clinical research to validate this proposed pathogenic link.
