Smach M A, Naffeti S, Charfeddine B, Ben Abdallah J, Othmen L B, Letaef A, Limem K
Department of Biochemistry, Faculty of Medicine of Sousse, 4002 Sousse, Tunisie.
Pathol Biol (Paris). 2013 Oct;61(5):184-92. doi: 10.1016/j.patbio.2012.04.003. Epub 2012 May 29.
Hyperhomocysteinemia is a risk factor for neurological diseases, but the underlying pathophysiology has not been adequately explained. Mild hyperhomocysteinemia, which is sometimes associated with a low plasma level of vitamin B9, B12 and folic acid, is responsible in the toxicity in neural cell by activating NMDA receptor. Indeed, even if vitamin supplementation has clearly proven its efficiency on lowering plasma levels of homocysteine, recent studies do not show any positive effect of vitamin therapy on cognitive function. The hypothesis that this therapy is inefficient has been recently reinforced by two randomized trials on the effects of vitamin supplementation. Several hypotheses still need to be explored: Mechanisms of homocysteine toxicity and that of total uselessness of vitamin supplementation; the possible need to complete the actual data with further, more powerful studies in order to prove the role of homocysteine in the development of neurodegenerative diseases and a clinical effect of vitamin therapy.
高同型半胱氨酸血症是神经疾病的一个风险因素，但其潜在的病理生理学机制尚未得到充分解释。轻度高同型半胱氨酸血症有时与血浆中维生素B9、B12和叶酸水平较低有关，它通过激活NMDA受体对神经细胞产生毒性作用。事实上，尽管补充维生素已明确证明其在降低血浆同型半胱氨酸水平方面的有效性，但最近的研究并未显示维生素疗法对认知功能有任何积极影响。关于这种疗法无效的假说最近因两项关于补充维生素效果的随机试验而得到加强。仍有几个假说有待探索：同型半胱氨酸毒性的机制以及补充维生素完全无效的机制；可能需要通过进一步更有力的研究来完善现有数据，以证明同型半胱氨酸在神经退行性疾病发展中的作用以及维生素疗法的临床效果。
