Homocysteine (Hcy): has been proven to be an independent risk factor for atherosclerosis, and recent studies have shown a close relationship between Hcy and the occurrence, development and prognosis of certain neurodegenerative diseases. Certain B vitamins, such as VB12, folic acid and VB6, play a very important role as enzyme cofactors in the metabolism of Hcy, and deficiency of folic acid, VB12 or VB6 can cause an increase in plasma Hcy levels, which can lead to impairment of brain function and trigger or promote the occurrence and development of neurodegenerative diseases. Therefore, it is possible to prevent and treat neurodegenerative diseases by intervening in the levels of Hcy and related B vitamins. Hcy is an intermediate product of the metabolism of the nutritionally essential amino acid methionine (Met), which is known as 2-amino-4 mercaptobutyric acid. The normal plasma concentration of Hcy is 5-15 μmolL-1. There are two main metabolic pathways for Hcy: first, the transsulfuration pathway, in which Hcy and serine are catalyzed by cystathione-β-synthase (CBS) to produce cystathionine, which is further broken down to produce cysteine and α-ketobutyric acid. The second is the remethylation pathway, in which Hcy is remethylated to produce Met, which is catalyzed by Met synthase (MS), and the required methyl group is provided by N5-methyltetrahydrofolate, which is catalyzed by N5,N10-methylenetetrahydrofolate via methylenetetrahydrofolate reductase (MTHFR). folic acid are important cofactors of the remethylation pathway. Folic acid and VB6 play very critical roles as important cofactors in the metabolism of Hcy, while CBS, MS and MTHFR are key enzymes in the metabolism of Hcy. Failure of any of them can lead to metabolic disorders of Hcy, resulting in elevated plasma Hcy levels and hyperhomocysteinemia. Studies have shown that hyperhomocysteinemia is closely related to the occurrence and development of cerebrovascular disease and certain neurodegenerative diseases. With further research into the pathogenesis and prevention of neurodegenerative diseases, the link between Hcy and B vitamin deficiency and these diseases is becoming a new breakthrough point in the understanding and prevention of neurodegenerative diseases. Both population studies and animal studies have confirmed a strong association between hyperhomocysteinemia and AD. Of 10 studies of the relationship between Alzheimer’s disease and Hcy, eight showed that plasma Hcy levels were significantly higher in Alzheimer’s patients than in controls. 1998 McCaddon et al. studied 30 individuals over 65 years of age with a clinical diagnosis of AD and found that their plasma Hcy levels correlated significantly with Cambridge Cognitive Performance Examination scores. A more recent study suggests that elevated blood Hcy levels may increase the risk of developing AD and suggests that Hcy is an independent risk factor for dementia and AD.