Vitamin B12 deficiency impairs neurological function through several mechanisms. First, vitamin B12 mediates two important enzymatic reactions in the body, one is the conversion of methylmalonyl CoA to succinyl CoA, and the other is the conversion of Hcy to methionine. In the latter reaction, methylcobalamin acts as a cofactor for methionine synthase, transferring the methyl group of 5methyltetrahydrofolate to Hcy to enable the formation of methionine. Adenosylated methionine (SAM) acts as a donor of methyl groups and is involved in the methylation of many important substances, including DNA, RNA, proteins, myelin and many neurotransmitters. Once vitamin B12 is deficient in the body, SAM production is blocked, leading to severe metabolic disorders and causing neuropathies such as impaired formation and loss of nerve myelin sheaths. Secondly, the accumulation of Hcy due to impaired conversion produces cytotoxic effects and impairs neurological function through mechanisms such as stimulation of N-methyl-D-aspartate (NMDA) receptors and activation of apoptosis-related proteins Bax and p53. Third, impaired methionine synthesis prevents the conversion of methyltetrahydrofolate to tetrahydrofolate, which leads to reduced production of methylenetetrahydrofolate. The latter is an important cofactor for the conversion of RNA precursor deoxyuridine into DNA precursor deoxythymidine, and its reduction causes blockage of DNA synthesis and neurological dysfunction, which is the so-called “folate trap” hypothesis. Finally, vitamin B12 deficiency causes the accumulation of S-adenosyl homocysteine (SAH), which is a powerful inhibitor of many methyltransferases, and its reduced amount inevitably leads to the blockage of methylation process and affects the normal metabolism of neuronal cells [4].