Acquired cobalamin (Cbl)-deficiency in human induces a neuropathy that is known as subacute combined degeneration or Cbl-deficient neuropathy. The neurologic features of Cbl-deficient neuropathy typically include a spastic paraparesis or tetraparesis, extensor plantar response, and impaired perception of position and vibration. The neurological disease affects both the central- and the peripheral nervous systems. Patients affected by other neurological disorders like Alzheimer's disease had significantly higher ratio of Cbl analogue/corrinoid than control subjects. The role of oxidative stress in the pathogenesis of Alzheimer's disease has been repeatedly reported. Several studies have confirmed the association between low concentrations of plasma Cbl, elevated homocysteine and Alzheimer's disease. Chronic cerebral oxidative stress may in turn cause depletion of B-vitamins thus explaining the association between Alzheimer's disease and low Cbl. Besides Cbl-deficient neuropathy and Alzheimer's disease, multiple sclerosis could also present Cbl abnormalities, although the exact pathogenetic role of Cbl in the diseases is unclear.