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Abstract
Cognitive difficulties in later life can be both aversive and disruptive to older adults and bring about the loss of functional independence. One precursor to cognitive impairment in late life may be vitamin B12 deficiency, and associated elevations in the metabolites methylmalonic acid (MMA) and homocysteine. However, there has been little consensus on a cause-effect relationship between B12 deficiency and cognitive decrements. Furthermore, there is some controversy with respect to the efficacy of B12 replacement in reversing associated cognitive decrements. The current experiments address such questions in a longitudinal study of cognitive ability in B12-deficient versus B12-adequate older adults before and following vitamin B12 supplementation. Participants were classified as B12 deficient based upon elevated MMA levels. Those with elevated MMA levels underwent oral B12 replacement therapy (1000 g pills) with measurement of serum vitamin levels, and measurement of performance on a battery of neuropsychological tests measuring memory, processing speed, reaction time, attention, verbal fluency and visual abstract reasoning being administered, at three time points over a period of twelve months. In the first experiment, participants with elevated MMA levels at baseline testing showed cognitive impairment relative to those with normal MMA levels in the domains of memory, verbal fluency and abstract reasoning. In the second experiment, following a twelve month trial of vitamin B12 supplementation, those responding metabolically to treatment demonstrated marked and significantly better improvements in memory and abstract reasoning relative to the placebo group. Findings suggest that reducing plasma MMA concentrations by administering vitamin B12 supplements may provide protection against cognitive decline as well as reverse potential cognitive deficits related to vitamin B12 deficiency in this and other elderly populations.