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Cognitive impairment is one of the processes that accompany aging and may depend on nutritional, genetic or environmental factors. The identification of modifiable risk factors provides a crucial approach for the prevention of cognitive decline and neurocognitive disorders. One of the risk factors is the high concentration of plasma homocysteine and it has been associated to histopathological changes in senile dementia and Alzheimer s disease. Clinical trials about this association has shown inconsistent and contradictory results. The purpose of this review is to describe the possible interaction of three factors related with cognitive impairment: a) nutritional factors (homocysteine, folic acid and vitamin B12), b) the use of mental tests such as the Mini Mental State Examination for the diagnosis of cognitive dys- function, and c) the presence of polymorphic genetic variants of the methylenete- trahydrofolate reductase enzyme. A direct consequence of this triple relationship is the treatment with folic acid and vitamin B12, which decrease high concentrations of plasma homocysteine, with a potential for improvement of the clinical symptoms of cognitive decline, and possibly a delay in the progression towards neurocognitive disorder. Public health policies focused on mental health of older adults can identify people with initial cognitive dysfunction through health promotion and preventive measures, where it can be possible to administer B vitamins in order to reduce or minimize the progression of cognitive decline, that could lead to mental disturbances such as neurocognitive disorders.

Homocisteína y trastornos neurocognitivos. ¿Una luz al final del túnel?