Vitamin B12 deficiency as an etiology of cognitive impairment and dementia

Abstract

Vitamin B12 is a chemically complex molecule, which requires a series of mechanisms that ensure its stability and absorption, it is found in various foods for daily consumption such as liver, fish, shellfish, and fortified cereals. It has been shown that this vitamin fungus works in various devices and systems, mainly at the hematological level, as an erythrocyte component, and at the neurological level in the composition of myelin. When there is vitamin 12 deficiency, due to alterations in intake or absorption, clinical and laboratory manifestations occur, such as megaloblastic anemia, neuropathy, myelopathy, predominantly behavioral neuropsychiatric alterations, ataxia, extrapyramidal signs, among others and in most these cases resolve with targeted treatment. There are studies that indicate that early replacement of vitamin B12 could contribute to symptomatic improvement, reversing the initial manifestations of cognitive impairment, dementia and myelopathy, while late replacement could be linked to irreversible changes. Despite these studies, there are no conclusive data on the interrelation between vitamin B12 deficiency and cognitive impairment and/or dementia, since the underlying pathophysiological mechanism is still unclear, but there is evidence of improvement at the cognitive level when replacement is generated, having ruled out other primary causes of deterioration or dementia.