Since its discovery during the epidemic of rickets in the early 1920s, ă the physiological effects of vitamin D on calcium/ phosphorus ă homeostasis have been thoroughly studied. Along with the understanding ă of its actions on skeletal diseases and advances in cellular and ă molecular biology, this misnamed vitamin has gained attention as a ă potential player in a growing number of physiological processes and a ă variety of diseases. During the last 25 years, vitamin D has emerged as ă a serious candidate in nervous system development and function and a ă therapeutic tool in a number of neurological pathologies. More recently, ă experimental and pre-clinical data suggest a link between vitamin D ă status and cognitive function. Human studies strongly support a ă correlation between low levels of circulating 25-hydroxyvitamin D ă (25(OH) D) and cognitive impairment or dementia in aging populations. In ă parallel, animal studies show that supplementation with vitamin D is ă protective against biological processes associated with Alzheimer's ă disease (AD) and enhances learning and memory performance in various ă animal models of aging and AD. These experimental observations support ă multiple mechanisms by which vitamin D can act against neurodegenerative ă processes. However, clinical interventional studies are disappointing ă and fail to associate increased 25(OH) D levels with improved cognitive ă outcomes. This review collects the current available data from both ă animal and human studies and discusses the considerations that future ă studies examining the effects of vitamin D status on neurocognitive ă function might consider.