Beyond the classically described role of regulation of calcium andbone metabolism, vitamin D exerts an effect on other target tissues,such as cortical and subcortical neurons, which are essential to cognition.Vitamin D has experimentally demonstrated neuroprotectiveproperties (including the regulation of calcium flux, antioxidant andanti-inflammatory effects) and may protect neurons against neurodegenerativemechanisms of Alzheimer’s disease (AD). The vast majorityof seniors have hypovitaminosis D. From the brain’s point of view, correctionof hypovitaminosis D is justified by numerous cross-sectionaland longitudinal studies reporting an association between low levelsof vitamin D and poor cognitive performance, specifically executivedysfunction. Similarly, observational studies have shown an associationbetween inadequate dietary intake of vitamin D and cognitivedisorders, including an increased risk of developing AD. Although nocontrolled trial against placebo has examined yet the efficacy of vitaminD supplements to prevent AD, several quasi-experimental studieshave found that older adults supplemented with vitamin D improvedtheir cognitive performance after 1-15 months of treatment. It appearsparticularly important to maintain vitamin D levels high enough toslow or prevent or correct the neurological disorders of AD. In particular,while cognitive decline is slowed down only transiently with communithesymptomatic antidementia treatments, future treatment optionscould be based on drug combinations in order to prevent several neurodegenerativemechanisms at once. As such, vitamin D enhances theefficacy of memantine in terms of neuronal protection and preventionof cognitive decline in AD.