Given the relevance of selenium metabolism in the brain4,53, the limited evidence available on the involvement of selenoprotein P in the etiology of neurological diseases in humans, and the inability of peripheral indicators (such as serum) of selenoprotein P status in relation to its central nervous system concentrations, further in vivo human studies assessing the relation between brain selenoprotein P and dementia risk are clearly warranted. The gene discussed is SELENOP; the disease is dementia.