Vitamin A and Alzheimer's disease

Abstract

The deposition of amyloid β-protein (Aβ) in the brain is an invariant feature of Alzheimer's disease (AD). Vitamin A, which has been traditionally considered an anti-oxidant compound, plays a role in maintaining higher function in the central nervous system. Plasma or cerebrospinal fluid concentrations of vitamin A and β-carotene have been reported to be lower in AD patients, and these vitamins have been clinically shown to slow the progression of dementia. Vitamin A (retinol, retinal and retinoic acid) and β-carotene have been shown in in vitro studies to inhibit the formation, extension and destabilizing effects of β-amyloid fibrils. Recently, the inhibition of the oligomerization of Aβ has been suggested as a possible therapeutic target for the treatment of AD. We have recently shown the inhibitory effects of vitamin A and β-carotene on the oligomerization of Aβ40 and Aβ42 in vitro. In previous in vivo studies, intraperitoneal injections of vitamin A decreased brain Aβ deposition and tau phosphorylation in transgenic mouse models of AD, attenuated neuronal degeneration, and improved spatial learning and memory. Thus, vitamin A and β-carotene could be key molecules for the prevention and therapy of AD.