Nutrition and Alzheimer’s disease: pre‐clinical concepts

Alzheimer’s disease (AD) is a progressive condition characterized by neurodegeneration and the dense deposition of proteins in the brain. There is no cure for AD and current treatments usually only provide a temporary reduction of symptoms. There is thus a strong unmet need for effective preventative and therapeutic strategies and the potential role for nutrition in such strategies is rapidly gaining interest. An Alzheimer’s brain contains fewer synapses and reduced levels of synaptic proteins and membrane phosphatides. Brain membrane phosphatide synthesis requires at least three dietary precursors: polyunsaturated fatty acids, uridine monophosphate (UMP) and choline. Animal studies have shown that administration of these nutrients increases the level of phosphatides, specific pre‐ or post‐synaptic proteins and the number of dendritic spines – a requirement for new synapse formation. These effects are markedly enhanced when animals receive all three compounds together. This multi‐nutrient approach in animals has also been shown to decrease amyloid beta protein (Aβ) plaque burden, improve learning and memory through increased cholinergic neurotransmission and have a neuroprotective effect in several mouse models of AD. Whether these potential therapeutic effects of a multi‐nutrient approach observed in animal models can also be replicated in a clinical setting warrants further investigation.