Synapse loss and synaptic dysfunction are established features of the neuropathological processes involved in the early stages of Alzheimer’s disease (AD). This early involvement of synapses is very likely the neuropathological substrate for the early symptoms. Indeed, synapse loss has been shown to be the closest pathological correlate of memory dysfunction. Consequently, synapse loss and membrane-related pathology provide viable targets for intervention in AD.
Studies have shown that blood levels of key nutrients, essential for the formation and turnover of synapses are lower in patients with AD. This includes uridine, docosahexaenoic acid, eicosapentaenoic acid, choline, phospholipids, in combinations with certain vitamins and cofactors such as folic acid, vitamins B12, B6, C, E, and selenium. Furthermore lower brain and CSF levels of these nutrients have been demonstrated in subjects with AD.
The specific nutrient combination Souvenaid, was developed to provide the key nutrients required for synapse formation and membrane-related pathology in order to ameliorate synapse dysfunction and loss in AD.
This talk will focus on the rationale and preclinical evidence behind the hypothesis, that providing nutritional precursors and cofactors will act together to support membrane formation, and the broad clinical study program investigating the potential of this nutrient combination in AD.