Alzheimer's Research UK 2016 Conference report.

The annual Alzheimer's Research UK (ARUK) Conference was hosted by the Manchester and North West Network Centre on March 8-9, 2016. In this report, we provide a summary of the research presented.

Report from the Alzheimer's Research UK Conference 2015.

On 10-11 March 2015 University College London hosted the annual Alzheimer's Research UK Conference. This report provides an overview of the presentations and discussions that took place.

Dietary (-)-epicatechin as a potent inhibitor of βγ-secretase amyloid precursor protein processing.

Flavonoids, a group of dietary polyphenols have been shown to possess cognitive health benefits. Epidemiologic evidence suggests that they could play a role in risk reduction in dementia. Amyloid precursor protein processing and the subsequent generation of amyloid beta (Aβ) are central to the pathogenesis of Alzheimer's disease, as soluble, oligomeric Aβ is thought to be the toxic species driving disease progression.

AMPA receptor activation promotes non-amyloidogenic amyloid precursor protein processing and suppresses neuronal amyloid-β production.

Soluble oligomeric amyloid β peptide (Aβ) generated from processing of the amyloid precursor protein (APP) plays a central role in the pathogenesis of Alzheimer's Disease (AD) and through actions at glutamatergic synapses affects excitability and plasticity. The physiological control of APP processing is not fully understood but stimulation of synaptic NMDA receptors (NMDAR) can suppress Aβ levels through an ERK-dependent increase in α-secretase activity. AMPA-type glutamate receptors (AMPAR) couple to ERK phosphorylation independently of NMDAR activation raising the possibility that stimulation of AMPAR might similarly promote non-amyloidogenic APP processing.