Approximately 15 percent of people who live to the age of 65 will develop some form of dementia; by age 85, that proportion increases to at least 35 percent. The most common of all the dementias is Alzheimer's disease which is predicted to afflict 22 million people around the world by 2025. Beta amyloid 42 is generally thought to play a pivotal role in the development of disease as a result of it's neurotoxic activity and the identification of molecules able to prevent it's accumulation represents a highly promising approach. In a recent dossier LeadDiscovery has described the development of a novel assay able to identify under high throughput conditions such molecules and this assay was able to identify a lead for novel therapeutic candidates (Click here for free access). 

Much of our understanding of Alzheimer's disease has resulted from the study of familial Alzheimer's disease (FAD) which is characterized by mutations in the gene coding the precursor of beta amyloid (APP) and also in genes coding presenilin 1 and presenilin 2, and each of these mutations has been suggested to contribute to the accumulation of beta amyloid 42. FAD and late-onset Alzheimer's disease share many characteristics including the accumulation of beta amyloid 42. 

Japanese researchers have now made a breakthrough screening for genes that can prevent neural cell death that results from both genetic mutations responsible for FAD and in response to beta amyloid itself. The gene encoding a novel peptide, humanin, and humanin itself were both shown to reduce neural cell death. Humanin is thought to exert its effect by reducing the effects of beta amyloid rather than by reducing it's accumulation and furthermore a synthetic analogue of humanin has now been shown to improve memory in the mouse scopolamine assay, a model of memory disorders including Alzheimer's disease. Further modelling of humanin or the identification of mimetics of this peptide should be of immense use in the development of novel therapies for Alzheimer's disease.