Alzheimer's Disease: Approaches to Pathogenesis in the Genomic Age

Abstract

The prevalence of Alzheimer’s disease (AD), the most common form of dementia, is rising rapidly worldwide. A seemingly imminent epidemic is predicted to have wide reaching societal and economic consequences, becoming the leading health issue for many countries by the middle of this century. This epidemic is driven by an ageing world population in combination with a lack of disease modifying treatments or preventive strategies. The popular amyloid cascade hypothesis suggests that AD is precipitated by the dysregulated metabolism of the amyloid precursor protein resulting in the accumulation of the betaamyloid peptide (A) in the brain. This hypothesis is the basis for most experimental treatments currently in clinical trials. However, not all evidence supports a precipitating role of abnormal A accumulation in the common forms of AD.