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Background Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by severe memory impairment and accumulation of neuropathological amyloid plaques and tau tangles. By contrast, ‘normal’ age-associated cognitive decline is less severe and generally occurs in the absence of neuropathology. Many believe agingand AD-related memory impairments result from separate etiologies, but this distinction is not entirely consistent with emerging evidence that both are linked to hippocampal dysfunction. As aging is the most significant risk factor for late-onset AD (LOAD), we hypothesize that memory deficits in both ‘normal’ aging and AD are driven in part by some common underlying mechanisms, which are exacerbated in AD by disease-specific insults such as neurodegeneration, neuroinflammation, and neuropathologies. In addition, heritability estimates suggest a strong genetic component (50-80%) in both conditions [1,2]. Thus, elucidating genetic correlates of memory decline in ‘normal’ aging may identify risk factors that influence susceptibility to LOAD.

Multi-scale study of normal aging predicts novel late-onset Alzheimer's disease risk variants