Environmental Exposures and the Risk for Alzheimer DiseaseCan We Identify the Smoking Guns?

Over the past 3 decades, the focus on the molecular pathogenesis of Alzheimer disease (AD) has led to remarkable advances in our understanding of the emergence of symptoms and the course of the disease.¹ Biomarkers derived from growing knowledge of the pathobiology have enabled identification of amyloid plaques in both symptomatic and cognitively normal individuals,² the latter potentially identifying a population at high risk for dementia. About 20 genes have been identified as being associated with increased or decreased risk for late-onset AD (LOAD).³ Most of these linked genes have been identified by genomewide association studies and meta-analyses.³ Each new gene linked to LOAD fills in another gap in our understanding of AD pathogenesis and also serves as a new potential therapeutic opportunity.

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