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Editorial
March 2014

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

Author Affiliations
  • 1Department of Medical Ethics and Health Policy, University of Pennsylvania Perelman School of Medicine, Philadelphia
  • 2Department of Neurology, University of Virginia School of Medicine, Charlottesville
  • 3Department of Psychiatry and Neurobehavioral Sciences, University of Virginia School of Medicine, Charlottesville
  • 4Department of Neurology and Psychiatry (Dual Primaries), Center for Cognitive Health and NFL Neurological Care, Mount Sinai Alzheimer’s Disease Research Center, New York, New York
JAMA Neurol. 2014;71(3):273-275. doi:10.1001/jamaneurol.2013.6031

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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