AUTHOR=Wildburger Norelle C. , Gyngard Frank , Guillermier Christelle , Patterson Bruce W. , Elbert Donald , Mawuenyega Kwasi G. , Schneider Theresa , Green Karen , Roth Robyn , Schmidt Robert E. , Cairns Nigel J. , Benzinger Tammie L. S. , Steinhauser Matthew L. , Bateman Randall J. TITLE=Amyloid-β Plaques in Clinical Alzheimer’s Disease Brain Incorporate Stable Isotope Tracer In Vivo and Exhibit Nanoscale Heterogeneity JOURNAL=Frontiers in Neurology VOLUME=9 YEAR=2018 URL=https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2018.00169 DOI=10.3389/fneur.2018.00169 ISSN=1664-2295 ABSTRACT=
Alzheimer’s disease (AD) is a neurodegenerative disorder with clinical manifestations of progressive memory decline and loss of executive function and language. AD affects an estimated 5.3 million Americans alone and is the most common form of age-related dementia with a rapidly growing prevalence among the aging population—those 65 years of age or older. AD is characterized by accumulation of aggregated amyloid-beta (Aβ) in the brain, which leads to one of the pathological hallmarks of AD—Aβ plaques. As a result, Aβ plaques have been extensively studied after being first described over a century ago. Advances in brain imaging and quantitative measures of Aβ in biological fluids have yielded insight into the time course of plaque development decades before and after AD symptom onset. However, despite the fundamental role of Aβ plaques in AD,