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The triplicate copy of amyloid precursor protein gene (APP; chromosome 21) in Down
syndrome (DS) genetically predisposes adults with DS to over production of amyloid-β
(Aβ) leading to increased Aβ plaque deposition and a higher prevalence of Alzheimer’s
disease (AD) and dementia. Patterned localization of Aβ plaques are a hallmark of
AD. This study investigated the relationship between co-localized Aβ deposition and
cortical atrophy in non-demented adults with DS.
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