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Plasma {beta}-amyloid and cognitive decline

Cosentino, Stephanie; Stern, Yaakov; Sokolov, Elizaveta; Scarmeas, Nikolaos; Manly, Jennifer J.; Tang, Mingxin; Schupf, Nicole; Mayeux, Richard Paul

The amyloid cascade hypothesis suggests that aberrant metabolism of the amyloid precursor glycoprotein, and subsequent accumulation of soluble oligomers β-amyloid 40 (Aβ40) and 42 (Aβ42), is the primary trigger for the development of Alzheimer disease (AD). The Tg2576 mouse model of AD has shown that plasma Aβ levels decrease as brain Aβ levels increase, generating interest in the suitability of plasma Aβ level as a risk biomarker for AD. Indeed, we have reported that elevated plasma Aβ42 at baseline and decreasing levels over time predict conversion to AD, and other studies support these findings. The current study sought to specify existing work by investigating the extent to which plasma Aβ levels (1) can be linked to specific cognitive changes that constitute conversion to AD and (2) may be relevant for cognition independent of dementia.

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Academic Units
Taub Institute
Publisher
American Medical Association
Published Here
January 27, 2016
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