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Plasma {beta}-amyloid and cognitive decline

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

Title:
Plasma {beta}-amyloid and cognitive decline
Author(s):
Cosentino, Stephanie
Stern, Yaakov
Sokolov, Elizaveta
Scarmeas, Nikolaos
Manly, Jennifer J.
Tang, Mingxin
Schupf, Nicole
Mayeux, Richard Paul
Date:
Type:
Articles
Department(s):
Taub Institute
Volume:
67
Persistent URL:
Book/Journal Title:
JAMA Neurology
Publisher:
American Medical Association
Abstract:
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.
Subject(s):
Mild cognitive impairment
Alzheimer's disease
Amyloid beta-protein precursor
Glycoproteins
Alzheimer's disease--Etiology
Cognitive neuroscience
Dementia
Neurosciences
Mental health
Publisher DOI:
https://doi.org/10.1001/archneurol.2010.189
Item views
81
Metadata:
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Suggested Citation:
Stephanie Cosentino, Yaakov Stern, Elizaveta Sokolov, Nikolaos Scarmeas, Jennifer J. Manly, Mingxin Tang, Nicole Schupf, Richard Paul Mayeux, , Plasma {beta}-amyloid and cognitive decline, Columbia University Academic Commons, .

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