<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cosentino, Stephanie A</style></author><author><style face="normal" font="default" size="100%">Stern, Yaakov</style></author><author><style face="normal" font="default" size="100%">Sokolov, Elisaveta</style></author><author><style face="normal" font="default" size="100%">Scarmeas, Nikolaos</style></author><author><style face="normal" font="default" size="100%">Manly, Jennifer J</style></author><author><style face="normal" font="default" size="100%">Tang, Ming Xin</style></author><author><style face="normal" font="default" size="100%">Schupf, Nicole</style></author><author><style face="normal" font="default" size="100%">Mayeux, Richard P</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Plasma ß-amyloid and cognitive decline.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Neurol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Neurol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged, 80 and over</style></keyword><keyword><style  face="normal" font="default" size="100%">Amyloid beta-Peptides</style></keyword><keyword><style  face="normal" font="default" size="100%">Apolipoproteins E</style></keyword><keyword><style  face="normal" font="default" size="100%">Cognition Disorders</style></keyword><keyword><style  face="normal" font="default" size="100%">Community Health Planning</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Longitudinal Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Peptide Fragments</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">67</style></volume><pages><style face="normal" font="default" size="100%">1485-90</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">OBJECTIVES: To determine if plasma β-amyloid (Aβ) levels (1) can be linked to specific cognitive changes that constitute conversion to Alzheimer disease (AD) and (2) correspond to cognitive change independent of dementia.

DESIGN: Longitudinal study including 3 visits during approximately 4¹/₂ years (2000-2006).

SETTING: Northern Manhattan community.

PARTICIPANTS: Eight hundred eighty individuals from a population-based and ethnically diverse sample who had 2 plasma Aβ measurements and were dementia free at the time of the first Aβ sample; 481 remained cognitively healthy, 329 were cognitively or functionally impaired but not demented at any point, and 70 developed AD.

MAIN OUTCOME MEASURES: General estimating equations tested the association between plasma Aβ (baseline and change in values) and cognitive change (composite score and memory, language, and visuospatial indices).

RESULTS: High baseline plasma Aβ42 (P = .01) and Aβ40 (P = .01) and decreasing/relatively stable Aβ42 (P = .01) values were associated with faster decline in multiple cognitive domains. In those who remained cognitively healthy, high baseline plasma Aβ42 (P = .01) and decreasing/relatively stable plasma Aβ42 (P = .01) was associated with faster cognitive decline, primarily in memory.

CONCLUSIONS: The association between plasma Aβ and multiple aspects of cognition more clearly specifies the previously documented downward trajectory of plasma Aβ with AD onset. The predominant association with memory seen only in healthy elderly individuals also suggests that plasma Aβ is linked with even earlier neurologic changes that may or may not culminate in dementia.</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20697031?dopt=Abstract</style></custom1></record></records></xml>