<?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%">Steinerman, Joshua R</style></author><author><style face="normal" font="default" size="100%">Irizarry, Michael</style></author><author><style face="normal" font="default" size="100%">Scarmeas, Nikolaos</style></author><author><style face="normal" font="default" size="100%">Raju, Susan</style></author><author><style face="normal" font="default" size="100%">Brandt, Jason</style></author><author><style face="normal" font="default" size="100%">Albert, Marilyn</style></author><author><style face="normal" font="default" size="100%">Blacker, Deborah</style></author><author><style face="normal" font="default" size="100%">Hyman, Bradley</style></author><author><style face="normal" font="default" size="100%">Stern, Yaakov</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Distinct pools of beta-amyloid in Alzheimer disease-affected brain: a clinicopathologic study.</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%">Alzheimer Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Amyloid beta-Peptides</style></keyword><keyword><style  face="normal" font="default" size="100%">Brain</style></keyword><keyword><style  face="normal" font="default" size="100%">Brief Psychiatric Rating Scale</style></keyword><keyword><style  face="normal" font="default" size="100%">Cross-Sectional Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</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%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Plaque, Amyloid</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">65</style></volume><pages><style face="normal" font="default" size="100%">906-12</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">OBJECTIVE: To determine whether beta-amyloid (Abeta) peptides segregated into distinct biochemical compartments would differentially correlate with clinical severity of Alzheimer disease (AD).

DESIGN: Clinicopathologic correlation study.

PARTICIPANTS: Twenty-seven patients from a longitudinal study of AD and 13 age- and sex-matched controls without a known history of cognitive impairment or dementia were included in this study.

INTERVENTIONS: Temporal and cingulate neocortex were processed using a 4-step extraction, yielding biochemical fractions that are hypothesized to be enriched with proteins from distinct anatomical compartments: TRIS (extracellular soluble), Triton (intracellular soluble), sodium dodecyl sulfate (SDS) (membrane associated), and formic acid (extracellular insoluble). Levels of Abeta(40) and Abeta(42) were quantified in each biochemical compartment by enzyme-linked immunosorbent assay.

RESULTS: The Abeta(42) level in all biochemical compartments was significantly elevated in patients with AD vs controls (P &lt; .01). The Abeta(40) levels in the TRIS and formic acid fractions were elevated in patients with AD (temporal, P &lt; .01; cingulate, P = .03); however, Triton and SDS Abeta(40) levels were similar in patients with AD and in controls. Functional impairment proximal to death correlated with Triton Abeta(42) (r = 0.48, P = .02) and SDS Abeta(42) (r = 0.41, P = .04) in the temporal cortex. Faster cognitive decline was associated with elevated temporal SDS Abeta(42) levels (P &lt; .001), whereas slower decline was associated with elevated cingulate formic acid Abeta(42) and SDS Abeta(42) levels (P = .02 and P = .01, respectively).

CONCLUSION: Intracellular and membrane-associated Abeta, especially Abeta(42) in the temporal neocortex, may be more closely related to AD symptoms than other measured Abeta species.</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18625856?dopt=Abstract</style></custom1></record></records></xml>