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Titolo:
Cerebrospinal fluid S100B is elevated in the earlier stages of Alzheimer'sdisease
Autore:
Peskind, ER; Griffin, WST; Akama, KT; Raskind, MA; Van Eldik, LJ;
Indirizzi:
Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98108 USA Vet Affairs Puget Sound Hlth Care Syst Seattle WA USA 98108 WA 98108 USA Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98108 USAUniv Washington Seattle WA USA 98108 t & Behav Sci, Seattle, WA 98108 USA VA Med Ctr, Ctr Geriatr Res Educ & Clin, Little Rock, AR 72205 USA VA Med Ctr Little Rock AR USA 72205 duc & Clin, Little Rock, AR 72205 USA Northwestern Univ, Sch Med, Inst Neurosci, Dept Mol & Cell Biol, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 & Cell Biol, Chicago, IL 60611 USA NW Drug Doscovery Program, Chicago, IL 60611 USA NW Drug Doscovery Program Chicago IL USA 60611 ram, Chicago, IL 60611 USA
Titolo Testata:
NEUROCHEMISTRY INTERNATIONAL
fascicolo: 5-6, volume: 39, anno: 2001,
pagine: 409 - 413
SICI:
0197-0186(200111/12)39:5-6<409:CFSIEI>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; FIBRILLARY ACIDIC PROTEIN; NEURON-SPECIFIC ENOLASE; S-100 PROTEIN; TRANSGENIC MICE; DOWNS-SYNDROME; COGNITIVE STATE; S100-BETA; OVEREXPRESSION; ASTROCYTES;
Keywords:
cerebrospinal fluid S100B; elevated; earlier stages; Alzheimer's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Peskind, ER Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, 116MIRECC,1660 S Columbian Way, Seattle, WA 98108 USA Vet Affairs Puget Sound Hlth Care Syst 116MIRECC,1660 S Columbian Way Seattle WA USA 98108
Citazione:
E.R. Peskind et al., "Cerebrospinal fluid S100B is elevated in the earlier stages of Alzheimer'sdisease", NEUROCHEM I, 39(5-6), 2001, pp. 409-413

Abstract

Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD. The hypothesis that the overexpression of S100B in Alzheimer brain is related to the progression of clinical symptoms was addressed in living persons by measuring S100B concentrations in cerebrospinal fluid (CSF) from AD patients with a broad range of clinical dementia severity and from healthy older persons. The effect of normal aging on CSF S100B concentrations also was estimated. CSF S100B did not differ between all 68 AD subjects (0.98 +/- 0.09 ng/ml (mean +/- S.E.M.)) and 25 healthy older subjects (0.81 +/- 0.13 ng/ml). When AD subjects were divided into mild/moderate stage and advanced stage clinical dementia severity by the established Clinical Dementia Rating Scale (CDR) criteria, S100B was significantly higher in the 46 mild/moderate stage AD subjects (1.17 +/-0.11 ng/ml) than in either the 22 advanced stage AD subjects (0.60 +/-0.12 ng/ml) or the healthy older subjects. Consistent with higher CSF S100B in mild to moderate AD, there was a significant correlation among all AD subjects between CSF S100B and cognitive status as measured by the Mini Mental State Exam (MMSE) score. CSF S100B did not differ between healthy oldersubjects and healthy young subjects. These results suggest increased CNS expression of S100B in the earlier stages of AD, and are consistent with a role for S100B in the initiation and/or facilitation of neuritic plaque formation in AD brain. (C) 2001 Published by Elsevier Science Ltd.

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Documento generato il 05/04/20 alle ore 22:25:00