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Titolo:
Neurofilament protein in cerebrospinal fluid: A marker of white matter changes
Autore:
Sjogren, M; Blomberg, M; Jonsson, M; Wahlund, LO; Edman, A; Lind, K; Rosengren, L; Blennow, K; Wallin, A;
Indirizzi:
Res Council, Stockholm, Sweden Res Council Stockholm SwedenRes Council, Stockholm, Sweden Huddinge Univ Hosp, Neurotec Inst, Dept Geriatr Med, S-14186 Huddinge, Sweden Huddinge Univ Hosp Huddinge Sweden S-14186 Med, S-14186 Huddinge, Sweden Univ Gothenburg, Inst Clin Neurosci, Gothenburg, Sweden Univ Gothenburg Gothenburg Sweden nst Clin Neurosci, Gothenburg, Sweden
Titolo Testata:
JOURNAL OF NEUROSCIENCE RESEARCH
fascicolo: 3, volume: 66, anno: 2001,
pagine: 510 - 516
SICI:
0360-4012(20011101)66:3<510:NPICFA>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
FRONTAL-LOBE DEGENERATION; APOLIPOPROTEIN-E GENOTYPE; BRAIN-BARRIER FUNCTION; NON-ALZHEIMER TYPE; VASCULAR DEMENTIA; TAU-PROTEIN; FRONTOTEMPORAL DEMENTIA; CLINICAL-DIAGNOSIS; BIOCHEMICAL MARKER; DIFFUSE PLAQUES;
Keywords:
white matter; dementia; axonal degeneration;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Sjogren, M Sahlgrens Univ Hosp, Inst Clin Neurosci, SE-43180 Molndal, Sweden Sahlgrens Univ Hosp Molndal Sweden SE-43180 0 Molndal, Sweden
Citazione:
M. Sjogren et al., "Neurofilament protein in cerebrospinal fluid: A marker of white matter changes", J NEUROSC R, 66(3), 2001, pp. 510-516

Abstract

The objective of this study was to compare cerebrospinal fluid (CSF) levels of the light subtype of the neurofilament proteins (NFL), tau, and beta -amyioid42 (A beta 42) in individuals with moderate or severe white matter changes (WMC) and in those with mild or no WMC. Twenty-two patients with Alzheimer's disease (AD), nine patients with subcortical vascular dementia (SVD), and 20 normal controls were included in the study. The occurrence of WMC was evaluated by a neuroradiologist using the Blennow-Wallin scale. Thirty-seven subjects had no or only punctate WMC 14 had moderate to severe WMC. Both diagnostic group and WMC, but not gender or apolipoproteinE E4 inheritance, contributed to the variance in the CSF levels of tau, NFL, and A beta 42. In patients with moderate to severe WMC, CSF NFL (P < 0.01), but not CSF tau or CSF A beta 42, was increased also after correction for age, gender, and degree of cognitive impairment. A comparison between patients and controls with any signs of WIVIC and those without such signs yielded a similar result: CSF NFL (P < 0.001) was increased in the group with signs of WMC. As in numerous previous studies, we found that CSF tau was increased in AD (P < 0.001) compared with controls. Furthermore, CSF NFL was increased in both AD and SVD compared with controls (P < 0.001 for both). Although diagnostic group seems to be a stronger predictor of the variance found in CSFNFL, a clear association between the presence of WIVIC and increased CSF NFL was found. Because NFL is located mainly in large myelinated axons, increased CSF NFL in individuals with WMC probably reflects axonal degeneration. (C) 2001 Wiley-Liss, Inc.

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Documento generato il 29/03/20 alle ore 08:57:58