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Titolo:
Expression of alpha-synuclein in the human brain: relation to Lewy body disease
Autore:
Wirdefeldt, K; Bogdanovic, N; Westerberg, L; Payami, H; Schalling, M; Murdoch, G;
Indirizzi:
Karolinska Inst, Dept Mol Med, S-17176 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17176 Med, S-17176 Stockholm, Sweden Karolinska Inst, Huddinge Hosp, NEUROTEC, Dept Geriatr Med, S-10401 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-10401 Med, S-10401 Stockholm, Sweden Oregon Hlth Sci Univ, Dept Neurol, Portland, OR USA Oregon Hlth Sci Univ Portland OR USA Univ, Dept Neurol, Portland, OR USA Oregon Hlth Sci Univ, Dept Neuropathol, Portland, OR USA Oregon Hlth Sci Univ Portland OR USA Dept Neuropathol, Portland, OR USA
Titolo Testata:
MOLECULAR BRAIN RESEARCH
fascicolo: 1-2, volume: 92, anno: 2001,
pagine: 58 - 65
SICI:
0169-328X(20010815)92:1-2<58:EOAITH>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULTIPLE SYSTEM ATROPHY; SPORADIC PARKINSONS-DISEASE; GLIAL CYTOPLASMIC INCLUSIONS; A-BETA COMPONENT; ALZHEIMERS-DISEASE; NEURODEGENERATIVE SYNUCLEINOPATHIES; PRECURSOR PROTEIN; SUBSTANTIA-NIGRA; MESSENGER-RNA; IN-VITRO;
Keywords:
Lewy body disease; Parkinson disease; alpha-synuclein; mRNA; gene expression; in situ hybridization;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Wirdefeldt, K Karolinska Inst, Dept Mol Med, L8-00, S-17176 Stockholm, Sweden Karolinska Inst L8-00 Stockholm Sweden S-17176 holm, Sweden
Citazione:
K. Wirdefeldt et al., "Expression of alpha-synuclein in the human brain: relation to Lewy body disease", MOL BRAIN R, 92(1-2), 2001, pp. 58-65

Abstract

alpha -Synuclein is mutated in some hereditary cases of Parkinson's disease and the protein precipitates in Lewy bodies, the pathological hallmark ofboth Parkinson's disease and Lewy body disease. Transgenic mice overexpressing human wild-type alpha -synuclein develop alpha -synuclein-immunoreactive inclusions in brain regions typically affected with Lewy body disease. We used in situ hybridization to characterize alpha -synuclein expression and examine mRNA levels in patients affected with Lewy body disease and controls. Substantia nigra was avoided because of the extensive neuronal loss and cingulate gyrus was chosen as it is one of the diagnostic regions in Lewybody disease where Lewy bodies most frequently are demonstrated. beta -tubulin was used to control for neuronal degeneration. The a-synuclein probe showed intense labeling of pyramidal cells in lamina III and V in both patients and controls. We found no difference in alpha -synuclein mRNA levels and beta -tubulin mRNA was not significantly altered (P=0.06) in patient brains. There was no difference in the ratio of alpha -Synuclein and beta -tubulin mRNA levels between patients and controls. Further, we found no relationship between alpha -synuclein mRNA levels and Lewy bodies. Great variability in alpha -synuclein mRNA levels among patients indicates that Lewy body disease may be a heterogeneous disorder with regard to alpha -synuclein involvement. (C) 2001 Elsevier Science BY. All rights reserved.

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Documento generato il 28/03/20 alle ore 10:59:00