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Titolo:
The cholinergic neuronal phenotype in Alzheimer's disease
Autore:
Blusztajn, JK; Berse, B;
Indirizzi:
Boston Univ, Sch Med, Dept Pathol & Lab Med, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 pt Pathol & Lab Med, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 Med, Dept Psychiat, Boston, MA 02118 USA
Titolo Testata:
METABOLIC BRAIN DISEASE
fascicolo: 1, volume: 15, anno: 2000,
pagine: 45 - 64
SICI:
0885-7490(200003)15:1<45:TCNPIA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; VESICULAR ACETYLCHOLINE TRANSPORTER; LEUKEMIA INHIBITORY FACTOR; AMYLOID-BETA-PROTEIN; ACETYL-COA METABOLISM; SEPTAL CELL-LINE; FACTOR PREVENTS DEGENERATION; ALPHA-SECRETASE CLEAVAGE; RAT SYMPATHETIC NEURONS; HUMAN APOLIPOPROTEIN-E;
Keywords:
acetylcholine; beta amyloid; choline acetyltransferase; vesicular acetylcholine transporter; apolipoprotein E; phosphatidylcholine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
177
Recensione:
Indirizzi per estratti:
Indirizzo: Blusztajn, JK Boston Univ, Sch Med, Dept Pathol & Lab Med, 85 E Newton St,Room M1009, Boston, MA 02118 USA Boston Univ 85 E Newton St,Room M1009 Boston MA USA 02118 SA
Citazione:
J.K. Blusztajn e B. Berse, "The cholinergic neuronal phenotype in Alzheimer's disease", METAB BRAIN, 15(1), 2000, pp. 45-64

Abstract

The synthesis, storage and release of acetylcholine (ACh) requires the expression of several specialized proteins, including choline acetyltransferase (ChAT) and the vesicular ACh transporter(VAChT). The VAChT gene is located within the first intron of the ChAT gene. This unique genomic organization permits coordinated activation of expression of the two genes by extracellular factors. Much less is known about factors that reduce the expression of the cholinergic phenotype. A cholinergic deficit is one of the primary features of Alzheimer's disease (AD), and AD brains are characterized by amyloid deposits composed primarily of A beta peptides. Although A beta peptides are neurotoxic, part of the cholinergic deficit in AD could be attributed to the suppression of cholinergic markers in the absence of cell death. Indeed, we and others demonstrated that synthetic A beta peptides, at submicromolar concentrations that cause no cytotoxicity, reduce the expression ofcholinergic markers in neuronal cells. Another feature of AD is abnormal phospholipid turnover, which might be related to the progressive accumulation of apolipoprotein E (apoE) within amyloid plaques, leading perhaps to thereduction of apoE content in the CSF of AD patients. ApoE is a component of very low density lipoproteins (VLDL). As a first step in investigating a potential neuroprotective function of apoE, we determined the effects of VLDL on ACh content in neuronal cells. We found that MDL increases ACh levels, and that it can partially offset the anticholinergic actions of A beta peptides.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 04:20:13