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Titolo:
Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer's disease: histotopographical correlation with amyloid plaques and hyperphosphorylated-tau protein
Autore:
Wevers, A; Monteggia, L; Nowacki, S; Bloch, W; Schutz, U; Lindstrom, J; Pereira, EFR; Eisenberg, H; Giacobini, E; de Vos, RAI; Steur, ENHJ; Maelicke, A; Albuquerque, EX; Schroder, H;
Indirizzi:
Univ Cologne, Dept Anat, D-50931 Cologne, Germany Univ Cologne Cologne Germany D-50931 Dept Anat, D-50931 Cologne, Germany Abbott Labs, Pharmaceut Discovery, Neurosci Res, Abbott Pk, IL 60064 USA Abbott Labs Abbott Pk IL USA 60064 Neurosci Res, Abbott Pk, IL 60064 USA Univ Penn, Sch Med, Dept Neurosci, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Neurosci, Philadelphia, PA 19104 USA Univ Maryland, Sch Med, Dept Neurosurg, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 t Neurosurg, Baltimore, MD 21201 USA Univ Geneva, Sch Med, Dept Geriatr, CH-1226 Thonex Geneva, Switzerland Univ Geneva Thonex Geneva Switzerland CH-1226 Thonex Geneva, Switzerland Lab Pathol Oost Nederland, NL-7512 AD Enschede, Netherlands Lab Pathol Oost Nederland Enschede Netherlands NL-7512 AD e, Netherlands Med Spectrum Twente, NL-7512 AD Enschede, Netherlands Med Spectrum TwenteEnschede Netherlands NL-7512 AD nschede, Netherlands Univ Mainz, Inst Physiol Chem & Pathobiochem, D-55128 Mainz, Germany Univ Mainz Mainz Germany D-55128 & Pathobiochem, D-55128 Mainz, Germany Univ Fed Rio de Janeiro, Ctr Hlth Sci, Inst Biomed Sci, Dept Basic & Clin Pharmacol, BR-2144 Rio De Janeiro, Brazil Univ Fed Rio de Janeiro Rio De Janeiro Brazil BR-2144 De Janeiro, Brazil
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 7, volume: 11, anno: 1999,
pagine: 2551 - 2565
SICI:
0953-816X(199907)11:7<2551:EONARS>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHOLINERGIC RECEPTOR; FRONTAL-CORTEX; HUMAN-BRAIN; PHARMACOLOGICAL PROPERTIES; MONOCLONAL-ANTIBODIES; CELLULAR-DISTRIBUTION; COGNITIVE IMPAIRMENT; XENOPUS-OOCYTES; SENILE DEMENTIA; MESSENGER-RNA;
Keywords:
alpha 4-subunit; alpha 7-subunit; beta-amyloid; cholinergic transmission; human brain;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Wevers, A Univ Cologne, Dept Anat, Joseph Stelzmann Str 9, D-50931 Cologne, Germany Univ Cologne Joseph Stelzmann Str 9 Cologne Germany D-50931 any
Citazione:
A. Wevers et al., "Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer's disease: histotopographical correlation with amyloid plaques and hyperphosphorylated-tau protein", EUR J NEURO, 11(7), 1999, pp. 2551-2565

Abstract

Impairment of cholinergic transmission and decreased numbers of nicotinic binding sites are well-known features accompanying the cognitive dysfunction seen in Alzheimer's disease (AD). In order to elucidate the underlying cause of this cholinoceptive dysfunction, the expression of two pharmacologically different nicotinic acetylcholine receptor (nAChR) subunits (alpha 4, alpha 7) was studied in the cerebral cortex of Alzheimer patients as compared to controls. Patch-clamp recordings of 14 dissociated neurons of controlcortices showed responses suggesting the existence of alpha 4- and alpha 7-containing functional nAChRs in the human cortex. In cortices of Alzheimerpatients and controls, the pattern of distribution and the number of alpha4 and alpha 7 mRNA-expressing neurons were similar, whereas at the proteinlevel a decrease in the density of alpha 4- and alpha 7-expressing neuronsof approximate to 30% was observed in Alzheimer patients. The histotopographical correlation of nAChR expression with accompanying pathological changes, e.g. accumulation of hyperphosphorylated-tau (HP-tau) protein and beta-amyloid showed that neurons in the vicinity of beta-amyloid plaques bore both nAChR transcripts. Neurons heavily labelled for HP-tau, however, expressed little or no alpha 4 and alpha 7 mRNA. These results point to an impaired synthesis of nAChRs on the protein level as a possible cause of the cholinoceptive deficit in AD. Further investigations need to elucidate whether interactions of HP-tau with nAChR mRNA, or alterations in the quality of alpha 4 and alpha 7 transcripts give rise to decreased protein expression at the level of individual neurons.

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Documento generato il 31/03/20 alle ore 16:27:38