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Titolo:
Diminished neuronal metabolic activity in Alzheimer's disease
Autore:
Salehi, A; Swaab, DF;
Indirizzi:
Netherlands Inst Brain Res, NL-1105 AZ Amsterdam, Netherlands Netherlands Inst Brain Res Amsterdam Netherlands NL-1105 AZ Netherlands
Titolo Testata:
JOURNAL OF NEURAL TRANSMISSION
fascicolo: 9-10, volume: 106, anno: 1999,
pagine: 955 - 986
SICI:
0300-9564(1999)106:9-10<955:DNMAIA>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; AMYLOID PRECURSOR PROTEIN; CHOLINE-ACETYLTRANSFERASE ACTIVITY; AMYOTROPHIC-LATERAL-SCLEROSIS; APOLIPOPROTEIN-E POLYMORPHISM; POSITRON EMISSION TOMOGRAPHY; BRAIN GLUCOSE-METABOLISM; FACTOR MESSENGER-RNA; RAT GOLGI-APPARATUS; NUCLEUS BASALIS;
Keywords:
Alzheimer's disease; ApoE; Golgi apparatus; metabolism; neuritic plaques; neurofibrillary tangles; neur otrophin receptors; neurotrophin; NGF; Nucleus basalis; trkA;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
187
Recensione:
Indirizzi per estratti:
Indirizzo: Salehi, A Stanford Univ, Dept Neurol & Neurol Sci, Sch Med, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 Med, Stanford, CA 94305 USA
Citazione:
A. Salehi e D.F. Swaab, "Diminished neuronal metabolic activity in Alzheimer's disease", J NEURAL TR, 106(9-10), 1999, pp. 955-986

Abstract

An increasing number of studies have appeared in the literature suggestingthat Alzheimer's disease (AD) is a hypometabolic brain disorder. Decreasedmetabolism in AD has been revealed by a variety of in vivo and postmortem methods and techniques including positron emission tomography and glucose metabolism. We used the: size of the Golgi apparatus (GA) and cell profile area as indicators of neuronal activity in postmortem material. Using an antibody against MG-160, a sialoglycoprotein of the medial cisternae of the GA, we were able to visualize ansi quantify the GA area. In a series of experiments, we tried to relate neuronal metabolism to different hallmarks of AD, i.e. plaques and tangles, and also to genetic risk factors for AD like age and (apolipoprotein E) ApoE polymorphism. Our results showed that in AD there is indeed a clear reduction in brain metabolism in several severely affected brain regions including the nucleus basalis of Meynert (NBM), the CA1 area of the hippocampus and the hyplothalamic tuberomamillary nucleus. However, the reduction in neuronal activity did not seem to be caused by the presence of neuropathological hallmarks of AD, i.e. plaques and tangles. There was, however, a clear relationship between the presence of ApoE epsilon4 alleles and a decrease in GA size. Our data suggest that decreased neuronal activity and neuropathological hallmarks of AD, such as plaques and tangles, are basically independent phenomena. Moreover, ApoE epsilon 4 may participate in the pathogenesis of AID by decreasing neuronal metabolism. The main implication of these findings is that therapeutic strategies in AD should be focussed on reactivation of neuronal metabolism.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 10:38:53