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Titolo:
Prospects for pharmacological intervention in Alzheimer disease
Autore:
Emilien, G; Beyreuther, K; Masters, CL; Maloteaux, JM;
Indirizzi:
Univ Catholique Louvain, Clin Univ St Luc, Pharmacol Lab, B-1200 Brussels,Belgium Univ Catholique Louvain Brussels Belgium B-1200 B-1200 Brussels,Belgium Univ Catholique Louvain, Clin Univ St Luc, Dept Neurol, B-1200 Brussels, Belgium Univ Catholique Louvain Brussels Belgium B-1200 B-1200 Brussels, Belgium Univ Heidelberg, Ctr Mol Biol, D-6900 Heidelberg, Germany Univ HeidelbergHeidelberg Germany D-6900 ol, D-6900 Heidelberg, Germany Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia Univ Melbourne Parkville Vic Australia 3052 arkville, Vic 3052, Australia Mental Hlth Res Inst, Parkville, Vic 3052, Australia Mental Hlth Res InstParkville Vic Australia 3052 le, Vic 3052, Australia
Titolo Testata:
ARCHIVES OF NEUROLOGY
fascicolo: 4, volume: 57, anno: 2000,
pagine: 454 - 459
SICI:
0003-9942(200004)57:4<454:PFPIIA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONTROLLED TRIAL; DEMENTIA; PROPENTOFYLLINE; ACTIVATION; GENERATION; TACRINE; DRUGS; BRAIN;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Emilien, G 127 Rue Henri Prou, F-78340 Les Clayes Bois, France 127 Rue Henri Prou Les Clayes Bois France F-78340 ois, France
Citazione:
G. Emilien et al., "Prospects for pharmacological intervention in Alzheimer disease", ARCH NEUROL, 57(4), 2000, pp. 454-459

Abstract

Alzheimer disease (AD) involves neuronal degeneration with impaired cholinergic transmission in the cerebral cortex and hippocampus in areas of the brain particularly associated with memory and higher intellectual functioning. Other neurotransmitter deficits also occur, hut the mechanisms underlying the widespread impairment of synaptic functions remain uncertain. Research on the molecular basis of AD has elucidated a pathogenic pathway from which a range of rational pharmacological interventions has emerged. Although at least 3 cholinesterase inhibitors (tacrine hydrochloride, donepezil, andrivastigmine tartrate) are non available and provide patients with modest relief, the most promising strategy involves approaches to retarding, halting, or preventing the formation or accumulation of beta-amyloid (A beta) plaques. Estrogen is believed to have antioxidant or other anti-A beta effects. as hormonal replacement therapy in women with menopause is associated with a reduced risk or delayed onset of AD. The association between nonsteroidal anti-inflammatory drugs and a reduced risk of AD has not yet been confirmed. but these agents may protect the brain from the reactive glial and microglial responses associated with LIP deposition Also, recent studies suggested that antioxidants, such as vitamin E taken alone or in combination with selegiline hydrochloride, can delay the progression of AD. Despite theseencouraging results, no current therapy has been shown to halt or reverse the underlying disease process. The proof of the principle that anti-A betadrugs will work in the transgenic models of AD is eagerly awaited with theexpectation that they will eventually prove successful in humans.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:16:16