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Titolo:
Ovariectomy and 17 beta-estradiol modulate the levels of Alzheimer's amyloid beta peptides in brain
Autore:
Petanceska, SS; Nagy, V; Frail, D; Gandy, S;
Indirizzi:
NYU, Nathan Kline Inst, Orangeburg, NY 10962 USA NYU Orangeburg NY USA 10962 , Nathan Kline Inst, Orangeburg, NY 10962 USA Wyeth Ayerst Res, Womens Hlth Res Inst, Radnor, PA USA Wyeth Ayerst Res Radnor PA USA Res, Womens Hlth Res Inst, Radnor, PA USA
Titolo Testata:
NEUROLOGY
fascicolo: 12, volume: 54, anno: 2000,
pagine: 2212 - 2217
SICI:
0028-3878(20000627)54:12<2212:OA1BMT>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRECURSOR PROTEIN; NEUROBLASTOMA-CELLS; SECRETASE CLEAVAGE; IN-VITRO; ESTRADIOL; ESTROGEN; DISEASE;
Keywords:
amyloid beta; estrogen replacement therapy; 17 beta-estradiol; guinea pigs;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Gandy, S NYU, Nathan Kline Inst, 140 Old Orangeburg Rd, Orangeburg, NY 10962 USA NYU 140 Old Orangeburg Rd Orangeburg NY USA 10962 g, NY 10962 USA
Citazione:
S.S. Petanceska et al., "Ovariectomy and 17 beta-estradiol modulate the levels of Alzheimer's amyloid beta peptides in brain", NEUROLOGY, 54(12), 2000, pp. 2212-2217

Abstract

Objective: To test whether female gonadal hormone status and estrogen modulate the metabolism of A beta peptides in vivo. Background: AD is a neurodegenerative disorder characterized by accumulation of aggregated forms of the 40- and 42-amino acid A beta peptides (A beta 40 and A beta 42). Estrogenreplacement therapy in postmenopausal women is associated with decreased risk for AD or delay in disease onset or both. The mechanism by which estrogen exerts this neuroprotective effect is elusive. 17 beta-estradiol (E2) was shown to reduce the release of A beta peptides by primary neuronal cultures of murine and human origin. Methods: For this purpose, four experimentalsets of guinea pigs were used: intact animals, ovariectomized animals (ovx), and ovariectomized animals that received E2 at two different doses (ovx+low-dose E2 and ovx+high-dose E2). Brain A beta 40 and A beta 42 levels were assessed using A beta 40 and A beta 42-specific ELISA assays. Results: Prolonged ovariectomy resulted in uterine atrophy and decreased serum E2 levels and was associated with a pronounced increase in brain A beta levels. Total brain A beta in the ovx animals was increased by 1.5-fold on average ascompared to intact controls. E2 treatment of ovariectomized animals led touterine hypertrophy and a dose-dependent increase in serum E2 levels. In addition, both doses of E2 significantly reversed the ovariectomy-induced increase in brain A beta levels. The high-dose E2 treatment did not lead to afurther decrease in brain A beta beyond that observed with the low-dose E2treatment. Conclusions: Our results infer that cessation of ovarian estrogen production in postmenopausal women might facilitate A beta deposition byincreasing the local concentrations of A beta 40 and A beta 42 peptides inbrain. In addition, our finding that E2 treatment is associated with diminution of brain A beta levels suggests that modulation of A beta metabolism may be one of the ways by which estrogen replacement therapy prevents or delays the onset of AD or both in postmenopausal women.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 01:20:51