Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Age-dependent cognitive deficits and neuronal apoptosis in cyclooxygenase-2 transgenic mice
Autore:
Andreasson, KI; Savonenko, A; Vidensky, S; Goellner, JJ; Zhang, Y; Shaffer, A; Kaufmann, WE; Worley, PF; Isakson, P; Markowska, AL;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Neurol, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 urosci, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Pathol, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Pediat, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 av Sci, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD 21205USA Johns Hopkins Univ Baltimore MD USA 21205 iol Sci, Baltimore, MD 21205USA Kennedy Krieger Inst, Baltimore, MD 21205 USA Kennedy Krieger Inst Baltimore MD USA 21205 Inst, Baltimore, MD 21205 USA Johns Hopkins Univ, Dept Psychol, Baltimore, MD 21218 USA Johns Hopkins Univ Baltimore MD USA 21218 sychol, Baltimore, MD 21218 USA Pharmacia Res & Dev, Peapack, NJ 07977 USA Pharmacia Res & Dev Peapack NJUSA 07977 Res & Dev, Peapack, NJ 07977 USA Pharmacia Res, St Louis, MO 63198 USA Pharmacia Res St Louis MO USA 63198Pharmacia Res, St Louis, MO 63198 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 20, volume: 21, anno: 2001,
pagine: 8198 - 8209
SICI:
0270-6474(20011015)21:20<8198:ACDANA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; INBRED MOUSE STRAINS; ALZHEIMERS-DISEASE; INDUCIBLE CYCLOOXYGENASE; GENE-EXPRESSION; POSTTRAINING INFUSION; HIPPOCAMPAL-FORMATION; PREFRONTAL CORTEX; PARIETAL CORTEX; RAT-BRAIN;
Keywords:
transgenic mouse; COX-2; spatial memory; aversive behavior; TUNEL; GFAP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Andreasson, KI Johns Hopkins Univ, Sch Med, Dept Neurol, 600 N Wolfe St,Meyer 5-119B, Baltimore, MD 21205 USA Johns Hopkins Univ 600 N Wolfe St,Meyer5-119B Baltimore MD USA 21205
Citazione:
K.I. Andreasson et al., "Age-dependent cognitive deficits and neuronal apoptosis in cyclooxygenase-2 transgenic mice", J NEUROSC, 21(20), 2001, pp. 8198-8209

Abstract

The cyclooxygenases catalyze the rate-limiting step in the formation of prostaglandins from arachidonic acid and are the pharmacological targets of (NSAIDs). In brain, cyclooxygenase-2 (COX-2), the inducible isoform of cyclooxygenase, is selectively expressed in neurons of the cerebral cortex, hippocampus, and amygdala. As an immediate-early gene, COX-2 is dramatically and transiently induced in these neurons in response to NMDA receptor activation. In models of acute excitotoxic neuronal injury, elevated and sustainedlevels of COX-2 have been shown to promote neuronal apoptosis, indicating that upregulated COX-2 activity is injurious to neurons. COX-2 may also contribute to the development of Alzheimer's disease, for which early administration of NSAIDs is protective against development of the disease. To test the effect of constitutively elevated neuronal COX-2, transgenic mice were generated that overexpressed COX-2 in neurons and produced elevated levels of prostaglandins in brain. In cross-sectional behavioral studies, COX-2 transgenic mice developed an age-dependent deficit in spatial memory at 12 and 20 months but not at 7 months and a deficit in aversive behavior at 20 months of age. These behavioral changes were associated with a parallel age-dependent increase in neuronal apoptosis occurring at 14 and 22 months but not at 8 months of age and astrocytic activation at 24 months of age. These findings suggest that neuronal COX-2 may contribute to the pathophysiology of age-related diseases such as Alzheimer's disease by promoting memory dysfunction, neuronal apoptosis, and astrocytic activation in an age-dependentmanner.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 23:07:59