Microglial receptor for advanced glycation end product-dependent signal pathway drives beta-amyloid-induced synaptic depression and long-term depression impairment in entorhinal cortex. (Articolo in rivista)

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Label
  • Microglial receptor for advanced glycation end product-dependent signal pathway drives beta-amyloid-induced synaptic depression and long-term depression impairment in entorhinal cortex. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Nicola Origlia, Camilla Bonadonna, Alfredo Rosellini, Elena Leznik, Ottavio Arancio, Shirley ShiDu Yan, Luciano Domenici (2010)
    Microglial receptor for advanced glycation end product-dependent signal pathway drives beta-amyloid-induced synaptic depression and long-term depression impairment in entorhinal cortex.
    in The Journal of neuroscience
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Nicola Origlia, Camilla Bonadonna, Alfredo Rosellini, Elena Leznik, Ottavio Arancio, Shirley ShiDu Yan, Luciano Domenici (literal)
Pagina inizio
  • 11414 (literal)
Pagina fine
  • 11425 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 30 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 34 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Nicola Origlia, Camilla Bonadonna, Alfredo Rosellini, Luciano Domenici: Neuroscience Institute, Italian National Research Council, Pisa, 56100 Pisa, Italy, Ottavio Arancio, Shirley ShiDU Yan: Departments of Pathology and Cell Biology and Surgery and Taub Institute for Research on Alzheimer's Disease and Aging Brain, Columbia University, New York, New York 10032, Luciano Domenici: Department of Biomedical Science and Technology, University of L'Aquila, 67010 L'Aquila, Italy (literal)
Titolo
  • Microglial receptor for advanced glycation end product-dependent signal pathway drives beta-amyloid-induced synaptic depression and long-term depression impairment in entorhinal cortex. (literal)
Abstract
  • Overproduction of beta-amyloid (Abeta) is a pathologic feature of Alzheimer's disease, leading to cognitive impairment. Here, we investigated the impact of cell-specific receptor for advanced glycation end products (RAGE) on Abeta-induced entorhinal cortex (EC) synaptic dysfunction. We found both a transient depression of basal synaptic transmission and inhibition of long-term depression (LTD) after the application of Abeta in EC slices. Synaptic depression and LTD impairment induced by Abeta were rescued by functional suppression of RAGE. Remarkably, the rescue was only observed in slices from mice expressing a defective form of RAGE targeted to microglia, but not in slices from mice expressing defective RAGE targeted to neurons. Moreover, we found that the inflammatory cytokine IL-1 (interleukin-1beta) and stress-activated kinases [p38 MAPK (p38 mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase)] were significantly altered and involved in RAGE signaling pathways depending on RAGE expression in neuron or microglia. These findings suggest a prominent role of microglial RAGE signaling in Abeta-induced EC synaptic dysfunction. (literal)
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