beta-Amyloid Monomers Are Neuroprotective (Articolo in rivista)

Type
Label
  • beta-Amyloid Monomers Are Neuroprotective (Articolo in rivista) (literal)
Anno
  • 2009-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1523/JNEUROSCI.1736-09.2009 (literal)
Alternative label
  • M.L. Giuffrida; F. Caraci; B. Pignataro; S. Cataldo; P. De Bona; V. Bruno; G. Molinaro; G. Pappalardo; A. Messina; A. Palmigiano; D. Garozzo; F. Nicoletti; E. Rizzarelli; A. Copani (2009)
    beta-Amyloid Monomers Are Neuroprotective
    in The Journal of neuroscience; Society of Neuroscience, Washington (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • M.L. Giuffrida; F. Caraci; B. Pignataro; S. Cataldo; P. De Bona; V. Bruno; G. Molinaro; G. Pappalardo; A. Messina; A. Palmigiano; D. Garozzo; F. Nicoletti; E. Rizzarelli; A. Copani (literal)
Pagina inizio
  • 10582 (literal)
Pagina fine
  • 10587 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
  • numero citazioni =55 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 29 (literal)
Rivista
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  • ImpactFactor=8,657 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Pharmaceutical Sciences, University of Catania, Catania 95125, Italy, Department of Physical-Chemistry, University of Palermo, Palermo 90100, Italy, Department of Chemical Sciences, University of Catania, Catania 95125, Italy, Department of Human Physiology and Pharmacology, University of Rome \"La Sapienza,\" Rome 00185, Italy, Istituto Neurologico Mediterraneo, Neuromed, Pozzilli 86077, Italy, Institute of Biostructure and Bioimaging, National Research Council, Catania 95125, Italy, Istituto di Chimica e Tecnologia dei Polimeri-Consiglio Nazionale delle Ricerche, Catania 95126, Italy Istituto Nazionale Biostrutture e Biosistemi, Rome 00136, Italy (literal)
Titolo
  • beta-Amyloid Monomers Are Neuroprotective (literal)
Abstract
  • The 42-aa-long B-amyloid protein--AB1-42--is thought to play a central role in the pathogenesis of Alzheimer’s disease (AD) (Walsh and Selkoe, 2007). Data from AD brain (Shankar et al., 2008), transgenic APP (amyloid precursor protein)-overexpressing mice (Lesné et al., 2006), and neuronal cultures treated with synthetic AB peptides (Lambert et al., 1998) indicate that self-association of AB1-42 monomers into soluble oligomers is required for neurotoxicity. The function of monomeric AB1-42 is unknown. The evidence that AB1-42 is present in the brain and CSF of normal individuals suggests that the peptide is physiologically active (Shoji, 2002). Here we show that synthetic AB1-42 monomers support the survival of developing neurons under conditions of trophic deprivation and protect mature neurons against excitotoxic death, a process that contributes to the overall neurodegeneration associated with AD. The neuroprotective action of AB1-42 monomers was mediated by the activation of the PI-3-K (phosphatidylinositol-3-kinase) pathway, and involved the stimulation of IGF-1 (insulin-like growth factor-1) receptors and/or other receptors of the insulin superfamily. Interestingly, monomers of AB1-42 carrying the Arctic mutation (E22G) associated with familiar AD (Nilsberth et al., 2001) were not neuroprotective. We suggest that pathological aggregation of AB1-42 may also cause neurodegeneration by depriving neurons of the protective activity of AB1-42 monomers. This \"loss-of-function\" hypothesis of neuronal death should be taken into consideration when designing therapies aimed at reducing AB burden. (literal)
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