Paper type: Journal Article, Research Support, Non-U. S. Gov'T,
Impact factor: 7.627, 5-year impact factor: 6.916
Url: Not available.
Keywords: Alzheimer Disease, Beta Monomers, Bdnf, Creb, Igf1-R, Alzheimer Disease Pathology
, Amyloid Beta-Peptides Metabolism Pharmacology
, Animals
, Brain-Derived Neurotrophic Factor Drug Effects Genetics
, Gene Expression Regulation Drug Effects
, Humans
, Neurons Drug Effects Metabolism
, Peptide Fragments Metabolism
, Rats
, Receptor, Igf Type 1 Drug Effects Genetics
, Somatomedin Drug Effects
, Signal Transduction Drug Effects
, S Disease
, Aβ Monomers,
Affiliations: *** IBB - CNR ***
Institute of Biostructures and Bioimaging, National Council of Research (IBB-CNR), Via Paolo Gaifami 18, 95126, Catania, Italy., Endocrinology, Department of Clinical and Experimental Medicine, Garibaldi-Nesima Medical Center, University of Catania, via Palermo 636, 95122, Catania, Italy., Department of Drug Sciences, University of Catania, Viale A. Doria 6, 95125, Catania, Italy., Department of Chemical Sciences, University of Catania, Viale A. Doria 6, 95125, Catania, Italy.,
Endocrinology, Department of Clinical and Experimental Medicine, Garibaldi-Nesima Medical Center, University of Catania, via Palermo 636, 95122, Catania, Italy.
Department of Drug Sciences, University of Catania, Viale A. Doria 6, 95125, Catania, Italy.
Department of Chemical Sciences, University of Catania, Viale A. Doria 6, 95125, Catania, Italy.
References: Not available.
Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type-1 insulin-like growth factor receptors in neuronal cells
Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with synaptic dysfunction, pathological accumulation of beta-amyloid (Abeta), and neuronal loss. The self-association of Abeta monomers into soluble oligomers seems to be crucial for the development of neurotoxicity (J. Neurochem., 00, 2007 and 1172). Abeta oligomers have been suggested to compromise neuronal functions in AD by reducing the expression levels of the CREB target gene and brain-derived neurotrophic factor (BDNF) (J. Neurosci., 27, 2007 and 2628; Neurobiol. Aging, 36, 2015 and 20406 Mol. Neurodegener., 6, 2011 and 60). We previously reported a broad neuroprotective activity of physiological Abeta monomers, involving the activation of type-1 insulin-like growth factor receptors (IGF-IRs) (J. Neurosci., 29, 2009 and 10582, Front Cell Neurosci., 9, 2015 and 297). We now provide evidence that Abeta monomers, by activating the IGF-IR-stimulated PI3-K/AKT pathway, induce the activation of CREB in neurons and sustain BDNF transcription and release.
Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type-1 insulin-like growth factor receptors in neuronal cells
Bruni AC, Bernardi L, Colao R, Rubino E, Smirne N, Frangipane F, Terni B, Curcio SA, Mirabelli M, Clodomiro A, Di Lorenzo R, Maletta R, Anfossi M, Gallo M, Geracitano S, Tomaino C, Muraca MG, Leotta A, Lio SG, Pinessi L, Rainero I, Sorbi S, Nee L, Milan G, Pappata S, Postiglione A, Abbamondi N, Forloni G, St George Hyslop P, Rogaeva E, Bugiani O, Giaccone G, Foncin JF, Spillantini MG, Puccio G * Worldwide distribution of PSEN1 Met146Leu mutation: A large variability for a founder mutation(1536 views) Neurology (ISSN: 0028-3878, 1526-632x, 1526-632xelectronic), 2010 Mar 9; 74(10): 798-806. Impact Factor:8.017 ViewExport to BibTeXExport to EndNote