http://www.cnr.it/ontology/cnr/individuo/prodotto/ID223351
HSV-1 promotes Ca2+ -mediated APP phosphorylation and Abeta accumulation in rat cortical neurons (Articolo in rivista)
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- Label
- HSV-1 promotes Ca2+ -mediated APP phosphorylation and Abeta accumulation in rat cortical neurons (Articolo in rivista) (literal)
- Anno
- 2011-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.neurobiolaging.2010.06.009 (literal)
- Alternative label
Roberto Piacentini a,1, Livia Civitelli b,1, Cristian Ripolia,1, Maria Elena Marcocci b,
Giovanna De Chiara c, Enrico Garaci d, Gian Battista Azzena a,
Anna Teresa Palamara e,f, Claudio Grassi a,* (2011)
HSV-1 promotes Ca2+ -mediated APP phosphorylation and Abeta accumulation in rat cortical neurons
in Neurobiology of aging
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Roberto Piacentini a,1, Livia Civitelli b,1, Cristian Ripolia,1, Maria Elena Marcocci b,
Giovanna De Chiara c, Enrico Garaci d, Gian Battista Azzena a,
Anna Teresa Palamara e,f, Claudio Grassi a,* (literal)
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- ISI Web of Science (WOS) (literal)
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- a Institute of Human Physiology, Catholic University Medical School, Rome, Italy
b Department of Public Health Sciences, Sapienza University of Rome, Rome, Italy
c Department of Cell Biology and Neuroscience, ISS, Rome, Italy
d Department of Experimental Medicine and Biochemical Sciences, University of Rome \"Tor Vergata\", Rome, Italy
e Department of Public Health and Infectious Diseases, Institute Pasteur Cenci Bolognetti Foundation, Sapienza University of Rome, Rome, Italy
f San Raffaele Pisana Scientific Institute for Research, Rome, Italy (literal)
- Titolo
- HSV-1 promotes Ca2+ -mediated APP phosphorylation and Abeta accumulation in rat cortical neurons (literal)
- Abstract
- Epidemiological and experimental findings suggest that chronic infection with Herpes simplex virus type 1 (HSV-1) may be a risk factor for Alzheimer's disease (AD), but the molecular mechanisms underlying this association have not been fully identified. We investigated the effects of HSV-1 on excitability and intracellular calcium signaling in rat cortical neurons and the impact of these effects on amyloid precursor protein (APP) processing and the production of amyloid-beta peptide (Abeta). Membrane depolarization triggering firing rate increases was observed shortly after neurons were challenged with HSV-1 and was still evident 12 hours postinfection. These effects depended on persistent sodium current activation and potassium current inhibition. The virally induced hyperexcitability triggered intracellular Ca2+ signals that significantly increased intraneuronal Ca2+ levels. It also enhanced activity- and Ca2+-dependent APP phosphorylation and
intracellular accumulation of Abeta42. These findings indicate that HSV-1 causes functional changes in cortical neurons that promote APP processing and Abeta production, and they are compatible with the co-factorial role for HSV-1 in the pathogenesis of AD suggested by previous findings. (literal)
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