Academic
Publications
HSV1 promotes Ca 2+-mediated APP phosphorylation and Aβ accumulation in rat cortical neurons

HSV1 promotes Ca 2+-mediated APP phosphorylation and Aβ accumulation in rat cortical neurons,10.1016/j.neurobiolaging.2010.06.009,Neurobiology of Agin

HSV1 promotes Ca 2+-mediated APP phosphorylation and Aβ accumulation in rat cortical neurons   (Citations: 7)
BibTex | RIS | RefWorks Download
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-β peptide (Aβ). 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 Aβ42. These findings indicate that HSV-1 causes functional changes in cortical neurons that promote APP processing and Aβ production, and they are compatible with the co-factorial role for HSV-1 in the pathogenesis of AD suggested by previous findings.
Journal: Neurobiology of Aging - NEUROBIOL AGING , vol. 32, no. 12, pp. 2323.e13-2323.e26, 2011
Cumulative Annual
View Publication
The following links allow you to view full publications. These links are maintained by other sources not affiliated with Microsoft Academic Search.
Sort by: