Interleukin 1β receptor and synaptic dysfunction in recurrent brain infection with Herpes simplex virus type-1

Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer's disease. However, the molecular mechanisms underlying this association are not completely understood. Among the molecular mediators of synaptic and cognitive dysfu...

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Published inNeural regeneration research Vol. 20; no. 2; pp. 416 - 423
Main Authors Piacentini, Roberto, Grassi, Claudio
Format Journal Article
LanguageEnglish
Published India Wolters Kluwer - Medknow 01.02.2025
Medknow Publications & Media Pvt. Ltd
Department of Neuroscience,Università Cattolica del Sacro Cuore,Rome,Italy
Fondazione Policlinico Universitario A.Gemelli,IRCCS,Rome,Italy
Wolters Kluwer Medknow Publications
Edition2
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ISSN1673-5374
1876-7958
DOI10.4103/NRR.NRR-D-23-01690

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Summary:Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer's disease. However, the molecular mechanisms underlying this association are not completely understood. Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role. Here, we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain, highlighting the role of interleukins and, in particular, interleukin 1β as a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.
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Author contributions: Manuscript was written and revised by RP and CG. Both authors approved the final version of the manuscript.
ISSN:1673-5374
1876-7958
DOI:10.4103/NRR.NRR-D-23-01690