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 in | Neural regeneration research Vol. 20; no. 2; pp. 416 - 423 |
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| Main Authors | , |
| Format | Journal Article |
| Language | English |
| 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 |
| Edition | 2 |
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| Online Access | Get full text |
| ISSN | 1673-5374 1876-7958 |
| DOI | 10.4103/NRR.NRR-D-23-01690 |
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| Abstract | 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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| AbstractList | 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.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. 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. |
| Author | Piacentini, Roberto Grassi, Claudio |
| AuthorAffiliation | Department of Neuroscience,Università Cattolica del Sacro Cuore,Rome,Italy;Fondazione Policlinico Universitario A.Gemelli,IRCCS,Rome,Italy |
| AuthorAffiliation_xml | – name: Department of Neuroscience,Università Cattolica del Sacro Cuore,Rome,Italy;Fondazione Policlinico Universitario A.Gemelli,IRCCS,Rome,Italy – name: 2 Fondazione Policlinico Universitario A. Gemelli, IRCCS, Rome, Italy – name: 1 Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy |
| Author_xml | – sequence: 1 givenname: Roberto orcidid: 0000-0003-4215-1643 surname: Piacentini fullname: Piacentini, Roberto – sequence: 2 givenname: Claudio surname: Grassi fullname: Grassi, Claudio |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38819045$$D View this record in MEDLINE/PubMed |
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| Keywords | interleukin 1β herpes simplex virus type 1 synaptic dysfunction neuroinflammation microglia |
| Language | English |
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| Snippet | Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer's disease. However, the... Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease. However, the... Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer's disease.However,the... |
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| SubjectTerms | herpes simplex virus type 1 interleukin 1β microglia neuroinflammation Review synaptic dysfunction |
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| Title | Interleukin 1β receptor and synaptic dysfunction in recurrent brain infection with Herpes simplex virus type-1 |
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