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dc.rights.licenseopenen_US
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorHASANTARI, Iris
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorNICOLAS, Nabil
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorALZIEU, Philippe
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorLEVAL, Lea
dc.contributor.authorSHALABI, Andree
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGROLLEAU, Sylvain
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDINET, Virginie
dc.date.accessioned2024-03-25T15:59:26Z
dc.date.available2024-03-25T15:59:26Z
dc.date.issued2024-02-14
dc.identifier.issn1422-0067en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/188968
dc.description.abstractEnThe complement is a component of the innate immune system designed to fight infections and tissue- or age-related damages. Complement activation creates an inflammatory microenvironment, which enhances cell death. Excessive complement inflammatory activity has been linked to alterations in the structure and functions of the blood-brain barrier, contributing to a poor prognosis for Alzheimer's disease (AD). In the AD preclinical phase, individuals are often clinically asymptomatic despite evidence of AD neuropathology coupled with heightened inflammation. Considering the involvement of the complement system in the risk of developing AD, we hypothesize that inhibiting complement activation could reduce this inflammatory period observed even before clinical signs, thereby slowing down the onset/progression of AD. To validate our hypothesis, we injected complement inhibitor factor H into the brain of APP/PS1 AD mice at early or late stages of this pathology. Our results showed that the injection of factor H had effects on both the onset and progression of AD by reducing proinflammatory IL6, TNF-α, IL1β, MAC and amyloid beta levels. This reduction was associated with an increase in VGLUT1 and Psd95 synaptic transmission in the hippocampal region, leading to an improvement in cognitive functions. This study invites a reconsideration of factor H's therapeutic potential for AD treatment.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enMice
dc.subject.enAnimals
dc.subject.enAlzheimer Disease
dc.subject.enAmyloid beta-Peptides
dc.subject.enAmyloid beta-Protein Precursor
dc.subject.enComplement Factor H
dc.subject.enMice
dc.subject.enTransgenic
dc.subject.enComplement Activation
dc.subject.enDisease Models
dc.subject.enAnimal
dc.title.enFactor H's Control of Complement Activation Emerges as a Significant and Promising Therapeutic Target for Alzheimer's Disease Treatment.
dc.title.alternativeInt J Mol Scien_US
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/ijms25042272en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed38396950en_US
bordeaux.journalInternational Journal of Molecular Sciencesen_US
bordeaux.volume25en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.issue4en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.identifierhal-04520560
hal.version1
hal.date.transferred2024-03-25T15:59:29Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
workflow.import.sourcepubmed
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=International%20Journal%20of%20Molecular%20Sciences&rft.date=2024-02-14&rft.volume=25&rft.issue=4&rft.eissn=1422-0067&rft.issn=1422-0067&rft.au=HASANTARI,%20Iris&NICOLAS,%20Nabil&ALZIEU,%20Philippe&LEVAL,%20Lea&SHALABI,%20Andree&rft.genre=article


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