Show simple item record

dc.contributor.authorFülöp, T.
dc.contributor.authorMunawara, U.
dc.contributor.authorLarbi, A.
dc.contributor.authorDesroches, M. 
dc.contributor.authorRodrigues, S. 
dc.contributor.authorCatanzaro, M.
dc.contributor.authorGuidolin, A.
dc.contributor.authorKhalil, A.
dc.contributor.authorBernier, F.
dc.contributor.authorBarron, A.E.
dc.contributor.authorHirokawa, K.
dc.contributor.authorBeauregard, P.B.
dc.contributor.authorDumoulin, D.
dc.contributor.authorBellenger, J.-P.
dc.contributor.authorWitkowski, J.M.
dc.contributor.authorFrost, E.
dc.date.accessioned2020-12-28T19:19:37Z
dc.date.available2020-12-28T19:19:37Z
dc.date.issued2020-05-26
dc.identifier.urihttp://hdl.handle.net/20.500.11824/1225
dc.description.abstractAlzheimer’s disease (AD) is the most prevalent dementia in the world. Its cause(s) are presently largely unknown. The most common explanation for AD, now, is the amyloid cascade hypothesis, which states that the cause of AD is senile plaque forma- tion by the amyloid β peptide, and the formation of neurofibrillary tangles by hyperphosphorylated tau. A second, burgeoning theory by which to explain AD is based on the infection hypothesis. Much experimental and epidemiological data support the involvement of infections in the development of dementia. According to this mechanism, the infection either directly or via microbial virulence factors precedes the formation of amyloid β plaques. The amyloid β peptide, possessing antimicrobial properties, may be beneficial at an early stage of AD, but becomes detrimental with the progression of the disease, concomi- tantly with alterations to the innate immune system at both the peripheral and central levels. Infection results in neuroinflam- mation, leading to, and sustained by, systemic inflammation, causing eventual neurodegeneration, and the senescence of the immune cells. The sources of AD-involved microbes are various body microbiome communities from the gut, mouth, nose, and skin. The infection hypothesis of AD opens a vista to new therapeutic approaches, either by treating the infection itself or modulating the immune system, its senescence, or the body’s metabolism, either separately, in parallel, or in a multi-step way.en_US
dc.description.sponsorshipBasque Government under the grant “Artificial Intelligence in BCAM number EXP. 2019/00432”en_US
dc.formatapplication/pdfen_US
dc.language.isoengen_US
dc.rightsReconocimiento-NoComercial-CompartirIgual 3.0 Españaen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/es/en_US
dc.titleTargeting Infectious Agents as a Therapeutic Strategy in Alzheimer’s Diseaseen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.identifier.doi10.1007/s40263-020-00737-1
dc.relation.publisherversionhttps://link.springer.com/article/10.1007%2Fs40263-020-00737-1en_US
dc.relation.projectIDES/1PE/SEV-2017-0718en_US
dc.relation.projectIDES/2PE/RTI2018-093860-B-C21en_US
dc.relation.projectIDEUS/BERC/BERC.2018-2021en_US
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen_US
dc.type.hasVersioninfo:eu-repo/semantics/acceptedVersionen_US
dc.journal.titleCNS Drugsen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

Reconocimiento-NoComercial-CompartirIgual 3.0 España
Except where otherwise noted, this item's license is described as Reconocimiento-NoComercial-CompartirIgual 3.0 España