Long-Term Dabigatran Treatment Delays Alzheimer's Disease Pathogenesis in the TgCRND8 Mouse Model

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dc.contributor.authorCortes-Canteli, Marta
dc.contributor.authorKruyer, Anna
dc.contributor.authorFernandez-Nueda, Irene
dc.contributor.authorMarcos-Diaz, Ana
dc.contributor.authorCeron, Carlos
dc.contributor.authorT. Richards, Allison
dc.contributor.authorC. Jno-Charles, Odella
dc.contributor.authorRodríguez Ramírez De Arellano, Ignacio
dc.contributor.authorCallejas, Sergio
dc.contributor.authorNorris, Erin H.
dc.contributor.authorSanchez-Gonzalez, Javier
dc.contributor.authorRuiz-Cabello Osuna, Jesús
dc.contributor.authorIbanez, Borja
dc.contributor.authorStrickland, Sidney
dc.contributor.authorFuster, Valentín
dc.date.accessioned2026-02-26T22:39:19Z
dc.date.available2026-02-26T22:39:19Z
dc.date.issued2019-10-15
dc.description.abstractAD is a multifactorial disorder with a chronic pro-thrombotic component. This study combined physiological and molecular techniques to demonstrate that long-term anticoagulation with dabigatran ameliorated AD pathogenesis in an AD transgenic mouse model. Dabigatran treatment impeded fibrin deposition and was able to prevent cognitive decline, maintain optimal cerebral perfusion, curb neuroinflammation, decrease amyloid pathology, and maintain the integrity of the BBB in the AD mouse brain. The use of dabigatran might be a future candidate treatment to normalize the sustained pro-coagulant state present in AD patients. Further studies are needed to warrant its use in the clinic.
dc.description.departmentDepto. de Química en Ciencias Farmacéuticas
dc.description.facultyFac. de Farmacia
dc.description.refereedTRUE
dc.description.statuspub
dc.identifier.citationCortes-Canteli M, Kruyer A, Fernandez-Nueda I, Marcos-Diaz A, Ceron C, Richards AT, Jno-Charles OC, Rodriguez I, Callejas S, Norris EH, Sanchez-Gonzalez J, Ruiz-Cabello J, Ibanez B, Strickland S, Fuster V. Long-Term Dabigatran Treatment Delays Alzheimer's Disease Pathogenesis in the TgCRND8 Mouse Model. J Am Coll Cardiol. 2019 Oct 15;74(15):1910-1923. doi: 10.1016/j.jacc.2019.07.081. PMID: 31601371; PMCID: PMC6822166.
dc.identifier.doi10.1016/j.jacc.2019.07.081
dc.identifier.issn0735-1097
dc.identifier.officialurlhttps://doi.org/10.1016/j.jacc.2019.07.081
dc.identifier.urihttps://hdl.handle.net/20.500.14352/133432
dc.issue.number15
dc.journal.titleJournal of the American College of Cardiology
dc.language.isoeng
dc.page.final1923
dc.page.initial1910
dc.publisherElsevier
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.cdu543
dc.subject.keywordCognitive impairment
dc.subject.keywordoral anticoagulation
dc.subject.keywordthrombin
dc.subject.keywordthrombosis
dc.subject.keywordneuroinflammation
dc.subject.keywordanimal models of human disease
dc.subject.ucmQuímica farmaceútica
dc.subject.ucmCardiología
dc.subject.unesco24 Ciencias de la Vida
dc.subject.unesco2302.20 Química Microbiológica
dc.titleLong-Term Dabigatran Treatment Delays Alzheimer's Disease Pathogenesis in the TgCRND8 Mouse Model
dc.typejournal article
dc.type.hasVersionAM
dc.volume.number74
dspace.entity.typePublication
relation.isAuthorOfPublication85f8ae35-f650-415c-bd71-06c07ee772b4
relation.isAuthorOfPublicationde9b6685-e822-4ea8-9ff8-5841cd12adc8
relation.isAuthorOfPublication.latestForDiscovery85f8ae35-f650-415c-bd71-06c07ee772b4

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