Cortes-Canteli, MartaKruyer, AnnaFernandez-Nueda, IreneMarcos-Diaz, AnaCeron, CarlosT. Richards, AllisonC. Jno-Charles, OdellaRodríguez Ramírez De Arellano, IgnacioCallejas, SergioNorris, Erin H.Sanchez-Gonzalez, JavierRuiz-Cabello Osuna, JesúsIbanez, BorjaStrickland, SidneyFuster, Valentín2026-02-262026-02-262019-10-15Cortes-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: PMC6822166.0735-109710.1016/j.jacc.2019.07.081https://hdl.handle.net/20.500.14352/133432AD 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.engAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/journal articlehttps://doi.org/10.1016/j.jacc.2019.07.081open access543Cognitive impairmentoral anticoagulationthrombinthrombosisneuroinflammationanimal models of human diseaseQuímica farmaceúticaCardiología24 Ciencias de la Vida2302.20 Química Microbiológica