RT Journal Article
T1 Long-Term Dabigatran Treatment Delays Alzheimer's Disease Pathogenesis in the TgCRND8 Mouse Model
A1 Cortes-Canteli, Marta
A1 Kruyer, Anna
A1 Fernandez-Nueda, Irene
A1 Marcos-Diaz, Ana
A1 Ceron, Carlos
A1 T. Richards, Allison
A1 C. Jno-Charles, Odella
A1 Rodríguez Ramírez De Arellano, Ignacio
A1 Callejas, Sergio
A1 Norris, Erin H.
A1 Sanchez-Gonzalez, Javier
A1 Ruiz-Cabello Osuna, Jesús
A1 Ibanez, Borja
A1 Strickland, Sidney
A1 Fuster, Valentín
AB AD 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.
PB Elsevier
SN 0735-1097
YR 2019
FD 2019-10-15
LK https://hdl.handle.net/20.500.14352/133432
UL https://hdl.handle.net/20.500.14352/133432
LA eng
NO Cortes-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.
DS Docta Complutense
RD 24 mar 2026