Long-term Treatment With Blood Thinner Delays Onset of Alzheimer’s

A research study published in the Journal of American College of Cardiology indicates how a common blood thinner, Dabigatran can stall the onset and progression of Alzheimer’s disease in mouse models. Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that involves the deposition of amyloid plaques, tau tangles, neuroinflammation and brain atrophy. It has a strong cardiovascular risk and often presents with blood-brain barrier disruption, reduced cerebral blood flow and fibrin clots. The team used TgCRND8 AD mice and nontransgenic littermates (as controls). The mice were provided by The Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Canada. Only female mice were used as male littermates were aggressive. The team obtained 70 female mice through in vitro fertilization - 7 TgCRND8 and 33 wild-type (WT) mice.

Two-month old TgCRND8 AD mice and nontransgenic littermates were randomized into groups which received food supplemented with 5 mg/g of dabigatran etexilate (BIBR 1048) or placebo. Both drug and placebo were provided by Boehringer Ingelheim, Germany. The mice were treated till they were 30 weeks old.

The team found that AD mice treated with dabigatran were able to successfully negotiate the test of Barnes maze to assess spatial memory at 25 weeks whereas placebo treated mice were not up to the task. The mice were then sacrificed at 30 to 60 weeks and blood and brain tissue were collected for histology and immunohistochemistry.

The mice treated with dabigatran showed positive improvement with prevention of memory decline, improved blood flow in the cerebral area and reduction of toxic fibrin deposits in the brain. The dabigatran treated mice also showed reduction in the deposit of amyloid plaques, oligomers, phagocytic microglia and infiltrated T cells.

This study proved that long term use of dabigatran can prevent cognitive decline, improve cerebral blood flow, reduce amyloid deposits and reduce neuroinflammation. Dabigatran actually inhibited thrombin and excessive deposition of fibrin in the brain thereby preserving blood flow, facilitating oxygen and rich nutrient delivery to the brain. The results open up a new field to study how this can be translated to therapeutic benefits for Alzheimer’s patients.

Reference:

1. Long-Term Dabigatran Treatment Delays Alzheimer’s Disease Pathogenesis in the TgCRND8 Mouse Model - (http://www.onlinejacc.org/content/74/15/1910)

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Source-Medindia