DELAYED onset of Alzheimer’s disease caused by a well-known anticoagulant has been demonstrated in a mouse model. The study was carried out by researchers from Centro Nacional de Investigaciones Cardiovasculares (CNIC), in Madrid, Spain, and The Rockefeller University, in New York City, New York, USA, and was co-ordinated by Dr Marta Cortés Canteli. The researchers sought to explore the effects of an existing anticoagulant which prevents blood clots instigated by the manifestation of Alzheimer’s causing patients to experience poor circulation of blood within the brain.
The therapy entailed administration of dabigatran etexilate, or of a placebo, for 1 year to female mice bioengineered by the researchers to experience symptoms of Alzheimer’s disease. Following this treatment, the researchers found the bioengineered mice in the treatment group experienced reduced cerebral blood flow, reduced biological markers of Alzheimer’s disease, and did not suffer any memory loss. There was a 23.7% reduction in amyloid plaques, 31.3% reduction in aggressive phagocytic microglia, and 32.2% reduction in infiltrated T cells.
Dabigatran etexilate is a known drug approved for other conditions and with which patients experience fewer side effects than other blood thinning drugs, and thus can be considered as a safe and reliable treatment. The is no known cure for Alzheimer’s disease and therapeutic strategies to delay the development of the disease and its symptoms is of great value. Dr Cortés Canteli commented on the importance of the findings: “This discovery marks an important advance toward the translation of our results to clinical practice to achieve an effective treatment for Alzheimer’s disease.”
