November 28, 2014 / Bio Valley BIOON / -- Amyotrophic lateral sclerosis (ALS), also known as Gram's disease, is a neurodegenerative disease that kills motor neurons and causes paralysis. And death. At present, ALS cannot be cured, and most of the drugs for developing ALS have failed during the experiment.
In a study published in the November 20 issue of the journal Annals of Clinical and Translational Neurology, the researchers showed that the ability of the brain to pump out toxins is enhanced in patients with ALS, and that this ability of the brain also pumps out drugs that treat ALS. Thereby reducing the efficacy of the drug. Research work has shown that when these pumps are blocked, treatment of ALS drugs becomes more effective in mouse models, and disease progression is slowing down.
This brain pumping mechanism usually protects the brain and spinal cord from environmental toxin damage and also pumps out the treatment, so studies suggest that blocking the pump or transporter increases the effectiveness of ALS.
In an earlier published study, the team showed that in mice, the pump changed its function as the disease progressed, and the pump became more active as the symptoms became more severe. To address this issue, the researchers used a combination of riluzole and pump blockers (elacridar) that have been approved for the treatment of ALS in a mouse model of ALS.
Previous work has shown that the drug loses its effectiveness as the patient progresses. The drug only prolongs the survival of patients with ALS for 3-6 months. The researchers chose riluzole to conduct animal studies because they knew that riluzole interacted with two drug-resistant pumps, P-glycoprotein (P-gp) and the breast cancer resistance protein BCRP.
Mice were treated with combination therapy with ALS drug (riluzole) and pump blocker (elacridar) and found to be a better prolonged life in mice compared to those treated with riluzole alone. (Bio Valley Bioon.com)
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