Alzheimer's disease: a new drug candidate
Caffeine has been found to have the ability to fight Alzheimer's disease
Copper news based on the materials of the University of Bonn: Caffeine against Alzheimer's diseaseAn international team of scientists has shown for the first time that caffeine is able to restrain the development of complexes of excessively phosphorylated tau proteins, the presence of which is a hallmark of Alzheimer's disease.
The results of a two-year study published in the journal Neurobiology of Aging (Laurent et al., Beneficial effects of caffeine in a transgenic model of Alzheimer's Disease-like Tau pathology) may lead to the creation of a new class of drugs for the treatment of this disease.
Caffeine, which is part of coffee, tea, cocoa, acts as an antagonist of the adenosine receptors of the brain: it binds to them and thereby reduces the effect of their work. Adenosine reduces the processes of excitation in the brain, and replacing it with caffeine, on the contrary, leads to a stimulating effect.
Previous research by scientists has shown that blocking adenosine receptors of the A2A subtype plays an important role in slowing the development of Alzheimer's disease. Based on these data, researchers from the University of Bonn in Germany and the University of Lille in France have isolated an ultrapure water-soluble substance acting as an antagonist of A2A receptors. This compound proved to be more effective and had fewer side effects than caffeine, as it selectively blocked only adenosine receptors of the A2A subtype.
The compound not named here (bottom right), MSX-3 hydrate, aka – 3,7-Dihydro-8-[(1E)-2-(3-Methoxyphenyl)ethenyl]-7-methyl-3-[3-(phosphonooxy)propyl-1-(2-propynyl)-1H-purine-2,6-dione disodium salt hydrate, can be ordered from Sigma-Aldrich for only 256 euros for 5 mg. Among other information, it is noted there that this is a candidate drug, a selective inhibitor of adenosine A2A receptors. The structural formula of caffeine – VM is shown at the top left for comparison.For several weeks, mice with a genetic mutation that promotes the formation of tau complexes in the brain and the early development of Alzheimer's disease were injected with an A2A receptor antagonist.
Compared with the control group receiving placebo, the animals from the experimental group showed much higher results in memory tests, thereby demonstrating a slowdown in cognitive decline. Histological analysis of the hippocampus, responsible for the transition of short-term memory into long-term memory, confirmed an improvement in the brain condition of animals from the experimental group.
Now scientists plan to expand their research and conduct them on other animal models of Alzheimer's disease. If the results are confirmed, the researchers will conduct clinical trials of a substance acting like caffeine, which in the future may lead to the development of a new class of drugs for the treatment of Alzheimer's type dementia.
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