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It is a work developed over three years by a team of Portuguese, French and German scientists, which reveals a new mechanism involved in aging-related memory loss. Research shows that "specific changes in signaling in circuits involved in memory induce an abnormal response of nerve cells in the brain that is associated with aging."
As the major risk factor for neurodegenerative diseases is the aging, understanding these processes are crucial in defining new therapeutic strategies. Luísa Lopes, Principal Investigator of the Institute of Molecular Medicine João Lobo Antunes (iMM), coordinated this study published in the scientific journal Molecular Psychiatry.
According to the iMM, researchers studied the brains of the elderly and discovered for the first time that an adenosine receptor, called A2A (target of the caffeine in the brain), is specifically located in neurons. "We already knew that this receptor was increased in these conditions s, but there was very little information about the type of cells in which the receptors would be located. We have shown that these receptors are mainly concentrated in neurons, nerve cells and less in glial cells, at least in older patients, "says Luísa Lopes
The study highlights the "iMM," opens new perspectives for the design of drugs that regulate this now-discovered aberrant signaling, "namely the caffeine family that has also been tested effectively in the # 39
study was an animal model that reproduces the increase of the adenosine receptor in the same brain areas as observed in patients that the team of researchers has could better perceive the process. The team found that in these neurons, there was an increase in the release of glutamate, the most abundant neurotransmitter in the brain. By using a combination of electrical readings and calcium measurements, it has been possible to detect that under such conditions there is overactivation of glutamate signaling. "The mere act of altering the amount of adenosine receptor in the hippocampal and cortex neurons has induced a profile that we have called early aging because it causes cognitive deficits and changes in neuronal transmission ", explains Mariana Temido. "To prove the importance of this discovery, we wanted to prove that this same mechanism actually exists in older animals and not just in our model." On the one hand, we showed that the overactivation of glutamate receptors and we found that the A2A receptor is actually involved in this circuit, because when we blocked its action, we normalized both the neuronal function and the memory deficits reversed, "explains Luísa Lopes
. study, says iMM, "opens up new prospects for the design of drugs that regulate this now-discovered aberrant signaling," including the caffeine family that has also been tested effectively in the study. "Plus, it helps create new useful models for understanding aging."
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