May 08, 2017 04:36 AM EDT
The nicotinic acetylcholine receptors connect three things that seem to be unrelated: pain, memory, and nicotine addiction. Researchers from Texas has developed a drug that could help people to enhance the performance of their brain that could ease the pain they feel, slow down the memory loss of people with Alzheimer's disease, and stop people from smoking.
In an article published in Science Daily, researchers from Texas A&M University has developed a drug that would involve the nicotinic acetylcholine receptors, which comes in different varieties that would determine their role in easing the pain, memory loss, and nicotine addiction. "Based on their location and subunit composition, nicotinic acetylcholine receptors have different functions, biophysical properties, and pharmacological characteristics," Ayman Hamouda from the Texas A&M University College of Pharmacy, said. He also said that his team is trying to develop drugs that could modulate these functions but in a more selective way than what is currently available on the market.
In the study published in Journal of Biological Chemistry titled "Unraveling amino acids residues critical for allosteric potentiation of (α4)3(β2)2-type nicotinic acetylcholine receptor responses," developing a drug called nicotinic acetylcholine agonist that could ease pain, memory loss, and nicotine addiction is relatively easy as it is a compound that could bind and activate a receptor. Years were invested in the development but researchers realized that their approach to a compound that could react to nicotinic acetylcholine receptors are revolutionary conserved to bind acetylcholine. In short, using an agonist similar to acetylcholine could activate multiple nicotinic acetylcholine receptor types and multiple side effects are more likely to occur.
Hamouda said that he believes his team's approach is a lot safer because they are not changing the pattern of neural activity that could reach their goal of easing the pain, memory loss, and nicotine addiction. "Instead, we're changing the extent of neural activity so that the same signal that the brain designed is now at a higher level," he said.
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