New step in the fight against Alzheimer’s disease. This neurodegenerative pathology is characterized in part by the formation of amyloid plaques, formed by the accumulation of a protein, the amyloid beta peptide. Amyloid plaques are toxic to the brain because they disrupt neural networks and cause them to die. And when the plaques are visible in the brain, the damage is already done: the memory damage are then important and irreversible. This is why neurobiology researchers at the Institut Pasteur in Paris are interested in the presence of amyloid beta peptide in the brain, before the formation of plaques. They focused their work on the hippocampus, a region of the brain that plays a central role in memory.
Mice protected against amyloid beta peptides
In this region, they looked at nicotinic receptors, also called acetylcholine receptors. These structures allow communication between the interior environment of the neuron and its environment and play a central role in memory, attention and even sleep. Usually, it is acetylcholine, a messenger naturally present in the body, which binds to it. But nicotine, which is similar in shape to acetylcholine, can also cling to it. It comes from an external source, in particular cigarettes. The researchers conducted experiments on mice in which they inactivated different parts of the nicotinic receptor. They were then able to determine that a region of the receptor, called the ß2 subunit, was the direct target of the amyloid beta peptide. Thus, mice in which this subunit was inactive proved to be protected from the toxic effects of the peptides. They did not suffer from memory problems or cognitive declinespecific to Alzheimer’s disease.
Find a molecule close to nicotine, without the harmful effects
And that is precisely what the nicotine causes: by binding to this receptor instead of acetylcholine, it blocks the ß2 subunit. Problem: As all smokers know, this substance is not without health hazards. “The challenge will therefore be to find a therapeutic molecule resembling nicotine but devoid of its harmful effects (addiction, premature cellular agingacceleration of cardiovascular activity, effects on the gastroenteric system, …)“, explains in a press release from the Pasteur Institute, Doctor Uwe Maskos, main author of this study published in the journal Neurobiology of Aging. Further work is needed to develop an effective therapeutic molecule in humans.
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