2023-08-28 16:06:01
Alzheimer’s disease, the most common cause of dementia, affects more than 50 million people worldwide. If the pathology remains incurable until now, scientific work is increasing in an attempt to counter the effects of this neurodegenerative disease.
Researchers from Laval and Lethbridge universities point out that even before the appearance of the first symptoms, brain activity is disturbed in individuals who will develop the disease. “There is neural hyperactivity and disorganization of signals in the brain,” they explain. “Our hypothesis is that a mechanism that regulates neuronal activity, specifically the one responsible for inhibiting neural signals, is disrupted.”
The main inhibitor of neural signals in the human brain is the neurotransmitter GABA. “It works in close collaboration with a cotransporter, KCC2. It is an ion pump, located in the cell membrane, which circulates chloride and potassium ions between the inside and the outside of neurons”, recall the authors. However, studies have already shown that the levels of KCC2 were reduced in the brains of patients who died of Alzheimer’s disease.
reverse the disease
By working on mice expressing manifestations of Alzheimer’s disease, the scientists observed that when these rodents reached the age of four months, the levels of KCC2 actually decreased in two regions of their brain: the hippocampus and the cortex. prefrontal. These two regions are also affected in people who suffer from Alzheimer’s.
The team then developed a molecule in the laboratory to activate KCC2 and prevent its reduction. “In the short term, the administration of this molecule to mice which already had reduced levels of KCC2 led to an improvement in their spatial memory and their social behavior”, rejoice the researchers. “In the long term, it protected them once morest a decrease in cognitive abilities and once morest neuronal hyperactivity. Our results do not imply that loss of KCC2 causes Alzheimer’s disease. On the other hand, it seems to cause an ionic imbalance leading to neuronal hyperactivity which can lead to the death of neurons. This suggests that preventing the loss of KCC2 might slow and possibly even reverse some manifestations of the disease. »
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