Hope in the face of Alzheimer’s: how researchers manage to ‘reverse’ symptoms

Scientists from Laval University and the University of Lethbridge in Canada have been able to reverse some of the cognitive manifestations associated with Alzheimer’s disease in mice. Explanations.

Alzheimer’s disease, the most common cause of dementia, affects more than 50 million people worldwide. If the pathology is still incurable, scientific work is increasing in attempts to counteract the consequences of this neurodegenerative disease.

Researchers from the universities of Laval and Lethbridge note that even before the first symptoms appear in people who develop the disease, brain activity is impaired.

“In the brain, there is hyperactivity of neurons and disorganization of signals,” they explain. “Our hypothesis is that the mechanism that regulates neuronal activity, in particular the one responsible for the inhibition of nerve signals, is disrupted.”

The main inhibitor of nerve signals in the human brain is the neurotransmitter GABA. “It works closely with the KCC2 cotransporter. It is an ion pump located in the cell membrane that circulates chloride and potassium ions between the inside and outside of neurons,” the authors recall.

However, studies have already shown that KCC2 levels were reduced in the brains of patients who died of Alzheimer’s disease.

reverse the disease

Working on mice with manifestations of Alzheimer’s disease, the scientists noticed that when these rodents reached four months of age, KCC2 levels actually decreased in two areas of their brains: the hippocampus and the prefrontal cortex. These two regions are also affected in people suffering from Alzheimer’s disease.

The team then developed a molecule in the lab that activates KCC2 and prevents it from being restored. “In the short term, administration of this molecule to mice that already had reduced levels of KCC2 led to improvements in their spatial memory and social behavior,” the researchers said. “In the long term, this protected them from cognitive decline and 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 hyperactivity of neurons, which can lead to their death. This suggests that preventing the loss of KCC2 may slow down and possibly even reverse some of the manifestations of the disease. “

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