2023-12-02 07:29:00
Géraldine Zamansky, journalist for the Health Magazine on France 5, today evokes a source of hope in the face of Alzheimer’s disease, thanks to the identification of new targets to slow its progression.
franceinfo: Would it be a question of acting very early on a dangerous inflammation of the brain?
Géraldine Zamansky : Exactly. A team of American researchers has just published results which are at the heart of major research into Alzheimer’s disease. They do not focus directly on the accumulation of some sort of toxic “waste” in the brain. But on the simultaneous development of inflammation, indeed very dangerous for the neurons.
The culprits here are cells whose role is essential: microglia. To put it simply, when everything is going well, they preserve an environment favorable to the proper functioning of neurons. With, for example, real cleaning capacity.
So these researchers discovered why these cells allow the “waste” of Alzheimer’s disease to multiply?
Yes, they actually go wrong. The more the “waste” of Alzheimer’s disease accumulates, the less successful these sentinels are in destroying it, and are content to sound the alarm. Biologically speaking, they begin to produce inflammatory molecules. And this can prevent the very subtle mechanisms that allow our neurons to communicate with each other.
So, by identifying each stage of this inflammation, we could find a way to stop it, as Professor Jacques Hugon, from the Center for Cognitive Neurology at Lariboisière Hospital in Paris, explained to me, one of the French pioneers of research in this domain. The challenge is to reach the very beginning of the clogging of the brain by Alzheimer’s lesions.
So this American team has found a target, a weak link in the inflammatory gear?
Exactly. Their starting point was a genetic abnormality known to be linked to Alzheimer’s. It is present on our famous sentinel cells. So these researchers from the largest universities in Boston, Chicago and New York joined forces to both prove and decipher its links with toxic inflammatory activation. With so much precision that it makes the prospect of treatment by this route quite close. (This is why their work was published in the prestigious scientific journal Nature Communications.)
Would this treatment be really close?
Rather yes. Over there in the United States. And here too. Professor Marie Sarrazin, head of the memory and language neurology unit at the Sainte-Anne Hospital Center, told me that she is currently coordinating a therapeutic trial with this type of target. The hope is to find solutions against Alzheimer’s, but not only that. Because these inflammation problems exist in other neurodegenerative diseases, such as Parkinson’s, for example.
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