A new avenue of research for treating early-stage Alzheimer’s disease has just been found. By making the plaques regress, it would prevent the progression of the symptoms of the pathology and may even reduce the cognitive decline already present.
Stimulating immune cells in the brain could halt the progression of Alzheimer’s disease. This result is from two studies published in the journal Neuron.
The authors, members of the medical research center of Sanford Burnham Prebys, present a new avenue to treat for this neurodegenerative disease.
A disease of the connections between nerve cells
People with Alzheimer’s disease lose their memory because the connections between their nerve cells, neurons, are damaged. The reason for this degradation – the most widely accepted within the scientific community – is the installation of plaques of a protein called “beta-amyloid” between neurons.
These plaques then prevent neurons from communicating with each other and interfere with the functioning of the brain. Researchers have long wanted to find out how the production of the protein could trigger Alzheimer’s. Some have tried to block its proliferation, via anti-beta-amyloid antibodies. Unsuccessful hypothesis.
“We are able to reduce behavioral deficits”
To prevent the buildup of this protein, researchers at Sanford Burnham Prebys studied the TREM2 receptor in mice. This is present in the cells of the microglia, that is to say the immune cells of the central nervous system which ensure its defense.
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Thus, they discovered that when the “beta-amyloid” proteins come into contact with TREM2, a chain reaction takes place in the nervous system: the immune cells break down and eliminate the beta-amyloid, at the origin of the pathology. . This reaction could slow the progression of Alzheimer’s disease because beta-amyloid proteins disappear.
A new mechanism for the elimination of beta-amyoid lacquers
In their second study, the researchers confirm and go beyond their hypothesis. They added TREM2 receptors to mice with an aggressive form of Alzheimer’s. The TREM2 protein prevented the progression of the disease and even reduced some of the cognitive decline already present.
The TREM2 protein therefore has an effect on the activation mechanisms of immune cells in the brain and reduces the symptoms of Alzheimer’s disease. “In addition to saving patients from this pathology, we are able to reduce behavioral deficits with TREM2,” continues Professor Huaxi Xu, author of the study.
A valid possibility at the early stage of the disease
Treatment could therefore be considered to decrease the levels of beta-amyloid proteins from immune cells in the brain. Nevertheless, Huari Xu retains some reservations about this discovery: “It could be beneficial in the early stages to activate the microglia to absorb beta-amyloid proteins. […], but if you over-excite them, they can release an overabundance of cytokines (causing extensive inflammation) that would damage healthy synaptic junctions. ”
In France, 900,000 people have Alzheimer’s disease and 225,000 new cases are diagnosed each year.
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