Another joint explanation put forward by the researchers: the effects linked to the drop in estrogen, a characteristic phenomenon of menopause, on the state of brain health. Before menopause, these estrogens play an anti-inflammatory role for this C3 protein.
Understanding the mechanism for better care
This research is important when in most cases, “Alzheimer’s disease is fatal ten years after the onset of the first symptoms, and there is currently no treatment to stop the progression of neurodegeneration, and even less to reverse it”, continues Professor Lipton. “If treatments are struggling to be developed, it is partly because we still know too little about how the disease works. »
In the future, Professor Lipton’s team intends to go further by testing the reactivation of this C3 protein on an animal model, hoping to identify a possible improvement in symptoms or even a brake on the progression of the disease.
Note: various proteins and inflammatory markers are already known to be involved in Alzheimer’s disease. Two examples in support: researchers have recently highlighted the presence of an enzyme in the genes of the X chromosome, responsible for an over-accumulation of the tau protein in the brain, a typical mechanism of the disease of Alzheimers. Finally, certain neuronal cells of microglia would be capable of destroying synapses, these areas making it possible to convey information between two neurons. This same loss of synapses would trigger the cognitive decline identified in patients with Alzheimer’s disease.
*Scripps Research and Massachusetts Institute of Technology (MIT)
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