Why are women more at risk of Alzheimer’s disease than men? Because the functioning of a protein, involved in cerebral connections, would be much more disturbed with the fairer sex..
Like many neurological pathologies, Alzheimer’s disease finds its origin in a molecular dysfunction. A track recently explored by American scientists* to explain the reasons why women seem more vulnerable to this disease, which is also ranked first – in terms of incidence – of neurodegenerative disorders.
How did they proceed? By observing 40 brain samples taken from patients, half of whom died of Alzheimer’s disease, and the other half of other causes. Each group was then divided according to gender, women on one side, men on the other. And what did they find? “A difference in the activity of a protein called C3, the expression of which proves to be much more inflammatory in women than in men. Its concentration is thus 6 times higher in women than in men”, declares the Pr Stuart Lipton, lead author of the study. And this C3 protein is precisely involved in many connections in the brain. This would explain the slowing of the processes of reflection, memorization or even the loss of spatio-temporal landmarks and motor difficulties.
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 following 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 regarding 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.
To note : different 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.
