Mice protected from Alzheimer’s disease thanks to a mutated protein. This is what a team led by the CNRS and Grenoble Alpes University has just discovered. This neurodegenerative disease, which affects nearly a million people in France, finds its origin in the appearance of two types of brain lesions: an abnormal accumulation of the protein beta-amyloidbeta-amyloid (amyloid plaques)) between neurons and an abnormal accumulation, inside neurons, of the Tau protein (neurofibrillar degeneration). These lesions disrupt communication between neurons, which eventually die when the aggregates are too large. To date, no treatment curativecurative is not available.
Discovered in Iceland, then tested on mice
More than ten years ago, scientists discovered a mutation that almost one in 100 Icelanders carry. It is a mutation in the beta-amyloid protein, which protects against Alzheimer’s disease, and whose carriers are little or less affected by cognitive decline. In the current study, scientists injected the mutated beta-amyloid protein, artificially recreated in the laboratory, into the brains of mouse models of Alzheimer’s disease. Results ? The researchers observed a reduction in toxic lesions linked to the beta-amyloid protein, but also in plaques formed by the Tau protein. They also noted an absence of memory loss.
Protection against all brain damage
According to the CNRS press release, the protein protected the brains of animals “ of all the dysfunctions linked to the disease », four months after the injection. Furthermore, on the mouse modelsmouse models, a single injection provided protection for several months. “ This result could thus be the starting pointstarting point of a new category of preventive therapies to treat people with neurodegenerative diseasesneurodegenerative diseases at early stages and block the evolution of the pathologypathologythanks to the injection of let’s praylet’s pray protectors », notes the CNRS in a press release.
Did you know ?
The beta-amyloid protein is also called “pseudo-prion”, due to a possible abnormal behavior, the same as that of the prion protein, involved in diseases of the central nervous system such as Creutzfeldt-Jakob disease. It can thus fold into an abnormal spatial configuration and transmit the abnormality to the surrounding normal proteins, in other words, the phenomenon that occurs in Alzheimer’s disease.
