Mice protected from Alzheimer’s disease thanks to a mutated protein. This is what a team led by the CNRS and the University of Grenoble Alpes has just discovered.
This neurodegenerative disease, which affects nearly a million people in France, originates from the appearance of two types of brain lesions: an abnormal accumulation of beta-amyloid protein (amyloid plaques) between neurons and an abnormal accumulation, inside neurons, of Tau protein (neurofibrillary degeneration).
These lesions disrupt communication between neurons, which eventually die when the aggregates are too large. To date, no curative treatment is available.
Mutation discovered in Iceland
More than a decade ago, scientists discovered a mutation that nearly one in 100 Icelanders carry; a mutation of the beta-amyloid protein that 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 mice modeling Alzheimer’s disease.
Results? The researchers observed a reduction in toxic lesions linked to 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 animals’ brains “of all the dysfunctions linked to the disease”, four months after infection. In addition, a single injection triggered protection for several months.
“This result could thus be the starting point for a new category of preventive therapies to treat people with neurodegenerative diseases at early stages and block the progression of the pathology, thanks to the injection of protective prions,” notes the CNRS in a press release.
To know : Beta-amyloid protein is also called “pseudo-prion” because of 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.
