Deficiencies of the RbAp48 protein in the hippocampus are thought to play a decisive role in the memory deteriorationlinked to aging, according to researchers at Columbia University in New York, United States. Reversing the process by filling in the deficiencies in the protein called RbAp48 could allow older people to regain their youthful memory, the researchers say.
Dr. Eric Kandel, co-winner of the 2000 Nobel Prize in Medicine and director of the study, insists, however, that the lapses of memory they studied have nothing to do with those seen with Alzheimer’s disease. Indeed the latter is a neurodegenerative disease to date incurable. Cognitive disorders linked to Alzheimer’s disease respond to dysfunctions of neurons that cannot be resolved by playing on a protein.
In the American journal Science Transnational Medicine, Dr. Kandel explains that these non-symptomatic Alzheimer’s memory losses originate in the serrated gyrus, a sub-region of the hippocampus. Genetic analyzes of serrated gyrus cells taken from the brains of eight deceased people (none of whom suffered from brain disease) have been confirmed by subsequent research using the brains of living mice.
In both cases, the activity of the RbAp48 gene declined with age. In young mice, when the expression of this gene was blocked, the rodents presented memory problems, which disappeared when the gene was reactivated.
Before any treatment for memory loss can be seen, scientists will need to have proof that the outcome of the Columbia experiment in live mice is verified by tests performed on human brains in Canada. life.
