Deficiencies in RbAp48 protein in the hippocampus would play a decisive role in the memory deteriorationlinked to aging, according to researchers at Columbia University in New York, USA. Reversing the process by addressing deficiencies in a protein called RbAp48 could allow older people to regain their youthful memories, the researchers suggest.
Dr. Eric Kandel, co-winner of the Nobel Prize for Medicine in 2000 and director of the study insists, however, that the memory lapses on which they leaned 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 neuron dysfunctions that cannot be resolved by acting on a protein.
In the American journal Science Transnational Medicine, Dr. Kandel explains that these non-symptomatic Alzheimer’s memory losses originate in the dentate gyrus, a sub-region of the hippocampus. Genetic analyzes of serratus gyrus cells extracted from the brains of eight deceased people (none of whom suffered from brain disease) were confirmed by subsequent research on the brains of living mice.
In both cases, RbAp48 gene activity declined with age. In young mice, when the expression of this gene was blocked, the rodents had 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 can be verified by tests performed on the brains of humans in life.
