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by Tiziana Di Giovannandrea 25 November 2019The aging of the brain, with the progressive decrease in the creation of new neurons, which leads to dementia caused by Alzheimer's disease, can be slowed down by recovering 80% of the defects caused by the disease in the initial phase. Even degenerative evolution can be reversed, favoring a real "rejuvenation" of the brain.

This is what was discovered by a group of Italian researchers from the Ebri Institute, who found that the emergence of new neurons in the adult brain (neurogenesis) is reduced at a very early stage of Alzheimer's disease. This alteration is caused by the accumulation in the brain stem cells of highly toxic aggregates of the beta amyloid protein, called A-beta oligomers. The team managed to neutralize the A-beta oligomers in the brain of an Alzheimer's patient by introducing the A13 antibody inside the brain's stem cells, reactivating the birth of new neurons and thus rejuvenating the brain.

The entirely Italian study, coordinated by Antonino Cattaneo, Giovanni Meli and Raffaella Scardigli, at the Ebri Rita Levi Montalcini Foundation, in collaboration with the CNR, the Scuola Normale Superiore and the Department of Biology of the University of Roma Tre, was published by recent in the Cell Death and Differentiation magazine.

"The importance of this research is twofold: on the one hand - explained Scardigli and Meli - we show that the decrease in neurogenesis anticipates the pathological signs typical of Alzheimer's disease, and could therefore help to identify the onset of the disease in a timely manner very early; on the other hand, we also observed the efficacy of our antibody in neutralizing A-beta oligomers right inside neurons in the mouse brain. "

For the first time the individual "toxic bricks" that will form the extracellular plaques of A-beta (the current therapeutic target of Alzheimer's disease) have been intercepted and neutralized before they cause irreversible neuronal damage.

The research therefore lays the foundation for the development of new strategies useful for the diagnosis and therapy of this neurodegenerative disease. "Being able to monitor neurogenesis in the adult population will offer a potential diagnostic tool in the future to signal the onset of Alzheimer's in a very early stage, that is when the disease is clinically pre-symptomatic. Furthermore - concludes Cattaneo - therapeutic use of the antibody A13 will allow to neutralize the A-beta oligomers inside the neurons, where they are formed for the first time, thus affecting the earliest possible event in the evolution of the pathology ".