ALZHEIMER’S DISEASE: EBRI RESEARCHERS DISCOVER A MOLECULE THAT REJUVENATES THE BRAIN
The antibody A13, developed at the EBRI (European Brain Research Institute) rejuvenates the brain by favoring the birth of new neurons and neutralizing the defects that accompany the early stages of Alzheimer's disease. A strategy that opens up new possibilities for diagnosis and treatment
Rome, NOVEMBER 25: EBRI researchers have discovered that the birth 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 of the highly toxic beta amyloid protein in the brain stem cells, called A-beta oligomers.
The research team managed to neutralize the A-beta oligomers in the brain of a mouse with Alzheimer’s disease by introducing the A13 antibody inside the brain's stem cells, reactivating the birth of new neurons and thus rejuvenating the brain. In particular, the researchers demonstrated how the strategy developed in the EBRI laboratories allows to re-establish the correct neurogenesis in the mouse model studied, recovering 80% of the defects caused by the Alzheimer's disease in the initial phase.
The study, conducted exclusively by Italian researchers, coordinated by Antonino Cattaneo, Giovanni Meli and Raffaella Scardigli at the EBRI Foundation Rita Levi-Montalcini, in collaboration with the CNR, the Scuola Normale Superiore and the Department of Biology of the University of Roma Tre, was recently published in the journal Cell Death and Differentiation (https://www.nature.com/articles/s41418-019-0409-3).
"The importance of this research is twofold: on the one hand - explain Scardigli and Meli - we demonstrate that the decrease of neurogenesis anticipates the pathological signs typical of Alzheimer's disease, and could therefore help to identify the onset of the disease at a very early stage; on the other hand, we also observed in vivo, in the mouse's brain, the effectiveness of our antibody in neutralizing A-beta oligomers right inside neurons ".
In fact, 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.
This research therefore lays the foundation for the development of new strategies useful for the diagnosis and treatment of this neurodegenerative disease. "The ability to monitor neurogenesis in the adult population will offer a potential diagnostic tool in the future to signal the onset of Alzheimer’s at a very early stage, that is when the disease is clinically pre-symptomatic. Moreover - concludes Cattaneo – the therapeutic use of the antibody A13 will allow the neutralization of the A-beta oligomers inside the neurons, where they are formed for the first time, thus affecting the earliest possible stage in the evolution of the pathology”.
TIMELINE FOR CLINICAL TRIALS
Our study was conducted on an animal model of Alzheimer's and has generated very promising results and completely new scientific evidence in this field. Nevertheless, our research is still at the preclinical stage. The transition from the preclinical phase to the clinical phase on patients is not immediate and strongly regulated by the appropriate agencies, requiring years of experimentation and major funding, to evaluate safety and effectiveness in humans. This long and rigorous process is necessary mainly to protect patients.
Scientific research is a slow process, but it is only on this basis that new solutions can be developed in the future.
Didascalia. Representative image of the beneficial effects of the A13 antibody on neuronal cells (in red). On the left the "sick" neurons are shown while on the right the neurons "treated" with the antibody developed by the EBRI research team (source: Scopa et al., Cell Death and Differentiation).