Editorial
The mechanism described in experiments conducted on experimental models associates the combined loss of dopamine and serotonin with the activation of inflammatory processes. These events trigger hyperphosphorylation of the tau protein and accelerate the deposition of amyloid plaques, resulting in a worsening of the cognitive symptoms typical of the disease. This is what emerges from the Italian study, coordinated by teacher. Marcello D'Amelio, Professor of Physiology at theUniversità Campus Bio-Medico di Roma and director of the Laboratory of Molecular Neuroscience at the Santa Lucia IRCCS in RomeIn partnership with the Catholic University of the Sacred Heart, the Fondazione Policlinico Universitario “A. Gemelli” IRCCS, the Department of Translational Research of the University of Pisa, and the IRCCS Neuromed of Pozzilli, which was published last October 13th on Molecular neurodegeneration.
Research has shown that damage to specific nuclei of the midbrain, responsible for the production of dopamine (ventral tegmental area and substantia nigra) and serotonin (interpeduncular nucleus), triggers powerful neuroinflammation processes in the hippocampus, one of the areas
The brain regions are most affected in Alzheimer's disease, whose degeneration leads to memory loss, a clinical sign of the disease. From a therapeutic perspective, researchers have observed that, in experimental models, increasing dopamine or serotonin levels can significantly reduce neuroinflammation and hyperphosphorylation of the tau protein.
These findings, of great translational relevance, pave the way for precision medicine strategies aimed at slowing the progression of Alzheimer's disease in patients with midbrain vulnerability."This study adds to previous findings from our team and contributes to understanding the role of degeneration of the Ventral Tegmental Area and other midbrain areas in Alzheimer's disease. – explains D'Amelio–- "This study sheds light on why patients with reduced volume in this important area and its associated anatomical and functional brain circuitry experience a more rapid progression from physiological aging to cognitive decline. Restoring the balance of the dopaminergic and serotonergic systems could therefore represent a new therapeutic approach to help slow the progression of the disease. In recent years," he continues, "MRI and brain connectivity studies conducted on patients have indicated that the midbrain is involved early in the Alzheimer's continuum. With this work, we show how its degeneration can fuel inflammation and tau-related processes in the hippocampus. It is not a cure, but it provides additional knowledge about a stage at which intervention could make a difference."
