Alzheimer’s, a CNR study demonstrates how a new drug works
At least slow down the degeneration of the disease, if it is not yet possible to eradicate it. This is the objective underlying the study of the Dell scientists” Institute of Neuroscience of the National Research Council (Cnr-In) which led to the discovery of the effectiveness of a drug in this direction.
The work, published in the specialist magazine ‘Brain‘, is the result of the collaboration between the Pisa research group coordinated by Nicola Origlia and that of Milan coordinated by Claudia Verderio. It is “an important step” in the understanding of the mechanisms that drive the neuro-degeneration associated with Alzheimer’s disease, opening up to “new possible therapeutic strategies” against the disease.
Alzheimer’s, symptoms caused by the accumulation of beta-amyloid proteins in the brain
Alzheimer’s disease is characterized by a progressive deterioration of cognitive functions: “in the early stages – recall from the CNR – it manifests itself with a gradual loss of memory due toaccumulation of beta-amyloid protein in brain tissue, which alters the functioning of synapsesup to leading to a cognitive decline due to the degeneration of large areas of the cerebral cortex “.
The study authors tried to understand how this neuro-degeneration process occurs. “The research – explains Origlia – has focused on the study of the entorhinal cortex, a brain area that seems to be particularly vulnerable to the accumulation of beta-amyloid protein. microglial cells, that is particular immune cells of the brain. As the disease progresses, neuro-degeneration spreads thanks to the microglial cells present in the entorhinal cortex to other brain areas, with consequent loss of the functions supported by them “.
A decisive role in this process, scientists point out, is played by extracellular vesicles containing the beta-amyloid protein produced by microglial cells which, moving along the neuronal connections, propagate the alterations through a circuit fundamental for memory, that is the one that connects the entorhinal cortex to the hippocampus.
Alzheimer’s, slow down the interaction between extracellular vesicles and neurons
Thanks to techniques of imagingduring the study, the interaction between the vesicles containing the beta-amyloid protein and the neuron’s surface was observed “demonstrating their movement along the axonal process, that is the process that transfers the nerve impulse to another cell “, explains Verderio.
In simpler wordsthe drug has shown the ability to slow down the movement of extracellular vesicles, carriers of the beta amyloid protein, which causes the degenerative process, so as to reduce their contact with brain tissue.
“It has therefore been shown that by reducing the motility of the vesicles, thanks to pharmacological treatment, the propagation of synaptic deficits between the entorhinal cortex and the hippocampus is prevented – explains the researcher Cnr-In -. This opens up new prospects for intervention. therapeutic aimed at slowing, if not stopping, the progression of the disease “.
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