- It is an experimental oral treatment to combat the disease, which aims to protect neurons.
- This compound, developed by scientists at Yale University, United States, could become a good treatment for Alzheimer’s.
- The study was published Wednesday in the scientific journal Science Translational Medicine.
To counteract Alzheimer’shave been able to reverse damage to brain synapses in a mouse model, without causing secondary damage; It is an experimental oral treatment to combat the disease, which aims to protect neurons.
This compound, developed by scientists at Yale University, United States, could become a good treatment for Alzheimer’sa disease that still has no cure.
The study was published Wednesday in the scientific journal Science Translational Medicine.
Alzheimer’s
Alzheimer’s —the most common form of dementia—is a complex, multifactorial disease that usually appears after the age of 65, and that it has a strong genetic component. It is believed that most cases are caused by the interaction of genetic and environmental factors.
Although the landscape of Alzheimer’s treatment remains very grim, scientists have made progress in understanding some of the genetic and molecular factors of the disease.
It is known that two of the main characteristics of Alzheimer’s disease are the accumulation of toxic Tau proteins and the gradual destruction of the synapses (connections) between neurons, which are the basis of all brain activities.
ABOUT THE STUDY
Scientists have shown that microglia, immune cells of the nervous system, can betray the brain and trigger synapse lossbut the reason for this is still unclear.
In the study, Joshua Spurrier and his Yale team evaluated the experimental compound BMS-984923, which targets a receptor called mGluR5, which has been linked to loss of connections between neurons.
Thanks to the magnetic resonance imaging and CT scans, the researchers observed for the first time that the compound acted effectively on the mGluR5 receptors in the brains of the monkeys and mice in which it was tested, without causing adverse effects.
In mouse models of Alzheimer’s disease, the treatment completely restored the density of the synapses and prevented them from being marked by the C1Q protein, which prevented them from being engulfed by microglia.
The authors also found that the benefits of BMS-984923 for synapses lasted for up to a month after treatment, suggesting that the compound should continue to be examined in follow-up studies.
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