- Alzheimer’s disease is characterized by the loss of synapses, the sites where nerve cells communicate with each other, in brain regions involved in cognitive function.
- Studies have shown that short chains of the beta-amyloid protein, called oligomers, can cause a dysfunction of synapses and their loss.
- A new study conducted using nerve cells from rodent brains has found a novel pathway through which beta-amyloid causes the loss of synapses.
- Mdm2, an enzyme belonging to this pathway, can be inhibited to prevent the loss of synapses and, thus, could be a target for the development of treatments for Alzheimer’s disease.
An aging population and the lack of effective treatments have made Alzheimer’s disease a global health crisis. Several Alzheimer’s disease treatments, including
However, therapies targeting molecules that mediate the toxic effects of beta-amyloid could be more effective in the treatment of Alzheimer’s disease.
A new study published in the journal eNeuro has uncovered a novel pathway through which beta-amyloid oligomers could cause a loss of synapses in brain regions impacted by Alzheimer’s disease.
The study also identified an enzyme in nerve cells called Mdm2 in this pathway that was necessary for beta-amyloid-mediated loss of synapses, which are the links between brain cells.
These results suggest that molecules such as Mdm2 in this novel pathway could be targeted for the treatment of Alzheimer’s disease.
Study author, Dr. Mark Dell’Acqua, a professor at the University of Colorado School of Medicine, told Medical News Today that, “[w]hile this is an early-stage discovery in a model system, it does give us a new lead to pursue in development of therapeutics to prevent neuronal synaptic dysfunction associated with Alzheimer’s disease.”
“In particular, our findings…
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