As amyloid beta peptides bind to prion proteins, a cascade of events, which include the accumulation of plaques, abnormal immune responses and damage to synapses, is triggered, eventually leading to the development of Alzheimer’s disease.
Fortunately, researchers have been working hard on a variety of treatment avenues. In one of the most recent attempts, detailed in a paper which came out in the journal Cell Reports on 2 January 2019, a group of researchers from Yale University have devised a new promising compound.
“We wanted to find molecules that might have therapeutic effect on this network,” said senior author Stephen Strittmatter, the Vincent Coates Professor of Neurology, professor of neuroscience, and director of the Yale Alzheimer Disease Research Centre.
After screening tens of thousands of different compounds, Strittmatter and research scientist Erik Gunther had discovered that an old antibiotic (Ceftazidime) showed promise in throwing a wrench into the process which leads to interactions between prion proteins and amyloid beta.
Once the compound was optimised and decomposed to form a polymer – the only way to make it active in a desirable manner – it was finally given to mice engineered to have a condition that mimics Alzheimer’s.
The drinkable cocktail of designer molecules was shown to have retained its beneficial effects and managed to cross the blood-brain barrier without problem. Most consequentially, the compound was found to effect synaptic repair in the brains of the lab mice, allowing them to recover lost memories.
Furthermore, a collaborating team at Dartmouth University also found the compound to have a positive impact on cells engineered to have Creutzfeldt-Jakob Disease, thereby providing additional support for its effectiveness.
Now, the research team plans to conduct further experiments to ensure the compound’s suitability for humans before moving to clinical trials.
Sources: study abstract, news.yale.edu.