In a paper published online in The Journal of Neuroscience, the researchers detailed that they carried out tests on animal brain cells and found restored memory to levels similar to those of normal cells. Should further tests succeed, the team says that trials to improve the wellbeing of human patients could start in five years. According to senior author Jack Jhamandas, a researcher with the Faculty of Medicine & Dentistry at the University of Alberta, their discovery is ‘very important’ because ‘it tells us that drugs like this might be able to restore memory, even after Alzheimer’s disease may have set in.’
It is believed that when you have Alzheimer’s, your memory is impaired because cells in your brain contain amyloid protein, which is found in particularly large amounts in cells from the memory and cognition parts of the brain. Jhamandas and his team have previously showed that AC253 could block the toxic effects of amyloid protein that lead to brain-cell death, and for this study they wanted to see how the memory capacity in cells extracted from brain tissue of healthy mice compared to mice that have been engineered to develop Alzheimer’s disease.
For the study, the team began by testing the memory capacity of normal brain cells and Alzheimer’s brain cells. They then tested the mice again after giving the drug AC253 to the Alzheimer’s brain cells, and found their memory was restored to levels similar to those of the normal cells. However, these promising results should be viewed with caution, as many problems need to be resolved before a drug based on these findings is ready for testing, such as developing a version of AC253 that can cross the blood-brain barrier.
Jhamandas concluded by saying, ‘I think what we discovered may be part of the solution, but I can’t say it will be the solution,’ as a long list of drugs have showed early promise against Alzheimer’s but in further tests proved not to be viable. He added, ‘I don’t think one drug or approach will solve Alzheimer’s disease because it’s a complicated disease, but I am cautiously optimistic about our discovery and its implications.’