Diabetes Drug May Restore Memory In Alzheimer's
The researchers write about their work in a paper published online in The Journal of Neuroscience on 28 November.
In a statement released on Tuesday, senior author Jack Jhamandas, a researcher with the Faculty of Medicine & Dentistry at the University of Alberta, says 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."
Estimates suggest in the next 30 years, 1,125,000 Canadians will be diagnosed with Alzheimer's disease.
Cells of people with Alzheimer's contain amyloid protein, which is found in particularly large amounts in cells from the memory and cognition parts of the brain. It is the presence of this protein that is believed to impair memory.
Last year, Jhamandas and his team showed that AC253 could block the toxic effects of amyloid protein that lead to brain-cell death.
For this latest study, they tested memory capacity in cells extracted from brain tissue of mice engineered to develop Alzheimer's disease and compared it to that of brain cells from healthy mice.
There is a way of testing memory capacity of cells in the lab by exposing them to a series of electrical shocks or impulses: the cells "remember" the experience.
First, the team tested the memory capacity of normal brain cells and Alzheimer's brain cells.
Then, after giving the drug AC253 to the Alzheimer's brain cells, they ran the electrical shock tests again and found their memory was restored to levels similar to those of the normal cells.
While these results show promise, the researchers caution there are a number of problems to resolve before a drug based on these findings is ready for testing. For example, AC253 doesn't cross the blood-brain barrier easily, so drug developers would have to design a version that could.
Jhamandas says clinical trials could start within about five years, should such problems be resolved and further tests succeed.
"I think what we discovered may be part of the solution, but I can't say it will be the solution," says Jhamandas, pointing to a long list of drugs that showed early promise against Alzheimer's but in further tests proved not to be viable.
"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," he adds.
In a group of tests that will take at least another year, the team is now trying to discover whether giving the drug before symptoms emerge can "stop the impairment of behaviour and cognition altogether in animals destined to develop Alzheimer's" says Jhamandas.
Funds for the study came from the Canadian Institutes of Health Research.
There is currently no cure for Alzheimer's, but evidence is gradually emerging of drugs that can help slow its progression, like galantamine, which not only appears to reduce mortality rates, but also slows down declines in cognitive impairment.
And recently, scientists from the University of California showed that an active lifestyle may also slow progression of Alzheimer's.
Written by Catharine Paddock PhD
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"Beta Amyloid-Induced Depression of Hippocampal Long-Term Potentiation Is Mediated through the Amylin Receptor"; Ryoichi Kimura, David
MacTavish, Jing Yang, David Westaway, and Jack H. Jhamandas; The Journal of Neuroscience, 28 November 2012, 32(48): 17401-17406; DOI:
10.1523/JNEUROSCI.3028-12.2012; Link to Abstract
Main source: The University of Alberta: News and Events.
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