A new study found that two drugs already on the market may be effective in slowing down the progression of neurodegeneration.
The study was conducted on mice and used medication that targeted an enzyme in the brain that researchers believe may turn off new protein production, disabling the brain to make the repairs needed to fight disease. Learn more about the study and its next steps.
In a new study presented at the Alzheimer’s Society annual research conference in Manchester, researchers said that two already licensed drugs have been effective in slowing the progression of Alzheimer’s in mice. Researchers call the results of the study “hugely promising” because the medications are already licensed, meaning they will be able to reach the public faster because they are already known to be safe.
Researcher and professor of clinical neuroscience at the University of Cambridge Giovanna Mallucci said, “It’s really exciting. They’re licensed drugs. This means you’d do a straightforward basic clinical trial on a small group of patients because these are not new compounds, they’re known drugs.”
Research manager from the Alzheimer’s Society, Clare Walton, also stressed the importance of the drugs being licensed saying, “The new results are hugely promising because the drugs are already given to people and we know they’re safe.”
Scientists are not revealing the names of the medication to avoid people using the drugs before a clinical trial can take place confirming its role in slowing brain degeneration. Before a trial occurs, researchers will need to conduct a brain imaging study to confirm that the drugs can help humans the way it helps mice. Professor Mallucci said of the need for brain scans:
“We need to do special scanning to show that what’s happening to the mice is happening to humans. The big, burning question is what is the relevance for human disease.”
The two drugs work to slow neurodegeneration by targeting an enzyme called Perk. That enzyme, if not inhibited, activates a defense mechanism which responds to the buildup of beta-amyloid plaque and turns off the production of all new proteins, disabling the brain’s ability to make repairs. This also suggests that beta amyloid proteins, commonly thought to be a root cause of Alzheimer’s, are actually a symptom of brain degeneration, but not the cause.
Carol Colton, professor of neurology at Duke University acknowledges the exciting results of the study but also cautions that so much is still unknown about the side effects of switching off a natural defense mechanism. She went on to say, “Time will tell. It would be a great thing if possible and new drugs are badly needed. Kudos to the authors and the Alzheimer’s Society for moving this concept along.”
Professor Mallucci remains hopeful, saying:
“Even delaying progress of Alzheimer’s by 10 years would have a massive effect. You have to re-adjust and understand that slowing Alzheimer’s would change the disease into something completely different and infinitely more acceptable to society.”
What do you think about using existing medication to slow Alzheimer’s? Is it a viable treatment method? Share your thoughts with us on the study in the comments below.
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