Study identifies existing drug which could protect against Alzheimer's memory-loss.
M2 EQUITYBITES-September 20, 2018-Study identifies existing drug which could protect against Alzheimer's memory-loss
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UK scientists have discovered a possible reason why many drug trials for Alzheimer's disease have failed.
The study, published in Translational Psychiatry, also identifies an existing drug which may halt the progress of the disease.
Alzheimer's disease is the most common cause of dementia, with minor memory problems usually showing as the first symptom.
As the condition develops, memory problems become more severe and additional symptoms can develop, such as: confusion, disorientation and getting lost in familiar places; difficulty planning or making decisions; and problems with speech and language.
Overproduction of the protein beta-amyloid is strongly linked to development of Alzheimer's disease but many drugs targeting beta-amyloid have failed in clinical trials, King's College London (KCL) reports. Beta-amyloid attacks and destroys synapses -- the connections between nerve cells in the brain -- and this results in memory problems, dementia and ultimately death.
In the new study, researchers at KCL found that when beta-amyloid destroys a synapse, the nerve cells make more beta-amyloid -- driving yet more synapses to be destroyed.
"We show that a vicious positive feedback loop exists in which beta-amyloid drives its own production," said senior author Dr Richard Killick from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at KCL. "We think that once this feedback loop gets out of control it is too late for drugs which target beta-amyloid to be effective, and this could explain why so many Alzheimer's drug trials have failed."
However, the study also identified a clinically approved drug which breaks the vicious cycle and protects against memory-loss in animal models of Alzheimer's.
Instead of targeting beta-amyloid itself, the researchers believe that targeting a protein called Dkk1 -- which stimulates production of beta-amyloid -- could be a better way to halt the progress of Alzheimer's disease by disrupting the vicious cycle of beta-amyloid production and synapse loss.
"Importantly, our work has shown that we may already be in a position to block the feedback loop with a drug called fasudil which is already used in Japan and China for stroke," Dr Killick said. "We have convincingly shown that fasudil can protect synapses and memory in animal models of Alzheimer's, and at the same time reduces the amount of beta-amyloid in the brain."
Welcoming the findings, Dr James Pickett, head of research at the Alzheimer's Society, said: "There haven't been any new drugs last 15 years, so it's very promising to have uncovered a reason why some of that research may have failed and a potential solution, which builds on our own previous research into this area."
Now, the researchers are seeking funding to run a trial in early-stage Alzheimer's patients to determine if fasudil improves brain health and prevents cognitive decline.
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|Publication:||M2 EquityBites (EQB)|
|Date:||Sep 20, 2018|
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