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The hope of a cure for Alzheimer's disease has been raised after scientists have discovered why decades of studies have failed to come up with a solution.
Attempts to stop the memory theft disorder in his tracks have targeted the toxic accumulation of beta-amyloid in the brains of patients.
This accumulation in the brain gradually destroys neurons and causes memory loss and confusion.
However, researchers at King's College London now claim that once these clusters are formed, it is "too late for the drugs to work".
Instead, they found that targeting a little-known protein that causes cluster development dramatically improves the signs of Alzheimer's disease in mice.
Drug treatments that block this protein are already available in China and Japan for stroke.
Scientists have sparked the hope of a cure for Alzheimer's disease after discovering why decades of studies have failed to find a solution. They claim that failed drugs often target protein clumps in the brain when it is "too late" to stop the disease (stock)
Alzheimer's disease – the most common form of dementia – affects about 5.5 million people in the United States and 500,000 in the UK, according to the figures.
The researchers, led by Dr. Christina Elliott, discovered that the progression of the disease works like a circuit.
When the beta-amyloid protein begins to agglomerate in a patient's brain, it begins to degrade nerve cells.
This causes these cells to produce more beta-amyloid, causing their own destruction.
Lead author, Dr. Richard Killick, said, "We show that there is a positive and vicious feedback loop in which beta-amyloid leads to its own production.
"We think that once this feedback loop has gone out of control, it's too late for the beta-amyloid targeting drugs to be effective."
He added: "This could explain why so many drug trials for Alzheimer's have failed."
Rather than focusing on beta amyloid itself, researchers believe that drug developers should target the protein Dkk1, which stimulates beta-amyloid production.
Scientists have studied mice with large amounts of beta-amyloid in their brains to test their theory.
When rodents were treated with fasudil, a blocking drug for Dkk1, for two weeks, their beta-amyloid levels dropped significantly.
The results were published in the journal Translational Psychiatry.
Dr. Killick said, "We have convincingly demonstrated that fasudil can protect synapses and memory in animal models of Alzheimer's, while reducing the amount of beta-amyloid in the brain.
Scientists plan to study whether fasudil could boost brain health and prevent cognitive decline in people with early-stage Alzheimer's.
The co-author of the study, Professor Dag Aarsland, added, "In addition to being a safe drug, fasudil appears to enter the brain in sufficient quantities to potentially be an effective treatment against beta -amyloid.
"We must now move forward in a clinical trial in people with early-stage Alzheimer's disease as soon as possible."
Although experts agree that the results of the study are promising, some are wondering how blocking Dkk1 could alleviate the symptoms of Alzheimer's disease.
Professor Tara Spiers-Jones, from the University of Edinburgh, welcomed the findings. She said, "This article is scientifically interesting.
"But there is a long way to go to find out if these results will lead to therapies that will help people with dementia."
In addition, the effects of fasudil were tested only in the laboratory and in the mouse. It is therefore difficult to know if the drug will benefit patients with Alzheimer's disease.
Dr. Carol Routledge, of Alzheimer's Research UK, said: "Fasudil is an approved drug for other health problems.
& # 39; But [it] is currently used in a critical care setting and is expected to undergo rigorous safety testing in trials of people with Alzheimer's disease.
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