Alfredhouse personal home care explores about Dementia care services and investigates about Alzheimer’s. Find out more in the article below.
For nearly half a century now, researchers and pharmaceutical companies have been engaged in what seems like a losing battle: the search for a cure—or at the very least an effective treatment—for Alzheimer’s. Efforts across the globe have been disappointing. In January of this year, an article published in The New England Journal of Medicine reported on the failure of the latest drug trial of an anti-amyloid drug named Solanezumab. At about the same time, another pharmaceutical giant, Pfizer, announced that it was ending its involvement in Alzheimer’s. In May, another pharmaceutical giant, Janssen, announced that it was ending clinical trials of one of its star drugs, the BACE inhibitor Atabecestat, after indications emerged that it is toxic to the liver. Such discouraging stories in the news raise the inevitable question: Will a cure for Alzheimer’s ever be found? The answer is somewhat complicated and runs along two main tracks.
One group of researchers maintains that we have been looking in the wrong place, and we need to start looking elsewhere. Until now, the leading theory of the cause of Alzheimer’s has been that the beta-amyloid plaques that build up around neurons in the brain as humans age (discussed in several previous newsletters) are responsible for the set of symptoms that have come to be known as Alzheimer’s Disease. This theory has led researchers to focus their attention on getting rid of the amyloid plaques, and perhaps even preventing their development. Scientists are now questioning the amyloid theory, and one scientist in particular, Dr. Paul Murphy of the University of Kentucky, in an editorial in the January 25, 2018 edition of The New England Journal of Medicine, went so far as to argue that it might well be time to let go of the amyloid theory and start looking elsewhere. Some researchers are turning their attention to the tau tangles that develop inside the neurons in the brain which are also associated with Alzheimer’s symptoms. Still others have begun looking at free radicals, inflammation in the brain, mitochondrial malfunction, and other possibilities.
The second approach to failures of the drug trials is to stick with the amyloid theory, but to increase the dosage of the drugs being tested and to start earlier in the process of amyloid plaque accumulation. So far, the experimental drugs have been tested only on those who have already developed Alzheimer’s and are thus in the advanced stages of plaque buildup. Dr. Reisa Sperling of the Brigham and Women’s Hospital, is currently engaged in a series of studies that will test Solanezumab on subjects aged 65 to 80 whose brain scans show amyloid buildup but who have not yet developed Alzheimer’s symptoms. In a future study, she will use subjects in their 50s who have a genetic predisposition to developing Alzheimer’s but show no signs of plaque buildup. The approach in this case is prevention, rather than cure.
Dr. Sperling is optimistic that a cure will be found and suggests that the answer may lie in combination therapies, that is, therapies that combine various theoretical approaches and target several possible causes at the same time, such as the amyloid plaques and the tau tangles. She suggests that the epic failures in the drug trials may be the result of the excessively narrow focus on a single cause, namely, the amyloid plaques. At the Krembil Research Institute in Toronto, Canada, Dr. Donald Weaver is engaged in a search for compounds that interact with both the amyloid plaques and the tau tangles. He has found several promising candidates and is working with a French pharmaceutical company to bring the best of them to clinical trial.
Will we find a cure? It is still too early to say, but there is sufficient reason to think that we are not chasing rainbows.
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