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The amyloid hypothesis is the theory that the accumulation of beta-amyloids in the brain leads to Alzheimer's Disease. These amyloids are "sticky" protein fragments, and the idea is that something in the body that normally regulates them fails and they accumulate in the brain. The idea was proposed in the early 1990s when it was observed that many Alzheimer's patients exhibited larger than normal amounts of amyloid plaques. This hypothesis has driven a very active area of research for drugs and treatments that address beta-amyloids.
In what some see as a fundamental blow to the hypothesis itself, it was recently announced that one of the leading drugs, solanezumab from Eli Lilly, has failed in a large trial of people with mild dementia. The clinical trial involved more than 2,100 people diagnosed with mild dementia due to Alzheimer’s disease, but the results showed only a small benefit of the drug. Eli Lilly has also been conducting prevention trials where the drug is given to people known genetically to be high-risk for the disease, and they said they will discuss with their clinical trial partners whether they will continue those studies.
Lilly’s result may say more about the characteristics of solanezumab than the accuracy of the underlying amyloid hypothesis, says Christian Haass, head of the Munich branch of the German Centre for Neurodegenerative Diseases. The antibody targets soluble forms of amyloid, he points out, so it “could be trapped in the blood without ever reaching the actual target in the brain in sufficient quantities”.
The appeal of the amyloid hypothesis is that it is a simple one. However, in the 25 years since it was proposed, it has led to essentially no progress in preventing or curing the disease. Criticism of the theory has grown with each failed result.
“We’re flogging a dead horse,” adds Peter Davies, an Alzheimer’s researcher at the Feinstein Institute for Medical Research in Manhasset, New York. “There’s no sign of anybody getting better, even for a short period, and that suggests to me that you have the wrong mechanism.”
(Score: 2, Interesting) by Anonymous Coward on Monday November 28 2016, @05:36AM
If amyloid plaques break connection networks in the brain, just removing the plaques isn't necessarily going to fix the connection networks -- the damage might have already been done. They could also be a symptom rather than the cause. In any case, getting negative results is more information than no information.
(Score: 2) by Fnord666 on Monday November 28 2016, @06:37AM
If amyloid plaques break connection networks in the brain, just removing the plaques isn't necessarily going to fix the connection networks -- the damage might have already been done. They could also be a symptom rather than the cause. In any case, getting negative results is more information than no information.
Several of the other studies are looking at people with a genetic predisposition to the condition. I think the hope was that they would be able to prevent any new plaques from forming.
(Score: 0) by Anonymous Coward on Monday November 28 2016, @07:43AM
The "diabetes type 3" theory seems more promising.
https://soylentnews.org/article.pl?sid=16/10/16/1657238 [soylentnews.org]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3709085/ [nih.gov]
The plaque stuff has never been convincing to me. It was like saying scar tissue is the problem. In some cases maybe but in most cases you should be looking for the real causes for the scar tissue.
(Score: 4, Interesting) by opinionated_science on Monday November 28 2016, @11:34AM
The Amyloid pre-cursor (AB) lives on Chr 21, for which Down's syndrome (21 trisomy) is the only one that lives to adulthood.
All Downs patients, will get Alzhemiers by virtue of the fact they have 3 copies of A-Beta.
There are variants from 36-43 amino acids long. The longer this peptide gets, the easier it aggregates.
If you take the gene from Human and give it to a mouse (which don't get Alz), they get it everytime.
It's definitely the gene. We simply don't know enough about the mechanism leading to the plaque aggregation and the damage that is done in the process (said elsewhere). So fixing this may not help the patient, as the damage is already done.
Source: designed some drugs that worked fine in the computer, less fine in the lab...
(Score: 2) by Hyperturtle on Monday November 28 2016, @03:34PM
Also note that removing a symptom does not mean the person is cured.
I am hoping that the preventative trials, when the medication is given to people that are genetically predisposed to the disease are provided the drug, that it in some way helps prevent or slow down the eventual onset.
In a way it may turn out to be like aspirin.
Aspirin does nothing to clean out cholesterol. But it can help prevent heart attacks by thinning the blood. Giving aspirin after a heart attack can't prevent the years of cholesterol build up, and can't repair damage. It can, however, help improve the odds of survival. It is no cure to lifelong damage that surgery was required to patch up, and it is no replacement for other therapies -- like behavioral changes that can further reduce the odds of another heart attack.
This drug solanezumab may prove to be similar in that an ounce of prevention is worth it because there is no cure. It isn't known if you can proberly exercise dementia away or keep it at bay. Probably, a healthy lifestyle will do you good in this regard as well.
Since this drug treats a symptom, the plaque build-up, it may very well be that by reducing the amount of plaque over many years, it can help prevent damage that occurs as a result of the plaque build-up, and thus result in lessened or more managable symptoms. For all we know, it may turn into a chronic disease to manage as a result of having to need to regularly take solanezumab to prevent issues from getting worse--especially upon the on-set of middle-age.
Like aspirin, better late than never -- but it may result in less spectacular results.
If everything wasn't so profit driven, we may have more drugs that help with prevention... but it costs so much to get modest results, and often failures--at least failures as per the measurements they are taking (modest diminishment of symptoms or delayed onset is a failure compared to a miraculous cure that raises the stock price overnight).
I hope that they put the drug on the market anyway. If people made homeopathy a multi-million dollar industry, then we have here a drug that very likely provides a real benefit -- even if minor. To throw it away... well. If it comes to that, maybe I can raise the funds to buy the rights to manufacture it and dilute it a million times and call it a treatment and recoup my investment?
(Score: 0) by Anonymous Coward on Monday November 28 2016, @04:40PM
all these stupid hacks ever do is try to treat the symptoms and use people as Guinea pigs so they can learn in general. your disease is just a way for them to get to hack on you. the researchers just want to learn. the drug makers and the government want control over mankind. reproduction, intelligence, life span, thoughts, everything. Chattle get sick and die from stupid shit anyways so you might as well experiment on them before they turn into compost.
(Score: 0) by Anonymous Coward on Wednesday November 30 2016, @03:32AM
Chattel + cattle?