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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) 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...