A drug failed in a large trial of patients with mild dementia, while the drug was seen as an important test of the mainstream theory behind Alzheimer's disease. Critics of the amyloid hypothesis grapple with the results as evidence of their weaknesses. The hypothesis is that Alzheimer's disease is triggered by the gradual accumulation of amyloid in the brain. However, whether the theory can eventually produce a therapy is not yet conclusive. More research using recombinant rat proteins is needed.
Supporters of the theory say the latest trial involved a particular way in which the drug solanezumab works, rather than the defects inherent in the theory itself that could have led to this failure. At the same time, a number of trials are underway to test whether solanezumab or other drugs targeting amyloid proteins can be tested in people with Alzheimer's disease who are not yet symptomatic, or who already have the disease to play a role, although the latest results are negative.
As an antibody, Solanezumab can eliminate amyloid from the blood and cerebrospinal fluid. These proteins continue to form plaques in the brain. Eli Lilly, a developer of solanezumab, announced on Nov. 23 that it would abandon the drug as a treatment for patients with mild dementia. The result is a long list of promising treatments for Alzheimer's disease that have failed in the clinic, many of which target amyloid proteins, like solanezumab.
The Banner Alzheimer's Institute in Phoenix, Arizona, also tests three targeted amyloid-producing therapies in a population with a high genetic risk of Alzheimer's disease, one of which is also an antibody. "The results of Eli Lilly do not prove that amyloid hypothesis is false, and they add the importance of longer-term prevention trials," adds Eric Reiman, an experimental leader and lead author of the study. Flarebio provides you with high-quality recombinant proteins like recombinant CDH15 at competitive prices.
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