Whether the treatment of amyloid protein hypothesis loses the scientific basis?

Eli Lilly and Company recently announced the results of its Phase 3 clinical trial of Alzheimer's disease (AD) drug candidate, solanezumab. Although the results using recombinant mouse proteins are not satisfactory, this doesn't mean that the treatment of amyloid protein hypothesis lost the scientific basis.

Amyloid hypothesis began in the 1980s and is an important theory which has the most research evidence to support the interpretation of AD causes. AD is the most important form of Alzheimer's disease. The deposition of amyloid protein (β-Amyloid, Aβ) is one of the important markers of AD. Amyloid Hypothesis think that Aβ levels in AD patients are abnormally elevated due to imbalance between production and degradation, leading to the deposition of Aβ in the brain and leading to neuronal damage and death in the brain. It is the root cause of memory and cognitive decline.

Based on this theory, different therapies targeting Aβ have been developed. Some of them attempt to target Aβ-producing proteases to prevent Aβ production, while others hope to bind free Aβ monomers in the blood, preventing them from entering the brain to produce deposits. The current trial results show that these therapies are not yet effective in preventing cognitive decline.

"This may be related to the characteristics of some of the therapies," says Christian Haass, MD, head of the Munich-based Neurodegenerative Disease Research." For example, some drugs can only bind to Aβ monomers, but not to deposited Aβ fibers; In addition, drugs injected into the patient's body may bind to Aβ monomers in the bloodstream, resulting in insufficient drug to enter brain, reducing Aβ monomer in the brain."

Other drugs with different mechanisms are expected to bring about a turn for the better. Aducanumab, which can target Aβ deposition in the brain, is one of them. In early clinical trials, this antibody can eliminate Aβ deposition in the brain and reduce memory loss. Its Phase 3 clinical trial is expected to end in 2020. The researchers believe that the different modes of action of Aβ may be the key to alleviating symptoms.

In summary, the current clinical trials in the setbacks encountered in progress, but it does not necessarily explain the amyloid hypothesis is wrong. New drug development is a long and thorny road. We hope that the new drug development of AD can find the direction of progress and ultimately bring new treatment for patients. Flarebio provides good-quality recombinant proteins such as recombinant Itgb2 for your research.