New antibody therapy of Alzheimer’s disease may come true someday

In study on degenerative nervous disease shows that an antibody therapy can reduce the light β- amyloid plaques in the brain of Alzheimer's patients. The study has been published in the British journal Nature this week. The study provides preclinical data and preliminary results of clinical trials in stageⅠ. Through research of recombinant proteins like recombinant dog proteins, it is found that both of them support to further develop the antibody for the treatment of Alzheimer's disease.

The gradual accumulation of β- amyloid proteins in the brain is a sign of of Alzheimer's disease. It is generally considered that β- amyloid-related toxicity triggers synaptic dysfunction and neurodegeneration, both of which can lead to Alzheimer's disease. However, clinical therapy targeted to β- amyloid proteins has always been unsuccessful currently.

This time, researcher Alfred Sang Duoke and colleagues from the famous American biotech company Biogen reported the development condition of human monoclonal antibody Aducanumab. The drug was developed by Biogen for treatment of Alzheimer's disease. It can be selectively directed to fight against β- amyloid proteins and is known as the "new hope to overcome Alzheimer's disease". Now, researchers say that in the genetically-modified mouse model, Aducanumab can enter the brain and dose dependently reduces soluble and insoluble β- amyloid proteins.

The authors also conducted a double-blind and randomized, placebo-controlled Phase Ⅰ clinical trial to evaluate the safety and tolerability showed by Alzheimer's patients after monthly injecting Aducanumab to patients with mild cognitive impairment or mild dementia and brain exist β- amyloid deposits. In one-year period, 165 patients were monthly injected placebo or Aducanumab. After 54 weeks of treatment, β- amyloid proteins in the brain of patients injected with Aducanumab significantly reduced. The higher the dose, the greater the decrease amplitude of plaque; while the brain of patients inhected with placebo showed no significant changes. During the research, 40 patients discontinued treatment, because 20 of them showed adverse reactions, including dose-dependent amyloid-related imaging abnormalities.

The authors conculded that demonstration that anti-β- amyloid therapy can delay cognitive decline will completely change the way of understanding, treatment and prevention of Alzheimer's disease. Flarebio provides you with high-quality recombinant proteins such as recombinant CDH12 at good prices.