Alzheimer's disease is the most important type of dementia, which is characterized by memory loss, impaired words, confusion of thinking, decreased judgment and other brain function abnormalities and changes of personality and behavior.

Two years ago, Jack Jhamandas, a well-known professor and neuroscientist at the University of Alberta, discovered a way to neutralize an abnormal protein associated with Alzheimer's disease. Now, he has discovered something new about the mystery of Alzheimer's disease, which has brought him one step closer to the treatment of Alzheimer's disease.

Jhamandas and his team found two short-chain amino acids. When injected these two amino acids once a day for 5 weeks into mice with Alzheimer's disease, the researchers found that the mice's memory was significantly improved. Treatment also reduces some of the harmful physiological changes in the brain associated with the disease.

As explained by Prof. Jhamandas, in mice that received these drugs, scientists found that amyloid plaque buildup was reduced and brain inflammation was reduced. This was very exciting because it not only improved the memory of the mice but also greatly improved the brain pathology of Alzheimer's disease. In fact, such a discovery is a bit unexpected for the research circle.

New discovery

Previous studies have shown that a compound called AC253 has a function of blocking the toxic effects of β-amyloid. β-amyloid is often abundantly present in the brains of patients with Alzheimer's disease and is therefore considered to be one of the leading causes of this disease. AC253 prevents beta-amyloid from binding to specific receptors in brain cells and Prof. Jhamandas likens this process to plugging keyholes.

However, although AC253 has been shown to prevent beta-amyloid deposition, there is no way to make it a drug because it is quickly metabolized in the blood and can't reach the brain effectively. Therefore, the theoretical use of AC253 requires very large doses - which is impractical, and high doses of compounds also increase the body's chance of developing an immune response to treatment. If AC253 can be converted from injection to an oral tablet, it is hopeful to solve the metabolic problem and improve the efficacy, but AC253 is too complicated to be made into an effective oral drug.

Prof. Jhamandas' solution is to cut AC253 into pieces to see if it can produce small molecule short peptides that block the accumulation of beta-amyloid like AC253. Through a series of experiments, the Jhamandas team discovered two AC253 short-chain amino acids that met the requirements.

New drug development

With the identification of short peptides, Prof. Jhamandas and his team, including the famous virologists Lorne Tyrell and Michael Houghton, are currently using computer modeling and artificial intelligence to develop a small molecule drug - similar to drugs that control high blood pressure or cholesterol.

The Jhamanda team is focused on creating an optimized oral small molecule drug that will allow human clinical trials to begin. For patients, small molecule drugs are more convenient, because they can not only be taken orally but are also easier to reach the brain through the blood. For pharmaceutical companies, small molecule drugs are cheaper. Prof. Jhamandas believes that this new drug has the potential to alter the treatment of Alzheimer's disease.

At the same time, however, this is still a tough job as the whole process may take 15 or 20 years, just like building a house, first we need to put down a brick, then lay another brick, and slowly lay the foundation to rebuild the house. But it is still exciting because this may fundamentally change the status quo of Alzheimer's treatment.

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Author's Bio: 

Creative Peptides is specialized in the process development and the manufacturing of bioactive peptides.