Blocking key enzyme could reverse Alzheimer’s disease, study finds

New York’s Staten Island. Alzheimer’s dementia is a global health issue with poorly known causes, and a new study in mice may help us better understand its triggers.

A study of mice found a particular enzyme that might be responsible for the buildup of a dangerous protein called tau, one of the disease’s main characteristics, according to a research in Nature Neuroscience.

Tau stabilizes and supports brain cells in a healthy brain, helping to move important chemicals across the cell to support appropriate function.

However, according to the National Institute on Aging, tau seems to act inappropriately in the brain of people with Alzheimer’s disease by accumulating inside and producing twisted clumps called neurofibrillary tangles that interfere with brain cell-to-cell communication. Thinking, action, and memory all depend on this communication.

A group of researchers from the United States utilized mice that had been genetically modified to have an excess of tau in their brains to simulate Alzheimer’s disease. They then discovered a particular enzyme that might be in charge of producing the harmful amount of tau.

Tyrosine kinase 2 (TYK2), an enzyme essential to the immune system, seems to hinder the brain’s ability to eliminate excess tau, leading to its accumulation.

The researchers then used genetic techniques to block TYK2 in the Alzheimer’s-affected animals, which reduced the total amount of tau in the brain, including the amount of disease-causing, toxic tau.

The researchers noted in Nature Neuroscience that the neurons, or brain cells, also displayed indications of healing. According to this finding, TYK2 blocking may be a means of lessening the accumulation of toxic tau and the harm it causes in conditions like Alzheimer’s.

Additionally, it might pave the way for novel medication development strategies to counteract toxic tau.

TYK2 inhibitor medications are already on the market and have been used to treat a variety of illnesses in people, such as inflammatory bowel disease and autoimmune disease.

Research is still required to determine whether the enzyme can readily enter the brain, change its levels there, and lessen Alzheimer’s disease symptoms.

According to reports, the study is pre-clinical and more is required because mouse results frequently do not translate to human outcomes.

Note: Every piece of content is rigorously reviewed by our team of experienced writers and editors to ensure its accuracy. Our writers use credible sources and adhere to strict fact-checking protocols to verify all claims and data before publication. If an error is identified, we promptly correct it and strive for transparency in all updates, feel free to reach out to us via email. We appreciate your trust and support!