(Technology) New Research Discovers the Deep Pathogenic Mechanism of Sporadic Alzheimer's Disease

Jerusalem, October 5th (Xinhua) - The Israeli Institute of Technology recently released a statement stating that an international team led by its researchers has found that the accumulation of toxic proteins in the brain of sporadic Alzheimer's disease patients is related to the failure of protein clearance mechanisms, and targeting specific proteins may alleviate the disease. The relevant paper was published in the UK journal Nature Communications

Jerusalem, October 5th (Xinhua) - The Israeli Institute of Technology recently released a statement stating that an international team led by its researchers has found that the accumulation of toxic proteins in the brain of sporadic Alzheimer's disease patients is related to the failure of protein clearance mechanisms, and targeting specific proteins may alleviate the disease. The relevant paper was published in the UK journal Nature Communications.

The communique states that Alzheimer's disease is highly prevalent in people over the age of 65, characterized by a gradual decline in cognitive ability as brain nerve cells degenerate and die. This disease is divided into familial and sporadic, characterized by the accumulation of toxic proteins in the brain. The former is related to the accumulation of related proteins caused by gene mutations, while the triggering mechanism of toxic protein accumulation in more common sporadic Alzheimer's disease is still unclear.

Researchers have proposed a hypothesis that the accumulation of toxic proteins in the brain is caused by the failure of the protein clearance mechanism (also known as the ubiquitin proteasome system). Ubiquitin is a small protein present in all eukaryotes, and its main function is to label the proteins that need to be broken down, causing them to be degraded by proteasomes. The ubiquitin proteasome system is the main pathway for intracellular protein degradation, participating in the degradation of the vast majority of intracellular proteins.

Next, the researchers designed a specific ribonucleic acid (RNA) molecule that can inhibit the expression of UBB+1. Researchers have found that inhibiting UBB+1 expression can prevent the emergence of the two pathological markers of Alzheimer's disease mentioned above.

Researchers say the research findings highlight the importance of the ubiquitin proteasome system in clearing "defective" proteins and maintaining cell health, which can help develop drugs for the treatment and prevention of sporadic Alzheimer's disease. Meanwhile, relevant RNA molecules may provide insights for the treatment of Alzheimer's disease. (End)

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