A mutation that impairs the function of ubiquitin will help in the discovery of a drug for Alzheimer's

According to their findings, the damaged proteins are inhibited on their way to the proteasome, accumulate and form the 'plaque'. According to Professor Michael Glickman, "the discovery opens a new avenue for the development of a drug for Alzheimer's disease."

A study conducted at the Faculty of Biology at the Technion paves a new avenue for the development of a drug for Alzheimer's disease
The researchers of the Faculty of Biology at the Technion have made a significant contribution to the understanding of the mechanism that creates the protein plaque ('plaque') that causes Alzheimer's disease. This is what the scientific journal Nature Chemical Biology publishes.

"The proteins, which are our building blocks, go through a kind of quality control during our lives," explains Professor Michael Glickman, under whose guidance Dr. Daria Kratouz made the surprising discovery during her doctoral thesis. "The damaged proteins are sent for degradation in the proteasome (a 'biological machine' that removes them by recycling them into new proteins), but a small part of them 'escapes' from this process. Proteins that have escaped degradation in the proteasome accumulate and may be harmful when they reach a critical mass, which usually happens in advanced age."

In their study, the researchers characterized a mutation that was known in Alzheimer's patients. The mutation, UBB+1, damages the ubiquitin protein, which marks other proteins for degradation in the proteasome. For the discovery of the ubiquitin protein, Professors Avraham Hershko and Aharon Chachanover from the Technion won the Nobel Prize in Chemistry (together with Ernie Rose from the USA).

Until now, the accepted explanation in the scientific community was that this mutation damages the function of the proteasome itself. Professor Glickman and his team, led by Noa Reiss and student Daria Kratouz, discovered that this assumption is incorrect. According to their findings, the damaged proteins are inhibited on their way to the proteasome, accumulate and form the 'plaque'. According to Professor Glickman, "the discovery opens a new avenue for the development of a drug for Alzheimer's disease."

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