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Home› Azerbaijan› Israeli researchers identify potential new target for neurodegenerative disease treatments

Israeli researchers identify potential new target for neurodegenerative disease treatments

AzerbaijanNov 3, 2026, 2:43 PM
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PUBLISHEDNov 3, 2026, 2:43 PM
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Baku, November 3, AZERTAC Israeli researchers have identified a cellular process that influences how cells protect themselves against damaged proteins, uncovering a potential new avenue for studying neurodegenerative diseases such as Alzheimer’s and Huntington’s, according to TPS-IL. The findings could point to a different approach to combating these diseases: rather than targeting harmful proteins directly, researchers may eventually be able to strengthen the cell’s natural defenses against protein buildup. The discovery could also help explain why these defenses weaken with age, making the brain more vulnerable to neurodegenerative diseases. Alzheimer’s disease is a progressive brain disorder and the most common cause of dementia, impairing memory, thinking and everyday functioning.

Huntington’s disease is an inherited neurological disorder that causes the progressive breakdown of nerve cells, leading to involuntary movements, cognitive decline and psychiatric symptoms. Both are associated with abnormal protein accumulation in the brain. In experiments involving microscopic worms, researchers found that reducing the activity of a process called UFMylation strengthened several natural defenses against damaged and misfolded proteins, helping the animals withstand harmful proteins associated with both diseases. UFMylation is a process in which cells attach a small protein called UFM1 to other proteins, changing how they function. Although it plays an important role in normal cell activity, its broader effects on aging and protein quality control have remained unclear. The intervention reduced paralysis in an Alzheimer’s disease model, improved movement in a Huntington’s disease model and extended the worms’ lifespans by approximately 13 percent. The findings, published in the…

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Main source: AZERTAC

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