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Health

IU1 Boosts Protein Clearance, Offering Potential Breakthrough in Parkinson’s Treatment

A compound known as IU1 may help improve the body’s ability to maintain healthy proteins by enhancing two key processes involved in clearing damaged proteins from cells, according to a recent study. These findings hold potential for treating age-related diseases like Parkinson’s.

The study, titled “Pharmacological inhibition of USP14 delays proteostasis-associated aging in a proteasome-dependent but foxo-independent manner,” was published in Autophagy.

As we age, our body’s ability to regulate protein quality, also known as protein homeostasis, declines. This can lead to the buildup of harmful proteins, which damage cells and contribute to conditions like Alzheimer’s and Parkinson’s disease. In Parkinson’s, aging accelerates nerve cell degeneration, leading to the accumulation of protein clumps, impaired mitochondrial function, and heightened inflammation. Mitochondrial dysfunction is closely linked to Parkinson’s development and progression.

Boosting Protein Homeostasis

In this study, researchers from Korea aimed to explore how two systems responsible for protein quality control—proteasomes and autophagy—could be activated together to slow this decline in protein homeostasis.

Proteasomes are complexes within cells that function like molecular trash compactors, breaking down damaged or unnecessary proteins. Autophagy, on the other hand, is a recycling process in which cells degrade and repurpose damaged or surplus components, including protein aggregates.

“I learned about IU1 at a conference and discovered that it enhances proteasomal activity, which prompted us to explore its anti-aging effects,” said Seogang Hyun, lead author of the study and professor at Chung-Ang University, in a press release.

The researchers tested IU1’s effects using fruit flies, which experience age-related muscle deterioration similar to humans. They found that IU1 treatment significantly boosted proteasome activity, promoting the breakdown of faulty proteins and reducing their aggregation. The compound also stimulated autophagy.

IU1 works by inhibiting an enzyme called ubiquitin-specific peptidase 14 (USP14). This enzyme removes a molecular tag known as ubiquitin, which cells use to mark proteins for degradation. By preventing USP14 from removing the ubiquitin tag, IU1 allows proteasomes to better identify and degrade faulty proteins.

“Inhibiting USP14 with IU1 not only enhanced proteasome activity but also activated autophagy simultaneously,” Hyun explained. “We demonstrated that this combined mechanism improved age-related muscle weakness in fruit flies and extended their lifespan.”

The study found similar results in human cells, suggesting that IU1 may offer potential therapeutic benefits for people as well.

“Reduced protein homeostasis is a hallmark of degenerative diseases like Alzheimer’s and Parkinson’s,” Hyun added. “Our findings could pave the way for developing treatments for various age-related diseases.”

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