Scientists have uncovered a nucleolar complex that plays a pivotal role in maintaining cellular health through protein homeostasis (proteostasis), which could be help in the fight against neurodegenerative diseases such as Alzheimer’s.
Proteostasis is a process by which cells maintain the balance and proper functioning of their proteins.
Researchers have now found that by suppressing this complex, the toxic effects of Alzheimer’s-causing proteins can be reduced and the cell’s natural defences are improved through enhanced degradation of hazardous proteins.
According to the researchers, this mechanism regulates proteostasis across tissues by modulating TGF-β signalling, a pathway involved in cell growth, differentiation, and tissue homeostasis.
“Our findings go beyond the lab bench,” said Hebrew University researcher, Professor Ehud Cohen.
“Neurodegenerative diseases affect millions of people worldwide, impacting families and caregivers. By uncovering how cells communicate to maintain protein integrity, we’re opening the door to the development of preventive therapeutic approaches that could delay disease onset and significantly improve quality of life of the elderly.”
This is because proteostasis begins to decline as we age, leading to the accumulation of toxic protein aggregates.
According to the team, a nucleolar complex, FIB-1-NOL-56, is a central player in the regulation of proteostasis at the cellular and organismal levels.
They found that when they supressed the activity of this complex, the toxic effects the Aβ peptide and another disease-causing protein were reduced, which the team say offers hope for future treatments that could delay or prevent a number neurodegenerative diseases.
