Scientists have advanced new ground in longevity research after formally proving the role of intracellular stress in mammalian aging.
Our cells are like small molecular factories, working to carry out all the processes our bodies need to survive. But like factories, the machinery within our cells wears out over time, causing them to become obsolete.
To build all these cellular gears and building blocks, our cells rely on molecular machines called ribosomes. Ribosomes translate the information in DNA into biological building blocks, proteins.
Ribosomes themselves are assembled into structures called nucleoli, which are located within the cell’s nucleus. It is this stress in the nucleolus that is thought to greatly contribute to cell aging.
In a new study published in the journal molecular cellResearchers at Spain’s National Cancer Research Center (CNIO) are now investigating how this nucleolar stress affects the rest of the cell, particularly in relation to the neurodegenerative disease amyotrophic lateral sclerosis. I investigated whether it would be given.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that occurs when neurons responsible for body movement, called motor neurons, begin to die. The exact cause of ALS has long eluded scientists, but this latest research may finally shed light on a solution: abnormalities in non-functional “junk proteins” in affected motor neurons. This is a great accumulation. Specifically, it is a ribosomal “junk” protein that is produced when something goes wrong inside the nucleolus.
”[Nucleolar stress causes cells to] The ability to produce new proteins is reduced,” said lead researcher Oscar Fernández Capetillo. newsweek. “In addition, our study shows that orphan R protein accumulation is also responsible for the toxicity experienced by cells during aging.
“These particular peptides have been specifically observed in certain ALS patients. However, the problem these toxins cause, the accumulation of orphan and dysfunctional ribosomal proteins, may be associated with nucleolar stress. It appears to be a common property of cells in other neurodegenerative diseases and initial evidence that [it is also observed] during normal aging. ”
CNIO
It is too early to know exactly how this age-related stress will affect humans. However, Professor Fernández-Cappetillo said studies in mice showed that nucleolar stress can accelerate aging in most of the organs tested.
More research is needed to truly understand the relationship between cell degeneration and longevity, but Professor Fernández-Cappetillo hopes their findings will pave the way for future anti-aging treatments.
”[Anti-aging] This is an area that we are very interested in and part of our research is that strategies to help reduce the accumulation of orphan R proteins could be used to treat neurodegenerative diseases such as ALS and aging in general. The purpose is to investigate whether it is effective or not. ” He said.
Fernández-Cappetillo added: “Our study opens a new door, a new angle, for explaining what the molecular origins of conditions such as ALS, and perhaps aging as a whole, are. But it is important to make clear that we are not.” Much work still needs to be done to suggest specific treatments, and we hope that others will also take inspiration from our ideas and help us address the therapeutic implications of our discoveries. I just hope so. ”
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