Scientists have advanced a new frontier in longevity research after formally proving the role of subcellular stress in mammalian aging.
Our cells are like tiny molecular factories, working to carry out all of the essential processes our bodies need to survive. However, like factories, the machinery in our cells gets worn out over time, which is what causes them to age.
In order to build all of these cellular cogs and components, our cells rely on molecular machines called ribosomes, which translate the information in our DNA into biological building blocks: proteins.
Ribosomes themselves are assembled in a structure called the nucleolus, which is located inside the nucleus of the cell. And it is stress in this nucleolus that appears to significantly contribute to cellular aging.
In a new study published in the journal Molecular Cell, researchers from the Spanish National Cancer Research Center (CNIO) investigated how this nucleolar stress can affect the rest of the cell, specifically in the context of the neurodegenerative disease Amyotrophic lateral sclerosis.
Amyotrophic lateral sclerosis, or ALS, is a neurodegenerative condition which occurs when the neurons that are responsible for our body’s movement—called motor neurons—begin to die. The exact cause of ALS has long evaded scientists, but the findings of this latest study may finally shed some light on a solution: the abnormal build-up of non-functional “junk proteins” in affected motor neurons. Specifically, ribosomal “junk” proteins, produced when things go wrong inside the nucleolus.
“[Nucleolar stress causes cells to] reduce their capacity to produce new proteins,” lead researcher Óscar Fernández-Capetillo, told Newsweek. “On top of that, our study indicates that the accumulation of orphan r-proteins is also a cause for the toxicity that cells experience during aging.
“These particular peptides have been observed specifically in certain ALS-patients. However, the problem that these toxins cause—namely, the accumulation of orphan and dysfunctional ribosomal proteins—seems to be a general property of cells experiencing nucleolar stress, which is observed in other neurodegenerative diseases and initial evidence indicate that [it is also observed] during normal aging.”
CNIO
It is too early to know exactly how humans are affected by this age-related stress. But Fernández-Capetillo said that studies in mice have shown that nucleolar stress can accelerate aging in the vast majority of tested organs.
More work needs to be done to truly understand the links between cellular degeneration and longevity, but Fernández-Capetillo hopes that their findings will pave the way for future anti-aging therapies in the future.
“[Anti-aging] is an area where we are very interested, and part of our studies are directed to investigate if strategies that can help to reduce the accumulation of orphan r-proteins, are efficacious for the treatment of neurodegenerative conditions such as ALS, or aging in general,” he said.
Fernández-Capetillo continued: “Our work opens a new door, a new angle, to explain what can be the molecular origin of pathologies such as ALS, and perhaps also of aging as a whole. However, it important to clarify that we are not proposing a specific therapy yet. Lots of work need to be done, and we can only hope that others also find inspiration in our ideas and help us address the therapeutic implications of our discoveries.”
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Uncommon Knowledge
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Newsweek is committed to challenging conventional wisdom and finding connections in the search for common ground.