Damaged ELLPs may let in DNA-damaging toxins that trigger gene-expression changes.

Damage to extremely long-lived proteins (ELLPs) that form transport channels into the nuclei of neurons could represent a key factor in the progression of aging and potentially age-related neurodegenerative disorders such as Alzheimer disease and Parkinson disease, researchers claim. A team at the Salk Institute has found that while nearly all proteins in the human proteome are recycled every few days to prevent functional deterioration and the accumulation of damage, ELLPs are not regularly turned over, and the nuclear pore complex ELLPs identified by the Salk researchers actually appear to last an entire lifetime.

The phenomenon means that as these ELLPs become damaged or deteriorate over time, the channels they form may become compromised, and start letting in DNA-damaging toxins that effect changes in DNA expression associated with age-related disorders.

“The fundamental defining feature of aging is an overall decline in the functional capacity of various organs such as the heart and the brain,” comments Martin Hetzer, Ph.D., lead investigator at the Salk’s molecular and cell biology laboratory. “Our results suggest that nuclear pore deterioration might be a general aging mechanism leading to age-related defects in nuclear function, such as the loss of youthful gene expression programs.”

Dr. Hetzer’s team says it is the only research group in the world looking specifically at the role of nuclear pore complex proteins in the aging process. The latest work is published in Science, in a paper titled “Extremely Long-Lived Nuclear Pore Proteins in the Rat Brain.”

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