Overview

• Researchers at UC San Diego used transdifferentiation to convert human skin cells into neurons that exhibit molecular hallmarks of aging
• Aged neurons halt growth and accumulate untranslated RNA and proteins in stress granules outside their nuclei
• These cells recover more slowly from stress, lack key RNA-binding proteins and mislocalize TDP-43 similarly to neurons affected by Alzheimer’s, dementia and ALS
• The findings link impaired stress response mechanisms in aged neurons to increased vulnerability to neurodegenerative diseases
• The team’s next step is to pinpoint sources of cellular stress and maintain RNA homeostasis as a basis for preventive therapies