Age-related degeneration is caused - at least in part - by accumulated cellular damage, including DNA damage, but how these types of damage drive aging remains unclear.
Dr. Paul Robbins and colleagues at the University of Pittsburgh sought to address this question using a mouse model of DNA repair deficiency. They found that DNA damage drives aging, in part, by activating NF-κB, a transcription factor that responds to cellular damage and stress. In a groundbreaking study, they report that inhibition of NF-κB reduces oxidative stress, oxidative DNA damage, oxidative protein damage, and cellular senescence induced by oxidative damage.
One of the methods used to inhibit the transcription factor involved removing a gene responsible for encoding a subunit of NF-κB. A compound known as NBD was also used. Together, these "delayed the age-related symptoms and pathologies of progeroid mice," and "reduced oxidative DNA damage and stress and delayed cellular senescence."
Their data suggest that NF-κB inhibitors could eventually be used in humans as a way of reducing age-related damage. The full report is published this week in the Journal of Clinical Investigation.