Targeting aging cells could slow intervertebral disk degeneration
Neck and low back pain affect millions worldwide and are a leading cause of disability. Degeneration of the disks that cushion the spine is a leading cause. Current treatments can relieve symptoms but do little to slow the underlying disease. Now, researchers from Thomas Jefferson University have shown that targeting harmful, aging cells early may preserve disk health and delay degeneration.
Intervertebral disk degeneration affects millions and leads to significant disability. Current treatments only alleviate symptoms, not stopping the disease's progression. Researchers from Thomas Jefferson University discovered that early intervention with aging cells may preserve disk health and slow degeneration.
The study, published in Bone Research, examined cellular senescence - a process where cells become dormant but still release inflammatory molecules that harm surrounding tissue. The team found that spinal disks of young mice with early-onset degeneration exhibited senescent cell characteristics similar to those in older mice. This suggests there may be a window to intervene before the disease worsens.
The researchers treated mice with a combination of drugs dasatinib and quercetin (DQ), targeting senescent cells. Mice treated with DQ had healthier disks, reduced inflammation, less tissue scarring, and more of the cells needed to maintain healthy spinal disks. Further analysis revealed DQ decreased activity in genes linked to inflammation, cell death, and aging.
Blocking JUN signaling, a key pathway identified, reproduced many protective effects seen with DQ treatment in human disk cells. Together, these findings suggest that removing senescent cells early could slow disk degeneration before irreversible damage occurs. Moreover, since dasatinib and quercetin have already been studied in people for other age-related conditions, this treatment approach could eventually be explored for disk-related low back pain.
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