Back and neck pain affect millions of people, and damaged spinal discs are a major reason why.
New research suggests that changes in gene activity may help drive this damage by causing tissues in the spine to become unusually hard and filled with minerals.
Spinal discs sit between the bones of the spine and act like soft cushions. They help absorb pressure when people walk, bend, lift or twist, but these discs can gradually wear down with age or disease.
This process is called intervertebral disc degeneration.
It can contribute to pain, stiffness and reduced movement, yet doctors currently have no medicine that can stop or reverse the underlying damage.
Scientists from the Universities of Edinburgh and Bristol studied the problem using zebrafish. Although zebrafish look very different from humans, their biology shares many important features with ours, making them useful for studying genes and diseases.
The researchers focused on a gene connected to collagen IX, a protein that helps support the structure of spinal discs. Variations involving this protein have previously been linked to disc problems that appear earlier in life.
The team bred zebrafish without a working copy of the gene and followed what happened as the animals grew older. Their spines gradually developed changes that looked surprisingly similar to features seen in human disc disease.
The tissue between the fish’s spinal bones began to harden as minerals collected where they should not normally build up. Eventually, neighboring bones of the spine fused together.
Importantly, the researchers saw an earlier warning sign before this mineral buildup appeared. A supportive scaffold in the developing spine started to break down, suggesting that structural damage may begin well before the later hardening becomes obvious.
The scientists then examined which genes became more or less active. They found changes in several biological systems, including the way cells handle fats, phosphate and vitamin A, as well as a growth-control system known as mTOR.
These findings gave the researchers clues about why the spine was becoming mineralized. They also suggested several possible ways to interfere with the process before severe damage develops.
In one experiment, the team used a type of medicine called a bisphosphonate. These medicines are already used in people with osteoporosis because they affect the way bone is broken down and rebuilt.
The treatment blocked the unwanted mineral buildup in the zebrafish. The researchers also found that restricting food intake or using drugs that reduced fat metabolism lowered the amount of spinal fusion.
These results raise the possibility that future treatments could target phosphate handling or fat metabolism. They also suggest that medicines already used for other bone conditions might provide useful starting points for research into spinal disc disease.
However, the results should not be interpreted as evidence that people with back pain should take osteoporosis medicines or change their food intake. The experiments were carried out in zebrafish, and treatments that work in fish may not have the same benefits or safety in humans.
The study was published in 2026 in the peer-reviewed journal Communications Biology. The research was led by Dr. Erika Kague from the University of Edinburgh’s Institute of Genetics and Cancer, with researchers from Edinburgh and Bristol.
The study is valuable because it connects a known genetic risk with specific biological changes that occur as spinal damage develops. It also goes beyond describing the disease by showing that some of those changes can be reduced experimentally.
At the same time, the study has important limits. Zebrafish are useful disease models, but the human spine carries different loads and has more complex discs, so clinical studies will be needed before researchers know whether these findings can lead to treatments for patients.
Overall, the research provides promising new directions rather than an immediate cure. Its strongest contribution may be identifying biological processes that scientists can now investigate as possible drug targets for a condition that currently has few ways to address the underlying damage.
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