The Sunday Times (London): It took my savings and 14 years — but I’m about to cure arthritis, 2024, Glen Keogh

sounds intriguing.... do we have a link to the phase II trial?
Is it's mechanism plausible @Jonathan Edwards ?

 

Interesting

Would love to know more about the possible mechanisms. And if this might work for chronic pain like Fibromyalgia as well as the osteo pain.

 

It’s a new treatment approach, not yet fully tested. But of course it would be wonderful if it did work. OA is very common and painful.


It doesn’t sound like a cure though does it?

 

Perhaps not cure, however, if it gets people moving more, doing things they want/need to do, it might be good enough for plenty people

 

For sure.

 

I recall an article about how damage to spinal discs causes nerves to grow into the cartilage, resulting in pain, so maybe that's the mechanism he's talking about.

 

It might be this paper.

Soluble low affinity nerve growth factor receptor sLNGFR may regulate pain in knee osteoarthritis
A. Altaie, T.M. Campbell, H. Owston, E. Jones, R. Doyle, R.J. Feibel, H. Pandit, S. Westbrook, D. Mcgonagle

OBJECTIVES
Nerve growth factor β (β-NGF) is a protein which is important to the development of neurons particularly those involved in the transmission of pain and is central to the experience of pain in osteoarthritis (OA). Direct NGF antagonism has been shown to reduce OA pain but is associated with rapidly progressive OA. The aim of the study is to investigate the ability of soluble neurotrophin receptors in the NGF pathway to modulate pain in OA.

METHODS
Synovial fluid (SF) was obtained from the knee joints of 43 subjects who underwent total knee arthroplasty. Visual analogue scale (VAS) pain scores were obtained prior to surgery. Customised-automated-ELISAs and commercial-ELISAs and LEGENDplex™ were used to measure soluble low-affinity nerve growth factor (LNGFR), soluble tropomyosin receptor kinase (TrkA), proNGF, β-NGF, other neurotrophins (NT) and cytokines including inflammatory marker TNF-α.

RESULTS
The VAS score positively correlated with β-NGF (r=0.34) and there was positive association trend with neurotrophin-3 (NT-3), BDNF and negative association trend with ProNGF. sLNGFR positively correlated with VAS (r=0.33). The β-NGF/soluble TrkA ratio showed a strong positive correlation with VAS (r=0.80). In contrast, there was no correlation between pain and the β-NGF/sLNGFR ratio (r=-0.08). TNF-α positively correlated with β-NGF (r=0.83), NT-3 (r=0.66), and brain-derived neurotrophic factor (BDNF) (r=0.50) and negatively with ProNGF (r= -0.74) and positively correlated with both soluble TrkA (r=0.62), sLNGFR (r=0.26).

CONCLUSIONS
This study suggests that endogenous or cleaved sLNGFR, but not soluble TrkA may participate in OA pain modulation thus supporting further research into soluble LNGFR as a therapeutic target in OA.

Link (Clin Exp Rheumatol)