Disturbances in sensory neurons may turn transient pain into chronic pain (Possible fixes)

Medical Xpress / University Medical Center Utrecht / Cell Reports Medicine ^ | Nov. 8, 2023 | Hanneke Willemen et al

[ConservativeMind]

Researchers have identified that a transient inflammatory pain causes mitochondrial and redox changes in sensory neurons that persist beyond pain resolution. These changes appear to predispose to a failure in resolving pain caused by subsequent inflammation. Additionally, targeting the cellular redox balance prevents and treats chronic inflammatory pain in rodents.

Pain often persists in patients with an inflammatory disease, even after the inflammation has subsided. For some time, there have been clues that mitochondrial dysfunction may be involved. In a clinical study, approximately 70% of patients with heritable mitochondrial diseases develop chronic pain.

To unravel the role of mitochondria in pain resolution, Hanneke Willemen Ph.D. used a model of hyperalgesic priming.

Hanneke and co-workers identified that hyperalgesic priming in mice causes mitochondrial and metabolic disturbances in sensory neurons. The investigators associate these disturbances with an increase in the expression of a mitochondrial protein (ATPSc-KMT) which in a previous study has been linked to chronic pain in patients.

By using genetic and pharmacological approaches they showed that inhibit mitochondrial respiration, ATPSCKMT expression and supplementation of one of the affected metabolites restores resolution of inflammatory pain and prevents chronic pain development.

"Thus, metabolic changes in sensory neurons result in failure of endogenous pain resolution pathways and drive the transition to chronic pain. Importantly, targeting mitochondrial respiration, scavenging reactive oxygen species, or supplementation with nicotinamide riboside (vitamin B3) both represent potential therapeutic strategies to restore failing pain resolution pathways, thereby treating chronic inflammatory pain."

Chronic pain is a leading cause of impaired quality of life. The current dogma is that pain resolution is the consequence of the dissipation of the drivers that induced the pain.

However, in 12–30% of rheumatic arthritis patients pain persists while they have minimal joint inflammation or even are in remission.

[ConservativeMind]

From the writeup:

“Importantly, targeting mitochondrial respiration, scavenging reactive oxygen species, or supplementation with nicotinamide riboside (vitamin B3) both represent potential therapeutic strategies to restore failing pain resolution pathways, thereby treating chronic inflammatory pain."

Nicotinamide riboside is available as a supplement. Nutritents that can help mitochondria include CoQ10, Omega-3s, magnesium, and various other vitamins and minerals. Also, a supplement called Urolithin A can cause mitophagy, which helps cells get rid of dysfunctional mitochondria, replacing them with young, healthy mitochondria.

These may be worth considering, if in chronic pain, as described in the article, above.

[ConservativeMind]

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[Larry Lucido]

Damn mitochondria. Has a better memory than the rest of me does.

[metmom]

Apparently, because of neuroplasticity, the retraining of the brain can actually help with that.

[metmom]

Nerves can become hypersensitized to pain when they experience a lot of it, making the pain actually feel worse than it actually is.

[Bigg Red]

MarQ

[Faith65]

Thanks.
bkmk