Duke University Study Describes a Breakthrough in Our Understanding of the Bioenergetics of Peripheral Sensory Nerves

Volume 9 | Issue 3

Dr. Richard Mann, DABPS, Ret., Chief Scientific Officer and Founder, Realm Labs®, sole US distributor of the NeuRemedy® line of benfotiamine products for the healthy function of the nerves in the feet and legs.*

A Duke University research group published a study in Nature describing a previously unrecognized way in which peripheral sensory neurons receive metabolic support. Satellite glial cells surrounding sensory neurons in the dorsal root ganglion transfer healthy mitochondria directly into the neurons, primarily through tunneling nanotube-like structures. This provides additional mitochondrial capacity to help meet the substantial energy requirements of normal nerve function.

Primary sensory neurons have exceptional energy requirements. A single dorsal root ganglion neuron may extend an axon from the spine to the foot or toes, requiring continuous energy over a remarkably long distance.

When investigators disrupted mitochondrial transfer in experimental models, nerve degeneration and neuropathic pain developed. Transfer was also impaired in association with diabetes and paclitaxel chemotherapy, both of which are associated with peripheral neuropathy. Conversely, healthy satellite glial cells or mitochondria delivered to the dorsal root ganglion reduced neuropathic pain. In diabetic mice, mitochondria from non-diabetic human satellite glial cells reduced mechanical hypersensitivity and increased intraepidermal nerve fiber density.

These findings may help explain the importance of energy availability in length-dependent peripheral neuropathy. Distal portions of long sensory neurons may be especially vulnerable when mitochondrial availability or ATP-generating capacity becomes inadequate. The study supports the concept that bioenergetic failure can contribute to nerve degeneration and neuropathic pain.

One fundamental requirement for mitochondrial energy production is adequate vitamin B1 (thiamine). Its active form, thiamine pyrophosphate (TPP), is an essential cofactor for enzymes required for efficient Krebs cycle activity and ATP production. Thiamine deficiency can therefore impair cellular energy metabolism. Thiamine deficiency and altered thiamine metabolism have been reported in individuals with diabetes and alcohol use disorder, as well as in older adults and in association with other clinical conditions and medications, including chronic use of loop diuretics.

Approaches used or studied with the intent of supporting neuronal bioenergetics include thiamine supplementation, particularly benfotiamine, a highly bioavailable derivative of thiamine that has been well studied and has a strong safety profile, as well as photobiomodulation and exercise. These were not investigated in the Duke study, and their effects on energy availability within human sensory neurons remain to be established. Nevertheless, the findings strengthen the concept that adequate energy availability is important to sensory nerve function and provide a rationale for clinicians to consider therapeutic approaches intended to support neuronal bioenergetics in patients with peripheral neuropathy.

Read the Duke University study in Nature

Reference

Xu J, Li Y, Novak C, et al. Mitochondrial transfer from glia to neurons protects against peripheral neuropathy. Nature. 2026;650:951–960. doi:10.1038/s41586-025-09896-x.