The Role of Neurotropic B Vitamins in Nerve Regeneration

Abstract

Damage and regeneration naturally occur in the peripheral nervous system. The neurotropic B vitamins thiamine (B1), pyridoxine (B6), and cobalamin (B12) are key players, which maintain the neuronal viability in different ways. Firstly, they constantly protect nerves against damaging environmental influences. While vitamin B1 acts as a site-directed antioxidant, vitamin B6 balances nerve metabolism, and vitamin B12 maintains myelin sheaths. However, nerve injury occurs at times, because of an imbalance between protective factors and accumulating stress and noxae. This will result in the so-called Wallerian degeneration process. The presence of vitamins B1, B6, and B12 paves the way out to the following important regeneration by supporting the development of new cell structures. Furthermore, vitamin B1 facilitates the usage of carbohydrates for energy production, whereas vitamin B12 promotes nerve cell survival and remyelination. Absence of these vitamins will favor permanent nerve degeneration and pain, eventually leading to peripheral neuropathy.

Vitamin B Complex and Experimental Autoimmune Encephalomyelitis –Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis

“…Thus, co-transplantation of both cell types has been proposed as a potential therapy for axonal regeneration of the injured nervous system, including CNS and peripheral nervous system (PNS) [ 38 ]. The literature data described that VBC, as additional therapy, improved nerve regeneration, by promoting an increase in the number of Schwann cells, which represent one of the most important glial cells of the PNS required for myelin formation and axonal recovery [ 23 , 39 ]. In the present study, the possible explanation for the rise in nuclear density in the affected femoral nerve after EAE induction could be in line with the infiltration process mediated by macrophages of different polarization which facilitate nerve regeneration, by clearing myelin debris and promoting the cell proliferation and migration [ 40 ].…”

“…Vitamins of the B group are water-soluble vitamins with many beneficial effects on the nervous system, which deficiency has been linked to different neurodegenerative diseases [ 20 ]. As demyelination and axonal deterioration are common for both vitamin B deficiency and many neurological diseases, including MS, it is believed that vitamin B treatment could aid in axonal recovery and improvement of neuronal function [ 21 , 22 , 23 , 24 ]. In our previously published paper [ 25 ], we have shown that VBC (a complex of vitamins B1, B2, B3, B5, B6, and B12) treatment enhanced the motor nerve regeneration and the recovery of muscle function in a rat model of peripheral nerve injury.…”

Engineering Proprioceptive Implants via Surgical and Regenerative Approaches: Preliminary Interpretations

“…55 Additionally, it has been previously reported by us that the titanium implants coated with PCL/gelatine nanofibrous scaffold, supports DPSCs, their proliferation and subsequent neural differentiation. 42 To ensure that the exogenous stem cells precisely participate in the terminal nerve repair at the interface we have systemically administered Neurobion Forte, as a peripheral nerve recovery agent 56,57 in the rabbit study model with test implant. However, additional specific interventional measures such as the inclusion of growth factors in relation to peripheral nerve regeneration, such as Neurotrophin-3, Neurotrophin-4, Recombinant human beta-NGF, and Fibroblast growth factors (FGF) protein 58 in the components of nanofibrous coating, could have certainly resulted in further improvement in the overall objectives of the trial.…”

“…55 Additionally, it has been previously reported by us that the titanium implants coated with PCL/gelatine nanofibrous scaffold, supports DPSCs, their proliferation and subsequent neural differentiation. 42 To ensure that the exogenous stem cells precisely participate in the terminal nerve repair at the interface we have systemically administered Neurobion Forte , as a peripheral nerve recovery agent 56,57 in the rabbit study model with test implant.…”

Vitamin B12 Reduces TDP-43 Toxicity by Alleviating Oxidative Stress and Mitochondrial Dysfunction

“…Vitamin B12 deficiency leads to demyelination and reduced neurotrophic activity, and it causes multiple sclerosis [ 27 ]. Many studies have shown that vitamin B12 accelerates nerve innervation and recovery in individuals with multiple sclerosis (MS) [ 28 , 29 ]. Vitamin B12 is known as a redox-active cofactor and it functions as an ROS scavenger [ 30 ].…”