Background/aim: Calcineurin, an inhibitor of calcium dependent phosphatase is highly presented in a brain of an Alzheimer's disease. Aging brain gets more sensitive to hyperactivation of calcineurin, and this event causes tau neurofibrillary plaque accumulation, which is one of the outcomes of this disease. The regions of hippocampus are much effected from the results of this process. Our hypothesis is that a calcineurin inhibitor, tacrolimus, could prevent the accumulation and the decrease of the neuronal cells. Therefore, this immunosuppressive drug could be a candidate for an early treatment of Alzheimer disease. Materials and methods: Fifteen male Wistar albino rats were divided to three groups; control, Alzheimer, and Alzheimer+Tacrolimus. The Alzheimer group received an injection of streptozotocin intracerebroventricularly for the purpose of modelling the disease via generating free radicals leading a cognitive impairment. Alzheimer+Tacrolimus group first received an oral drug, a calcineurin inhibitor for 10 days afterwards prepared for the model as same as the Alzheimer group received. Finally, all groups performed the Morris water maze test for four days then sacrificed. For the aim of counting neurons in the hippocampus stereological methods, as well as for an evaluation of cellular response to stress in dentate gyrus, a c-Fos immunohistochemistry was performed. Results: According to the probe trial of Morris water maze test, the latency time was dramatically higher at both Alzheimer and Alzheimer+Tacrolimus group (p < 0.01). We confirmed these results with our stereology data. The results from stereology technique indicate that there was a neuronal decrease at the hippocampus regions in Alzheimer and Alzheimer+Tacrolimus group. Our outcomes from immunohistochemical data showed a significant increase in the number of c-Fos-positive cells in Alzheimer group when comparing with Alzheimer+Tacrolimus group (p < 0.001). Conclusion: There was none preventive effect for neuronal loss in the hippocampus under the effect of tacrolimus drug according to stereological results. However, tacrolimus administration may have reduced cellular stress and cell damage.

The purpose of this study was to investigate the effect of dietary sesame oil and ginger oil supplements on the dorsal root ganglia following a sciatic nerve crush model in male Wistar albino rats....

It is widely known that each tissue has unique mechanisms to respond to injury and maintain homeostasis effectively. Although peripheral nerves have limited regeneration capacity, they conduct a complicated regeneration process by orchestrating multiple cell complexes after injury. In addition to drawing attention to anterograde and retrograde transportation, the absence of a cell body in the damaged area also points to the significance of immune and glial cells in the environment. Cellular reorganization following injury in the dorsal root ganglion, which takes place in the cell bodies of sensory peripheral nerve fibers, has attracted much attention. Growing research has been focused on investigating the molecular and cellular interactions occurring in sensory neurons and glial cells within the dorsal root ganglia after injury. It is clearly becoming that the sensory neurons and glial cells in the dorsal root ganglion are derived from the same embryological origins. Therefore, this information attracts attention to the potential of these two cells to differentiate into each other in case of injury. The focus of these studies is to illuminate the genes and pathways responsible for an increase in the plasticity of the neurogenic cell line following nerve injury. This review explores and discusses the underlying mechanisms responsible for maintaining homeostasis in the dorsal root ganglion and regeneration of peripheral nerves and how neuronal plasticity functions in the regeneration of the injury.

Peripheral nerve injuries (PNIs) constitute a significant concern as they predominantly affect young and productive age groups of the population, causing social and economic pressure on patients. PNIs are a global problem that can result in disability because of the disruption of nerve function. PNI leads to a reduction in nerve conduction velocity, which worsens or impairs the mobility of the innervated area. Managing PNI remains a major clinical challenge. Coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant first identified in 1957. It is an important antioxidant necessary for the organs to maintain their normal function and the body’s chemical processes. It scavenges free radicals and reduces oxidative stress. Studies showed that antioxidants such as CoQ10 a potent antioxidant, help the regeneration of PNIs. It has been observed to increase the myelination process in nerve fibres and promote nerve regeneration in rats after injury. Therefore, this review handles the current positive effects of CoQ10 on peripheral nerve regeneration following injury.