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Functional recovery following spinal cord injury will require the regeneration and repair of damaged neuronal pathways. It is well known that the tissue response to injury involves inflammation and the formation of a glial scar at the lesion site, which significantly impairs the capacity for neuronal regeneration and functional recovery. There are initial attempts by both supraspinal and intraspinal neurons to regenerate damaged axons, often influenced by the neighboring tissue pathology.

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The purpose of this study was to investigate the effects of weight- and non-weight-bearing exercises on the Basso-Beattie-Bresnahan (BBB) locomotor rating scale, corticospinal axon regrowth and regeneration-related proteins following spinal cord injury (SCI). Twenty-four male Sprague-Dawley rats were randomly divided into four groups: control group (n=6), SCI+sedentary group (SED, n=6), SCI+treadmill exercise group (TREAD, n=6), and SCI+swimming exercise group (SWIM, n=6). All rats in the SCI group were given the rest for 2 weeks after SCI, and then they were allowed to engage in low-intensity exercise for 6 weeks on treadmill device.

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Neurons in the CNS lose regenerative potential with maturity, leading to minimal corticospinal tract (CST) axon regrowth after spinal cord injury (SCI). In young rodents, knockdown of PTEN, which antagonizes PI3K signaling by hydrolyzing PIP3, promotes axon regeneration following SCI. However, this effect diminishes in adults, potentially due to lower PI3K activation leading to reduced PIP3.

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The ability of neurons to sense and respond to damage is crucial for maintaining homeostasis and facilitating nervous system repair. For some cell types, notably dorsal root ganglia (DRG) and retinal ganglion cells (RGCs), extensive profiling has uncovered a significant transcriptional response to axon injury, which influences survival and regenerative outcomes. In contrast, the injury responses of most supraspinal cell types, which display limited regeneration after spinal damage, remain mostly unknown.

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