Spinal cord injury (SCI) leads to loss of motor and sensory function below the injury level
and imposes a considerable burden on patients, families, and society. Repair of the injured …

Spinal cord injury (SCI) induces a pronounced neuroinflammation driven by activation and
proliferation of resident microglia as well as infiltrating peripheral monocyte-derived …

Traumatic spinal cord injury (SCI) induces irreversible autonomic and sensory‐motor
impairments. A large number of patients exhibit chronic SCI and no curative treatment is …

Extensive oligodendrocyte death after acute traumatic spinal cord injuries (TSCI) leads to
axon demyelination and subsequently may leave axons vulnerable to degeneration. Despite …

The inflammatory host tissue response, characterized by gliosis and neuronal death at the
neural interface, limits signal transmission and longevity of the neural probe. Substance P …

Compression injuries of the murine spinal cord are valuable animal models for the study of
spinal cord injury (SCI) and spinal regenerative therapy. The calibrated forceps model of …

Endogenous neural stem cells (NSCs) are the most promising sources for replacing cells
lost after spinal cord injury (SCI). We have previously shown that substance P (SP), a …

Following spinal cord injury (SCI), microglia gradually migrate to the edge of the lesion,
interweaving around the border of the lesion to form the microglial scar, which performs …

Two waves of oligodendrogenesis in the ventricular zone of the spinal cord (SC‐VZ) during
rat development, which take place between embryonic days 14 and 18 (E14–E18) and E20 …

Following incomplete spinal cord injuries, neonatal mammals display a remarkable degree
of behavioral recovery. Previously, we have demonstrated in neonatal mice a wholesale re …