Both the ApoE genotype and the sex of the mouse impacted the manner in which the animals with spinal cord injury responded to hypoxia treatment. Females with the ApoE e4 gene had a negative response to intermittent hypoxia.
People with spinal cord injuries have the same brain activity during processing speed tasks as healthy older adults. The findings suggest the theory of accelerated cognitive aging following SCI is correct.
Research shows it is possible to stimulate stem cells in the spinal cord to produce large amounts of new oligodendrocytes.
Axon regeneration and dramatic improvements in functional recovery occurred when lactate was applied to damaged neural tissue. Treatment with lactate also significantly improved locomotion and restored some walking capability in mouse models of SCI.
A newly designed synthetic compound could act as a prototype for a novel class of drugs to treat neurological damage.
The application of synchronized transcranial magnetic stimulation (TMS) and peripheral nerve stimulation (PNS) restored the ability to walk in a patient with spinal cord injury.
Researchers implanted specialized neural stem cell grafts directly into mice with spinal cord injuries. As the grafts grew, they integrated with and mimicked the animal's existing neural network.
Spinal cord injuries cause stem cells in the bone marrow to rapidly divide. Following the cell division, the stem cells become trapped in the bone marrow.
LIN28, a molecule that regulates cell growth could help in the treatment of spinal cord injury and optic nerve damage. When expressed above normal levels, the molecule fuels axon growth in mice with injury, enabling the body to repair damaged nerves.
Researchers were able to restore the sense of touch to a 28-year-old who suffered a spinal cord injury with the help of new brain-computer interface technology.