Neuroplasticity Research

KEY FINDING: Chronic SCI results in expansion and rostral displacement of trunk motor representations in the cortex, with the greatest significant increase observed for rostral (to injury) trunk.

KEY FINDING: Increased use of a limb, facilitated by CI therapy, leads to an expansion of the cortical representation zone of that body part.

KEY FINDING: Baseline BDNF levels in participants were lower than those reported in previous research on individuals with SCI and healthy adults.

KEY FINDING: Viral-mediated Rac1 knockdown in motor neurons after SCI significantly restored rate-dependent depression (RDD) of the H-reflex, indicating reduced hyperreflexia.

KEY FINDING: Most SCI research focuses on corticospinal, rubrospinal, and raphespinal pathways, neglecting many other important supraspinal populations.

KEY FINDING: Genetic deletion of RhoA and RhoC suppresses axon retraction or dieback after spinal cord injury.

KEY FINDING: Identified druggable targets to intervene with secondary brain injuries like ischemia, hemorrhage, and mitochondrial dysfunction after TBI.

KEY FINDING: EA significantly reduced Modified Neurological Severity Scores (mNSS), cerebral infarct volume, and apoptosis of neuronal cells in rats with permanent middle cerebral artery occlusion (p-MCAO).

KEY FINDING: Active regeneration of nerve gaps through the conduit was confirmed from 10 days onwards, with varied GAP-43 expression throughout the regeneration tissue.

KEY FINDING: dPSNs in animals without injury had dendrites mainly distributed in a top-bottom direction. Injury caused the dendrites to retract in this direction and extend sideways.