The extent of irreversible neuroaxonal (nerve cells and their processes) damage is the key determinant of permanent disability in traumatic and inflammatory conditions of the central nervous system (CNS). Structural damage is nevertheless in part compensated by neuroplastic events. However, it is unknown whether the same kinetics and mechanisms of neuroaxonal de- and regeneration take place in inflammatory and traumatic conditions. These investigators analysed neuroaxonal degeneration and plasticity in early MS lesions and traumatic brain injury (TBI). Neuroaxonal degeneration identified by the presence of SMI31+ neurons and SMI32+ axonal profiles were characteristic features of leukocortical TBI lesions (SMI is a staining technique to pick up damage axons). Axonal transport disturbances as determined by APP+ spheroids were present in both TBI and MS lesions to a similar degree. APP refers to amyloid precursor protein, which accumulates in bulbs and indicates that axons have been transected. Neurons expressing GAP43 and synaptophysin (Syn) were found under both pathological conditions. GAP43 and
synaptophysin are proteins that are produced at the synapse and are indicative of synaptic recovery. However, axonal swellings immunopositive for GAP43 and Syn clearly prevailed in subcortical MS lesions suggesting a higher regenerative potential in MS. In this context, GAP43+/APP+ axonal spheroid ratios correlated with macrophage infiltration in TBI and MS lesions supporting the idea that phagocyte activation might promote neuroplastic events. Furthermore, axonal GAP43+ and Syn+ swellings correlated with prolonged survival after TBI indicating a sustained regenerative response.
Multiple Sclerosis Research: Research: Brain Plasticity16 Feb 2012