Research: Nerve regeneration is more in MS than after brain trauma

EpubSchirmer et al. Neuroaxonal regeneration is more pronounced in early multiple sclerosis than in traumatic brain injury lesions. Brain Pathol. 2012 May 21. 

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.

We have talked about neuro plasticity, by which damaged nerves form new connections to overcome the damage. The authors looked for SMI-32 expression, This is reacts with a nonphosphorylated (no phosphorous) epitope in neurofilament heavy chain a nerve protein of most mammalian species. This is often expressed by nerves in distress. Amyloid precursor protein (APP) is shuttled down the nerve and whenthe nerve is cut a stump forms and the APP being transported down the nerve accumulates in the stump and forms a bulb called a spheroid (round like a sphere). GAP43 a nerve growth protein found in the tips of growing nerve processes and synaptophysin another protein found around synapses of nerves. More of this was found in the MS lesions compared to the brain injury suggesting that they have a greater capacity to make new nerve connections in MS. This was associated with inflammation, namely macrophages that may be clearing damaged nerves and myelin. This suggests that the MS brain is plastic, and capable of recovery, as we have previously reported:

Multiple Sclerosis Research: Research: Brain Plasticity16 Feb 2012

Multiple Sclerosis Research: Education: Targeting Progressive MS …09 Sep 2011

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  • Finally good news. I think with the advent of neuroprotective agents both natural and laboratory – based, along with more powerful immune-modifying drugs, physical therapy, and functional training, MS may soon be able to be halted. Remyelination/MSC's will also overlap these. Things are looking good as long as we can speed up these trials.

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