Spinal cord regeneration / iron chelators

2005-12-22 11:02:17 PM
1: Eur J Neurosci. 2005 Dec;22(12):3047-58. Related Articles, Links
Suppression of fibrous scarring in spinal cord injury of rat promotes
long-distance regeneration of corticospinal tract axons, rescue of
primary motoneurons in somatosensory cortex and significant functional
recovery.
Klapka N, Hermanns S, Straten G, Masanneck C, Duis S, Hamers FP, Muller
D, Zuschratter W, Muller HW.
Molecular Neurobiology Laboratory, Department of Neurology,
Heinrich-Heine-University, Moorenstrasse 5, D-40225 Dusseldorf,
Germany.
Abstract Traumatic injury of the central nervous system results in
formation of a collagenous basement membrane-rich fibrous scar in the
lesion centre. Due to accumulation of numerous axon-growth inhibitory
molecules the lesion scar is considered a major impediment for axon
regeneration. Following transection of the dorsal corticospinal tract
(CST) at thoracic level 8 in adult rats, transient suppression of
collagenous scarring in the lesion zone by local application of a
potent iron chelator and cyclic adenosine monophosphate resulted in the
delay of fibrous scarring. Treated animals displayed long-distance
growth of CST axons through the lesion area extending for up to 1.5-2
cm into the distal cord. In addition, the treatment showed a strong
neuroprotective effect, rescuing cortical motoneurons projecting into
the CST that normally die (30%) after thoracic axotomy. Further,
anterogradely traced CST axons regenerated through both grey and white
matter and developed terminal arborizations in grey matter regions. In
contrast to controls, injured animals receiving treatment showed
significant functional recovery in the open field, in the horizontal
ladder and in CatWalk locomotor tasks. We conclude that the fibrous
lesion scar plays a pivotal role as a growth barrier for regenerating
axons in adult spinal cord and that a delay in fibrotic scarring by
local inhibition of collagen biosynthesis and basement membrane
deposition is a promising and unique therapeutic strategy for treating
human spinal trauma.
PMID: 16367771 [PubMed - in process]
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