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Progress and Setbacks in the Study of CNS Axonal Plasticity and Regeneration
Author(s) -
Tuszynski Mark H,
Kadoya Ken,
Lu Paul,
Blesch Armin,
Rosenzweig Ephron,
Brock John,
Loew Karin
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.60.2
Subject(s) - remyelination , neuroscience , regeneration (biology) , biology , lesion , central nervous system , myelin , medicine , microbiology and biotechnology , pathology
Understanding of basic mechanisms underlying the refractory state of axonal regeneration in the CNS has advanced remarkably in the last 50 years. Mechanisms that underlie the failure of central regeneration include: 1) an absence of permissive extracellular matrices in lesion sites, 2) insufficient secretion of trophic molecules, 3) the presence of growth‐inhibitory molecules in the CNS, and 4) an intrinsic failure of adult CNS neurons to upregulate extensive sets of growth‐related genes. Addressing several of these mechanisms simultaneously, it is possible to elicit growth of select spinal cord axonal populations into and beyond lesion sites, and to reinnervate normal targets. However, several critical challenges remain in SCI research, including: 1) elicitation of regeneration or corticospinal axonal systems; 2) remyelination of regenerating axons; 3) elicitation of substantial growth at chronic stages after SCI, and 4) translation of these findings to primate systems, given fundamental differences in axonal organization and function between rodent and primate models. This talk will summarize these topics and highlight future directions of research.