Linked Life Data

20103844

Source:http://linkedlifedata.com/resource/pubmed/id/20103844

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-1-27
pubmed:abstractText
Injuries to the adult central nervous system (CNS), such as spinal cord injury and brain contusion, can cause permanent functional deficits if axonal connections are broken. Spontaneous functional recovery rarely occurs. It has been widely accepted that the extracellular environment of the CNS inhibits neuronal regeneration. However, it should be noted that another reason for injured neurons failing to regenerate is their weak intrinsic ability to do so. The regeneration of injured neurons is a process involving many intracellular phenomena, including cytoskeletal changes, gene and protein expression, and changes in the responsiveness to extracellular cues. The capacity of injured neurons to regenerate is modulated to some extent by changes in the expression of intracellular signaling molecules such as glycogen synthase kinase-3beta and cyclic adenosine 3',5'-monophosphate. Knowledge of these effects has guided the development of animal models for regenerative therapies of CNS injury. Enhancing the intrinsic regenerative machinery of injured axons in the adult CNS is a potentially powerful strategy for treating patients with a CNS injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1881-7823
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
179-83
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Intrinsic regenerative mechanisms of central nervous system neurons.
pubmed:affiliation
Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan. muramatsu@molneu.med.osaka-u.ac.jp
pubmed:publicationType
Journal Article, Review