Abstract:
:Niemann-Pick C (NPC) disease is an autosomal recessive lipidosis characterized by lysosomal accumulations of unesterified cholesterol. Cultured NPC cells exhibit a defect in the intracellular trafficking of LDL-derived cholesterol that leads to lysosomal accumulations of unesterified cholesterol. We found in a preliminary study that the myelination of regenerating axons was retarded in the NPC mouse following sciatic nerve crush. Because lipoprotein-mediated cholesterol transport is involved in myelination during nerve regeneration, we investigated whether this cholesterol reutilization pathway was perturbed in the NPC mouse. Mice received intraneural injections of [3H]acetate to label myelin cholesterol, and 2 weeks later the injected nerves were crushed above the injection site. Four weeks after crush, the nerves were examined by electron microscopic autoradiography. In normal mice, regeneration was well advanced, with thick myelin sheaths surrounding the regenerated axons and very little myelin debris remaining. The new myelin sheaths were well labeled, indicative of efficient cholesterol reutilization. In NPC mice, the new myelin sheaths were thinner and contained little label, indicative of retarded regeneration and little or no cholesterol reutilization. These data suggest the possibility of a causal link between compromised cholesterol reutilization and delayed or slowed regeneration of myelin sheaths.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Goodrum JF,Pentchev PGdoi
10.1002/(sici)1097-4547(19970801)49:3<389::aid-jnrsubject
Has Abstractpub_date
1997-08-01 00:00:00pages
389-92issue
3eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19970801)49:3<389::AID-JNRjournal_volume
49pub_type
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