Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination

Area of Science:

• Neuroscience
• Biochemistry
• Pathology

Background:

• Apolipoprotein E (apo E) is implicated in lipid transport following peripheral nerve injury.
• Its role in demyelination, distinct from Wallerian degeneration, requires further investigation.

Purpose of the Study:

• To investigate apo E release from rat peripheral nerve following selective demyelination without significant axonopathy.
• To compare apo E release in response to tellurium (Te) toxicity, chronic lead (Pb) poisoning, and nerve crush injury.

Main Methods:

• Quantification of apo E release from excised sciatic nerve segments using an immunoturbidimetric assay.
• Induction of demyelination via Te toxicity and Pb poisoning; Wallerian degeneration induced by nerve crush.
• Morphological assessment using nerve-fiber teasing and light/electron microscopy.

Main Results:

• Wallerian degeneration significantly increased apo E release, consistent with prior studies.
• Te-induced neuropathy showed a tenfold increase in apo E release during acute demyelination and remyelination.
• Chronic Pb poisoning resulted in a fourfold increase in apo E release with ongoing demyelination.

Conclusions:

• Peripheral nerve demyelination, similar to Wallerian degeneration, elevates apo E release.
• Apo E is crucial for lipid transport during both Wallerian degeneration and demyelinating neuropathies.
• These findings highlight apo E's central role in myelin repair and lipid homeostasis in the peripheral nervous system.