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Peripheral sensory nerve defects in apolipoprotein E knockout mice

S M Fullerton¹, W J Strittmatter, W D Matthew

¹Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, North Carolina 27710, USA.

Experimental Neurology

|September 23, 1998

Summary

Apolipoprotein E (apoE) deficiency in mice leads to abnormal sciatic nerve structure and reduced sensitivity to pain. This suggests apoE is crucial for peripheral nervous system health and unmyelinated axon survival.

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Area of Science:

Neuroscience
Cell Biology
Genetics

Background:

Apolipoprotein E (apoE) is a lipoprotein involved in lipid metabolism.
Emerging evidence suggests apoE plays roles in the central and peripheral nervous systems.
Schwann cells in the peripheral nervous system produce apoE, indicating a potential role in supporting sensory afferents.

Purpose of the Study:

To investigate the function of apoE in the peripheral nervous system.
To examine the structural and functional consequences of apoE deficiency in sciatic nerves.

Main Methods:

Utilized apoE-deficient (apoE KO) mice for the study.
Conducted electron microscopy to analyze sciatic nerve ultrastructure.
Assessed thermal sensory perception in apoE KO mice.

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Main Results:

ApoE KO mice exhibited abnormal and reduced numbers of unmyelinated axons in the sciatic nerve.
Unmyelinated axons in apoE KO mice were irregularly shaped with minimal Schwann cell cytoplasm.
Myelinated fibers and myelin structures were unaffected in apoE KO mice.
ApoE KO mice showed decreased sensitivity to noxious thermal stimuli.

Conclusions:

Apolipoprotein E is essential for the structural integrity and function of unmyelinated axons in the peripheral nervous system.
These findings provide in vivo evidence that apoE supports neuronal health and survival.
The study highlights a critical role for apoE in sensory nerve function and pain perception.