Abstract

Axonal transport is essential for the development, function, and survival of neurons, and impaired axonal transport has been implicated in many neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease

Highlights

  • J Neurol Neuromedicine (2016) 1(8): 19-21. Jlp ablations for this study[7], and these mice might serve as a useful animal model for studying the molecular mechanisms of neurodegenerative disorders

  • Histological analysis of 24-week-old mice revealed the specific loss of Purkinje cells (PCs) and the presence of swollen PC axons in mice with a conditional double KO of Jsap[1] and Jlp (Jsap1:Jlp cDKO), but not in control mice or those with a single Jsap[1] or Jlp cKO

  • The authors found that the PC counts were comparable in control and Jsap1:Jlp cDKO mice at 8 weeks of age; after this age, the PC counts decreased in cDKO mice compared to control mice

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Summary

Introduction

Jlp ablations for this study[7], and these mice might serve as a useful animal model for studying the molecular mechanisms of neurodegenerative disorders. Axonal transport is a complex and highly regulated process that is essential for neuronal development, function, and survival, and defective axonal transport has been implicated in many neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease[1,2].

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