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Fenbendazole improves pathological and functional recovery following traumatic spinal cord injury

  • C. G. Yu
  • , R. Singh
  • , C. Crowdus
  • , K. Raza
  • , J. Kincer
  • , J. W. Geddes

Producción científica: Articlerevisión exhaustiva

10 Citas (Scopus)

Resumen

During a study of spinal cord injury (SCI), mice in our colony were treated with the anthelmintic fenbendazole to treat pinworms detected in other mice not involved in the study. As this was not part of the original experimental design, we subsequently compared pathological and functional outcomes of SCI in female C57BL/6 mice who received fenbendazole (150. ppm, 8. mg/kg body weight/day) for 4. weeks prior to moderate contusive SCI (50. kdyn force) as compared to mice on the same diet without added fenbendazole. The fenbendazole-treated mice exhibited improved locomotor function, determined using the Basso mouse scale, as well as improved tissue sparing following contusive SCI. Fenbendazole may exert protective effects through multiple possible mechanisms, one of which is inhibition of the proliferation of B lymphocytes, thereby reducing antibody responses. Autoantibodies produced following SCI contribute to the axon damage and locomotor deficits. Fenbendazole pretreatment reduced the injury-induced CD45R-positive B cell signal intensity and IgG immunoreactivity at the lesion epicenter 6. weeks after contusive SCI in mice, consistent with a possible effect on the immune response to the injury. Fenbendazole and related benzimadole antihelmintics are FDA approved, exhibit minimal toxicity, and represent a novel group of potential therapeutics targeting secondary mechanisms following SCI.

Idioma originalEnglish
Páginas (desde-hasta)163-169
Número de páginas7
PublicaciónNeuroscience
Volumen256
DOI
EstadoPublished - ene 3 2014

Nota bibliográfica

Funding Information:
This research was supported by grants from KSCHIRT #7-6A and 11-19A, and NIH P30 NS051220. We thank Linda Simmerman for expert assistance with microscopy and imaging. The authors declare no conflict-of-interests.

Financiación

This research was supported by grants from KSCHIRT #7-6A and 11-19A, and NIH P30 NS051220. We thank Linda Simmerman for expert assistance with microscopy and imaging. The authors declare no conflict-of-interests.

FinanciadoresNúmero del financiador
KSCHIRT7-6A, 11-19A
National Institutes of Health (NIH)
Institute of Neurological Disorders and Stroke National Advisory Neurological Disorders and Stroke CouncilP30NS051220

    ASJC Scopus subject areas

    • General Neuroscience

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