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Related Experiment Videos

Caprine beta-mannosidosis. Abnormal thyroid structure and function in a lysosomal storage disease.

P J Boyer1, M Z Jones, R F Nachreiner

  • 1Department of Pathology, Michigan State University, East Lansing.

Laboratory Investigation; a Journal of Technical Methods and Pathology
|July 1, 1990
PubMed
Summary

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Beta-mannosidosis in goats causes thyroid abnormalities and decreased thyroid hormone levels. This thyroid hormone deficiency may contribute to hypomyelination in affected animals.

Area of Science:

  • Veterinary Pathology
  • Endocrinology
  • Lysosomal Storage Diseases

Background:

  • Caprine beta-mannosidosis is an inherited neurovisceral storage disease caused by beta-mannosidase deficiency.
  • Previous studies noted severe thyroid abnormalities in affected neonatal goats.
  • Thyroid hormone is crucial for central nervous system myelination.

Purpose of the Study:

  • To characterize thyroid structure and function in caprine beta-mannosidosis.
  • To investigate the developmental progression of thyroid abnormalities.
  • To determine if thyroid dysfunction contributes to hypomyelination.

Main Methods:

  • Light and electron microscopy of thyroids from affected and control goats (gestation to 3 days postnatal).
  • Histopathological analysis of thyroid follicle morphology and cellular vacuolation.

Related Experiment Videos

  • Measurement of thyroid hormone concentrations in neonatal goats.

    • Main Results:

    • Thyroid follicle irregularities and lysosomal storage vacuoles were observed in affected goats from 96/150 days gestation.
    • Cytoplasmic vacuolation in thyroid cells increased with age in affected animals.
    • Affected neonatal goats exhibited significantly decreased thyroid hormone concentrations compared to controls.

    Conclusions:

    • Thyroid structure and function are significantly impaired in caprine beta-mannosidosis.
    • Thyroid hormone deficiency is hypothesized to play a role in the pathogenesis of hypomyelination.
    • This study provides the first report of endocrine organ dysfunction in a lysosomal storage disease and suggests systemic effects on the CNS.