Truncating neurotrypsin mutation in autosomal recessive nonsyndromic mental retardation

Science. 2002 Nov 29;298(5599):1779-81. doi: 10.1126/science.1076521.

Abstract

A 4-base pair deletion in the neuronal serine protease neurotrypsin gene was associated with autosomal recessive nonsyndromic mental retardation (MR). In situ hybridization experiments on human fetal brains showed that neurotrypsin was highly expressed in brain structures involved in learning and memory. Immuno-electron microscopy on adult human brain sections revealed that neurotrypsin is located in presynaptic nerve endings, particularly over the presynaptic membrane lining the synaptic cleft. These findings suggest that neurotrypsin-mediated proteolysis is required for normal synaptic function and suggest potential insights into the pathophysiological bases of mental retardation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Brain / embryology
  • Brain / metabolism*
  • Female
  • Fetus / metabolism
  • Gene Expression
  • Genes, Recessive
  • Humans
  • Immunohistochemistry
  • Intellectual Disability / genetics*
  • Intellectual Disability / metabolism
  • Male
  • Microsatellite Repeats
  • Microscopy, Immunoelectron
  • Pedigree
  • Sequence Deletion*
  • Serine Endopeptidases / chemistry
  • Serine Endopeptidases / genetics*
  • Serine Endopeptidases / metabolism
  • Spinal Cord / embryology
  • Spinal Cord / metabolism
  • Synapses / metabolism*
  • Synapses / ultrastructure
  • Synaptic Membranes / metabolism

Substances

  • Serine Endopeptidases
  • neurotrypsin