TDP-43 pathology in a case of hereditary spastic paraplegia with a NIPA1/SPG6 mutation

Acta Neuropathol. 2012 Aug;124(2):285-91. doi: 10.1007/s00401-012-0947-y.

Abstract

Mutations in NIPA1 (non-imprinted in Prader-Willi/Angelman syndrome) have been described as a cause of autosomal dominant hereditary spastic paraplegia (HSP) known as SPG6 (spastic paraplegia-6). We present the first neuropathological description of a patient with a NIPA1 mutation, and clinical phenotype of complicated HSP with motor neuron disease-like syndrome and cognitive decline. Postmortem examination revealed degeneration of lateral corticospinal tracts and dorsal columns with motor neuron loss. TDP-43 immunostaining showed widespread spinal cord and cerebral skein-like and round neuronal cytoplasmic inclusions. We ruled out NIPA1 mutations in 419 additional cases of motor neuron disease. These findings suggest that hereditary spastic paraplegia due to NIPA1 mutations could represent a TDP-43 proteinopathy.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Female
  • Humans
  • Inclusion Bodies / genetics*
  • Inclusion Bodies / metabolism
  • Inclusion Bodies / pathology
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Mutation
  • Neurons / metabolism*
  • Neurons / pathology
  • Spastic Paraplegia, Hereditary / genetics*
  • Spastic Paraplegia, Hereditary / metabolism
  • Spastic Paraplegia, Hereditary / pathology
  • Spinal Cord / metabolism*
  • Spinal Cord / pathology

Substances

  • DNA-Binding Proteins
  • Membrane Proteins
  • NIPA1 protein, human