Neuronal gene expression in amyotrophic lateral sclerosis

Brain Res Mol Brain Res. 1990 Jan;7(1):75-83. doi: 10.1016/0169-328x(90)90076-p.

Abstract

To characterize neuronal gene expression in amyotrophic lateral sclerosis (ALS), we quantitated one glial and three neuronal mRNAs in spinal cords of 7 subjects with ALS and 11 controls. The ALS cases showed no loss of mRNA for the neurofilament light subunit when assessed with in situ hybridization. Northern analysis, and RNase protection assay; and no loss of mRNA for amyloid precursor protein or a growth-associated protein (GAP-43/B-50) on Northern analysis. ALS cords also showed no significant change in glial mRNA. Our findings indicate that expression of these neuronal mRNAs is well maintained in ALS-afflicted spinal cord. They do not support the hypothesis of a generalized impairment of neuronal gene transcription in the pathogenesis of this disorder.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Amyloid / genetics*
  • Amyloid / metabolism
  • Amyloid beta-Protein Precursor
  • Amyotrophic Lateral Sclerosis / genetics*
  • Amyotrophic Lateral Sclerosis / metabolism
  • Female
  • GAP-43 Protein
  • Gene Expression Regulation*
  • Humans
  • Intermediate Filament Proteins / genetics*
  • Intermediate Filament Proteins / metabolism
  • Male
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Middle Aged
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / metabolism
  • Neurofilament Proteins
  • Protein Precursors / genetics*
  • Protein Precursors / metabolism
  • RNA, Messenger / metabolism*
  • Spinal Cord / metabolism*

Substances

  • Amyloid
  • Amyloid beta-Protein Precursor
  • GAP-43 Protein
  • Intermediate Filament Proteins
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Neurofilament Proteins
  • Protein Precursors
  • RNA, Messenger