Dendritic and histochemical development and ageing in patients with Down's syndrome

J Intellect Disabil Res. 1994 Jun;38 ( Pt 3):265-73. doi: 10.1111/j.1365-2788.1994.tb00394.x.

Abstract

Mental retardation and dementia characteristic of Down's syndrome (DS) have a complex pathogenesis. Golgi and immunohistochemical studies were done on DS patients and controls from foetuses and elderly adults. Golgi studies on the cerebral cortex revealed that the postsynaptic spines on the basal dendrites increase from neonate to 15 years of age and gradually decrease after 20 years in controls, but poorly increase in children and rapidly decrease in adults with DS. This deficient synaptogenesis and dendritic atrophy may be related to mental retardation. On the other hand, immunohistochemistry on proteins, whose genes are located on chromosome 21, revealed that c-terminal protein of beta-amyloid appears in neurons of DS, S-100-positive glia increases in the hippocampus of neonates and adults, and membrane protein OK-2 is expressed earlier and is more widespread in the DS brains. The overexpression and early appearance of gene products in DS brains may be related to the pathogenesis of or predisposition to mental disorders or to dendritic hypogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / pathology*
  • Amyloid beta-Peptides / analysis
  • Cell Count
  • Cellular Senescence / physiology*
  • Cerebral Cortex / pathology
  • Child
  • Child, Preschool
  • Dendrites / pathology*
  • Down Syndrome / pathology*
  • Female
  • Gestational Age
  • Hippocampus / pathology
  • Humans
  • Immunoenzyme Techniques
  • Infant
  • Infant, Newborn
  • Male
  • Membrane Proteins / analysis
  • Middle Aged
  • Neurofibrillary Tangles / pathology
  • Neurons / pathology
  • Pregnancy
  • S100 Proteins / analysis
  • Synapses / pathology

Substances

  • Amyloid beta-Peptides
  • Membrane Proteins
  • S100 Proteins