Acta Neuropathologica

, Volume 106, Issue 4, pp 291–302

Reelin-immunoreactive Cajal-Retzius cells: the entorhinal cortex in normal aging and Alzheimer's disease

  • Anett Riedel
  • Riitta Miettinen
  • Jens Stieler
  • Mia Mikkonen
  • Irina Alafuzoff
  • Hilkka Soininen
  • Thomas Arendt
Regular Paper

DOI: 10.1007/s00401-003-0729-7

Cite this article as:
Riedel, A., Miettinen, R., Stieler, J. et al. Acta Neuropathol (2003) 106: 291. doi:10.1007/s00401-003-0729-7

Abstract

Alzheimer's disease (AD) is a disorder of brain self organization associated with morphodysregulation at the synaptic level. Disturbances follow a hierarchical spatio-temporal pattern throughout the cortex and involve the re-activation of developmental molecular programs. The large glycoprotein reelin, synthesized by Cajal-Retzius (CR) cells, is an important component of a signaling pathway involved in embryonic development and modulation of synaptic circuitry, but is also implicated in the pathogenetic cascade in AD. Although the majority of CR cells sequentially disappears from the postnatal cortical layer I, a few of them persist in the normal adult brain. They continue to produce reelin, express a variety of other proteins, and are characterized by a typical morphology. Recently, CR cells have been reported to be altered in number and morphology in a variety of neurological and psychiatric diseases linked to maldevelopment. In the present study we show that reelin-positive CR cells persist in the layer I of the entorhinal cortex in normal senescent brains and are also preserved in AD. The majority of CR cells in AD is morphologically and cytochemically—as revealed by double labeling with calcium-binding proteins—indistinguishable from normal cases, suggesting that they are not dramatically altered in the entorhinal cortex of AD patients. Nevertheless, CR cells seem to be partially affected by the formation of paired helical filaments, indicating subtle changes that are suggested to be a result rather than a cause of the pathogenetic cascade of AD.

Keywords

Human Intermediate subfield Calcium-binding proteins β-Amyloid Tau phosphorylation 

Copyright information

© Springer-Verlag 2003

Authors and Affiliations

  • Anett Riedel
    • 1
  • Riitta Miettinen
    • 2
  • Jens Stieler
    • 1
  • Mia Mikkonen
    • 2
  • Irina Alafuzoff
    • 2
  • Hilkka Soininen
    • 2
  • Thomas Arendt
    • 1
  1. 1.Department of Neuroanatomy, Paul Flechsig Institute for Brain ResearchUniversity of LeipzigLeipzigGermany
  2. 2.Departments of Neurology and Neurosciences and PathologyUniversity and University Hospital of KuopioKuopioFinland

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