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Experimental Synaptic Degeneration as a Model for the Pathogenesis of Alzheimer’s Disease: Monoclonal Antibodies and a Protein Kinase Inhibitor Block Synapse Formation and Maintenance Between Cultured CNS Neurons

  • Yoichiro Kuroda
  • Kazuo Kobayashi
  • Kazuyo Muramoto
  • Akihiko Ogura
  • Yoshihisa Kudo
  • Satoshi Nakanishi
Part of the Advances in Behavioral Biology book series (ABBI, volume 38A)

Abstract

A “tracing circuit” model has been proposedl, where in neuronal circuits are maintained by activity-dependent elimination of ex-circuit synapses and resultant sprouting of in-circuit axonal terminals, a process that might corre pond to human memory. Since synaptic and neuronal degeneration2, even following abnor-mal synapse formation3,4, represents the possible pathogenesis of the dementia of Alzheimer’s disease, the search for unknown molecules involved in the maintenance and formation of synaptic contacts is a promising approach to understanding of the disease.

Keywords

Synaptic Contact Synapse Formation Protein Kinase Inhibitor Cerebral Cortical Neuron Hippocampal Neuron Culture 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Yoichiro Kuroda
    • 1
  • Kazuo Kobayashi
    • 1
  • Kazuyo Muramoto
    • 1
  • Akihiko Ogura
    • 2
  • Yoshihisa Kudo
    • 2
  • Satoshi Nakanishi
    • 3
  1. 1.Dept.of NeurochemTokyo Metropolitan Institute for Neuro sciencesTokyo 183Japan
  2. 2.Dept.of NeurosciMitsubishi-kasei Institute of Life ScienceTokyo 194Japan
  3. 3.Tokyo Research LabKyowa Hakko Kogyo Co,LtdTokyo 194Japan

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