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Molecular Cloning of Human Growth Inhibitory Factor CDNA and Its Down-Regulation in Alzheimer’s Disease

  • S. Tsuji
  • H. Kobayashi
  • Y. Uchida
  • Y. Ihara
  • T. Miyatake
Part of the Advances in Behavioral Biology book series (ABBI, volume 44)

Abstract

Alzheimer’s disease (AD) is the most common dementing illness in man (Mann et al., 1988). AD is characterized by the presence of numerous senile plaques and neurofibrillary tangles throughout the cerebral cortex (Hirano and Zimmerman 1962; Kidd 1964; Schoenberg et al., 1987; Yamaguchi et al., 1988; Wisniewski et al., 1989). The major protein in senile plaques has been identified as a 39 ~ 42-amino-acid polypeptide referred to as the β/A4 protein (Masters et al., 1985; Selkoe et al., 1986). The major component of neurofibrillary tangles has also been identified as tau, a microtubule-associated phosphoprotein (Kondo et al., 1988; Wischik et al., 1988). The molecular mechanisms which lead to neuronal loss, and the accumulation of senile plaques followed by neurofibrillary tangles in AD, however, remain unexplained.

Keywords

Neurofibrillary Tangle Growth Inhibitory Activity Growth Inhibitory Factor Neurotrophic Activity Immunohistochemical Observation 
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

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • S. Tsuji
    • 1
  • H. Kobayashi
    • 1
  • Y. Uchida
    • 2
  • Y. Ihara
    • 3
  • T. Miyatake
    • 4
  1. 1.Department of NeurologyBrain Research Institute Niigata UniversityAsahimachi-dori, Niigata 951Japan
  2. 2.Departments of NeuropathologyTokyo Metropolitan Institute of GerontologyItabashiku, Tokyo 173Japan
  3. 3.Department of Neuropathology Institute of Brain Research, Faculty of MedicineUniversity of TokyoBunkyoku, Tokyo 113Japan
  4. 4.Department of NeurologyTokyo Medical and Dental UniversityYushima, Bunkyoku, Tokyo 113Japan

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