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4 - Neuronal cell death in human neurodegenerative diseases and their animal/cell models

Published online by Cambridge University Press:  03 March 2010

By
Lee J. Martin ,
Zhiping Liu ,
Juan Troncoso  and
Donald L. Price
Edited by
Martin Holcik ,
Eric C. LaCasse ,
Alex E. MacKenzie  and
Robert G. Korneluk
Lee J. Martin
Affiliation:
Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Zhiping Liu
Affiliation:
Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Juan Troncoso
Affiliation:
Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Donald L. Price
Affiliation:
Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Martin Holcik
Affiliation:
University of Ottawa
Eric C. LaCasse
Affiliation:
University of Ottawa
Alex E. MacKenzie
Affiliation:
University of Ottawa
Robert G. Korneluk
Affiliation:
University of Ottawa
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Summary

Introduction

Cell death is important in the normal histogenesis of organs, steady state kinetics of healthy adult tissues, pathogenesis of tissue damage and disease, and disease therapy. Pathologists conceived the concept of cell death as a mechanism for disease to aid in diagnosis and therapy (Virchow, 1858). Developmental biologists then realized the essential role of cell death in tissue and organ development (Glücksmann, 1951; Lockshin and Williams, 1964; Saunders, 1966). This idea was at first received with skepticism, but now it is dogma that cell number in tissues is controlled precisely in developing and adult tissues. The absence of this precise control of cell number in tissues causes cancer (impaired apoptosis is a central step toward neoplasia). Pathologic stimuli can be extrinsic or intrinsic and can inactivate normal cell death networks or can cause abrupt or delayed cell death. Cell demise can occur as multiple types of death (Schweichel and Merker, 1973; Lockshin and Zakeri, 2002). It is compelling that a goal of human disease therapy is, on the one hand, to prevent cell death in neurologic disease and, on the other hand, to stimulate cell death in malignancy. Thus, the study of cell death is fundamental to human pathobiology and disease treatment. In this chapter, recent critical views on the contributions of the different forms of cell death to human neurodegenerative diseases and their animal and cell models will be presented.

Type
Chapter
Information
Apoptosis in Health and Disease
Clinical and Therapeutic Aspects
 , pp. 96 - 155
Publisher: Cambridge University Press
Print publication year: 2005

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  • Neuronal cell death in human neurodegenerative diseases and their animal/cell models
    • By Lee J. Martin, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Zhiping Liu, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Juan Troncoso, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Donald L. Price, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  • Edited by Martin Holcik, University of Ottawa, Eric C. LaCasse, University of Ottawa, Alex E. MacKenzie, University of Ottawa, Robert G. Korneluk, University of Ottawa
  • Book: Apoptosis in Health and Disease
  • Online publication: 03 March 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511663543.005
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  • Neuronal cell death in human neurodegenerative diseases and their animal/cell models
    • By Lee J. Martin, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Zhiping Liu, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Juan Troncoso, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Donald L. Price, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  • Edited by Martin Holcik, University of Ottawa, Eric C. LaCasse, University of Ottawa, Alex E. MacKenzie, University of Ottawa, Robert G. Korneluk, University of Ottawa
  • Book: Apoptosis in Health and Disease
  • Online publication: 03 March 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511663543.005
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  • Neuronal cell death in human neurodegenerative diseases and their animal/cell models
    • By Lee J. Martin, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Zhiping Liu, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Juan Troncoso, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, Donald L. Price, Departments of Pathology, Division of Neuropathology, Neuroscience, and Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  • Edited by Martin Holcik, University of Ottawa, Eric C. LaCasse, University of Ottawa, Alex E. MacKenzie, University of Ottawa, Robert G. Korneluk, University of Ottawa
  • Book: Apoptosis in Health and Disease
  • Online publication: 03 March 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511663543.005
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