Apoptotic and Oxidative Indicators in Alzheimer’s Disease

  • Arun K. Raina
  • Lawrence M. Sayre
  • Craig S. Atwood
  • Catherine A. Rottkamp
  • Ayala Hochman
  • Xiongwei Zhu
  • Mark E. Obrenovich
  • Shun Shimohama
  • Akihiko Nunomura
  • Atsushi Takeda
  • George Perry
  • Mark A. Smith
Part of the Neuromethods book series (NM, volume 37)


Dogma suggests that cell death mechanisms can present with either a necrotic or an apoptotic phenotype. Recent evidence, however, seems to point to a far more complex picture, in which apoptotic and necrotic phenotypes might present simultaneously (1). For example, TUNEL positivity in cardiomyocytes does not necessarily entail the presence of cell death that has an apoptotic phenotype (2). Complicating the matter further is the promiscuous use of the same term, apoptosis, to mean different things at different times, by conflating process (a cell death program) with product (the apoptotic phenotype). Cell death can be classified into programmed cell death, which entails a global/extrinsic program of cell death, and a cell death program(s), which entails a local/intrinsic/ cellular death program (3). The latter can present in a variety of phenotypes ranging from necrosis to apoptosis or as a combination phenotype (1), while the former is seen primarily during development and presents with an apoptotic phenotype. These ideas are useful when we come across novel phenomena or in situations where there is ambiguity as to the nature of cell death, i.e., Alzheimer’s disease (AD), where the earliest perceptible event is the presence of oxidative stress (4,5). Indeed, the presence of oxidative stress markers in AD parallels neuronal susceptibility to cell death in AD (4,6,7). Here we will review methods to detect both the proximal event (oxidative stress) as well as the most distal event (cell death) in AD.


Senile Plaque Oxidative Stress Marker Cell Death Program Vulnerable Neuron Apoptotic Phenotype 
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

© Humana Press Inc., Totowa, NJ 2002

Authors and Affiliations

  • Arun K. Raina
    • 1
  • Lawrence M. Sayre
    • 2
  • Craig S. Atwood
    • 2
  • Catherine A. Rottkamp
    • 1
  • Ayala Hochman
    • 3
  • Xiongwei Zhu
    • 1
  • Mark E. Obrenovich
    • 1
  • Shun Shimohama
    • 4
  • Akihiko Nunomura
    • 5
  • Atsushi Takeda
    • 6
  • George Perry
    • 1
  • Mark A. Smith
    • 1
  1. 1.Institute of PathologyCase Western Reserve UniversityCleveland
  2. 2.Department of ChemistryCase Western Reserve UniversityCleveland
  3. 3.Department of Biochemistry, George S. Wise Faculty of Life SciencesTel Aviv UniversityTel AvivIsrael
  4. 4.Department of Neurology, Graduate School of MedicineKyoto UniversityKyotoJapan
  5. 5.Department of Psychiatry and NeurologyAsahikawa Medical CollegeAsahikawaJapan
  6. 6.Department of NeurologyTohoku University School of MedicineSendaiJapan

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