In Situ Immunodetection of Neuronal Caspase-3 Activation in Alzheimer Disease (original) (raw)

Journal Article

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Department of Pathology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

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Department of Molecular Biology and Pharmacology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

Department of Neurology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

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Department of Molecular Biology and Pharmacology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

Department of Neurology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

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,

Department of Pathology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

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IDUN Pharmaceuticals Inc., La Jolla, California

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Eugene M. Johnson, Jr., Phd

Department of Molecular Biology and Pharmacology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

Department of Neurology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

Search for other works by this author on:

Department of Pathology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

Department of Molecular Biology and Pharmacology, Center for Study of Nervous System Injury, Alzheimer Disease Research Center,

Washington University

School of Medicine, St. Louis, Missouri

Correspondence to: Dr. Kevin A. Roth, Washington University School of Medicine, Department of Pathology, 660 South Euclid Avenue; Box 8118, St. Louis, MO 63110.

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This work was supported by the Washington University Alzheimer Disease Research Center P50 AG05681 and NIH grants NS35I07, NS35484, and NS35902.

Author Notes

Published:

01 September 1999

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Lee A. Selznick, David M. Holtzman, Byung Hee Han, Murat Gökden, Anu N. Srinivasan, Eugene M. Johnson, Kevin A. Roth, In Situ Immunodetection of Neuronal Caspase-3 Activation in Alzheimer Disease, Journal of Neuropathology & Experimental Neurology, Volume 58, Issue 9, September 1999, Pages 1020–1026, https://doi.org/10.1097/00005072-199909000-00012
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Abstract

The mechanism by which cells die in Alzheimer disease (AD) is unknown. Several investigators speculate that much of the cell loss may be due to apoptosis, a highly regulated form of programmed cell death. Caspase-3 is a critical effector of neuronal apoptosis and may be inappropriately activated in AD. To address this possibility, we examined cortical and hippocampal brain sections from AD patients, as well as 2 animal models of AD, for in situ evidence of caspase-3 activation. We report here that senile plaques and neurofibrillary tangles in the AD brain are not associated with caspase-3 activation. Furthermore, amyloid beta (Aβ) deposition in the APPsw transgenic mouse model of AD does not result in caspase-3 activation despite the ability of A|3 to induce caspase-3 activation and neuronal apoptosis in vitro. AD brain sections do, however, exhibit caspase-3 activation in hippocampal neurons undergoing granulovacuolar degeneration. Our data suggests that caspase-3 does not have a significant role in the widespread neuronal cell death that occurs in AD, but may contribute to the specific loss of hippocampal neurons involved in learning and memory.

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Author notes

This work was supported by the Washington University Alzheimer Disease Research Center P50 AG05681 and NIH grants NS35I07, NS35484, and NS35902.

© 1999 by the American Association of Neuropathologists

Topic:

• apoptosis
• alzheimer's disease
• amyloid beta-protein
• death
• hippocampus
• mice, transgenic
• animal model
• neurofibrillary tangles
• neurons
• senile plaques
• brain
• memory
• tissue degeneration
• neuron death
• caspase-3

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