Progressive Neuronal Injury Associated with Amyloid Plaque Formation in Alzheimer Disease (original) (raw)

Journal Article

,

Department of Geriatrics,

University of Arkansas for Medical Sciences

, Little Rock, AR 72205

Department of Neurology, Rui-Jin Hospital,

Shanghai Second Medical University

, Shanghai 200025

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,

Department of Geriatrics,

University of Arkansas for Medical Sciences

, Little Rock, AR 72205

Department of Neurology, Rui-Jin Hospital,

Shanghai Second Medical University

, Shanghai 200025

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,

Department of Veterans'

Affairs Medical Center

Department of Pathology,

University of Arkansas for Medical Sciences

, Little Rock, AR 72205

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Geriatrics Research,

Education and Clinical Center

Department of Veterans'

Affairs Medical Center

Department of Geriatrics,

University of Arkansas for Medical Sciences

, Little Rock, AR 72205

Correspondence to: Professor W. Sue T. Griffin, Geriatric Research, Education and Clinical Center, Department of Veterans' Affairs Medical Center, 4300 West Seventh Street, Little Rock, AR 72205/

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Jin G. Sheng, Xue Q. Zhou, Robert E. Mrak, W.S.T. Griffin, Progressive Neuronal Injury Associated with Amyloid Plaque Formation in Alzheimer Disease, Journal of Neuropathology & Experimental Neurology, Volume 57, Issue 7, July 1998, Pages 714–717, https://doi.org/10.1097/00005072-199807000-00008
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Abstract

Neuronal injury associated with amyloid plaque progression in Alzheimer disease was examined using TUNEL combined with β-amyloid immunolabeling. There was a progressive increase in the frequency of TUNEL-positive neurons associated with plaque types representing a hypothesized sequence of plaque evolution, from 20% of neurons not associated with plaques to 40%, 70–80%; and 100% of neurons in diffuse, neuritic, and dense-core non-neuritic plaques, respectively. The total number of neurons associated with end-stage, dense-core, non-neuritic plaques declined by 70% (per unit plaque area) compared with neuritic plaque forms. This decline, together with the fact that virtually all of those remaining were TUNEL-positive, suggests that neuronal cell damage increases as plaques evolve from diffuse to more complex forms and that eventually all plaque-associated neurons are lost. This novel demonstration of neurotoxicity associated with amyloid plaque formation and progression suggests that plaque-associated neuronal injury is a major cause of neuronal loss in Alzheimer disease.

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© 1998 by the American Association of Neuropathologists, Inc.

Topic:

• amyloid
• alzheimer's disease
• neurotoxicity syndromes
• in situ nick-end labeling
• neurons
• senile plaques
• cell injury

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