Interleukin-1 Expression in Different Plaque Types in Alzheimer's Disease: Significance in Plaque Evolution (original) (raw)

Journal Article

,

Arkansas Children's Hospital Research Center,

University of Arkansas for Medical Sciences

, Little Rock, Arkansas

Department of Anatomy,

University of Arkansas for Medical Sciences

, Little Rock, Arkansas

Correspondence to; Professor W. Sue T. Griffin, Arkansas Children's Hospital Research Center, 800 Marshall Street, Little Rock, AR 72202-3591.

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Arkansas Children's Hospital Research Center,

University of Arkansas for Medical Sciences

, Little Rock, Arkansas

Department of Neurology, Rui-Jin Hospital,

Shanghai Second Medical University

, Shanghai, China

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,

Department of Molecular Neuropathology,

SmithKline Beecham Pharmaceuticals

, Essex, United Kingdom

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Robert E. Mrak, M.D., Ph.D.

Department of Veterans Affairs Medical Center,

University of Arkansas for Medical Sciences

, Little Rock, Arkansas

Department of Anatomy,

University of Arkansas for Medical Sciences

, Little Rock, Arkansas

Department of Pathology,

University of Arkansas for Medical Sciences

, Little Rock, Arkansas

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W. Sue T. Griffin, Jin Gen Sheng, Gareth W. Roberts, Robert E. Mrak, Interleukin-1 Expression in Different Plaque Types in Alzheimer's Disease: Significance in Plaque Evolution, Journal of Neuropathology & Experimental Neurology, Volume 54, Issue 2, March 1995, Pages 276–281, https://doi.org/10.1097/00005072-199503000-00014
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Abstract

The histologically apparent polymorphism of plaques containing β-amyloid in Alzheimer's disease is thought to represent different stages in plaque evolution, β-amyloid-immunopositive plaques were classified according to the pattern of β-amyloid distribution (diffuse vs dense-core) and the presence or absence of dystrophic β-amyloid precursor protein-immunopositive (β-APP+) neurites (neuritic vs non-neuritic). The potential contribution of microglia-derived interleukin-1 (IL-1), an immune response cytokine that induces synthesis and processing of β-APP, to the possible sequential development of these plaque types was examined through determination of the number of IL-1α+ microglia associated with each of four identified plaque types. Diffuse non-neuritic plaques had the least dense and most widely dispersed β-amyloid, did not exhibit β-APP+ dystrophic neurites, but most (78%) contained activated IL-1α+ microglia (2 ± 0.2/plaque; mean ± SEM). Diffuse neuritic plaques had more dense, but still widely dispersed β-amyloid, displayed a profusion of β-APP+ dystrophic neurites, and had the greatest numbers of associated activated IL-1±+ microglia (7 ± 0.8/plaque). Dense-core neuritic plaques had both compact and diffuse β-amyloid and had fewer IL-1±+ microglia (4 ± 0.4/plaque). Dense-core, non-neuritic plaques had compact β-amyloid, lacked associated diffuse β-amyloid, and were devoid of both IL-1α+ microglia and β-APP+ dystrophic neurites. These results suggest an important immunological component in the evolution of amyloid-containing plaques in Alzheimer's disease and further suggest that IL-1-expressing cells are necessary to initiate dystrophic neurite formation in diffuse β-amyloid deposits. Our data indicate that activation of microglia with expression of IL-1 in Alzheimer's disease is required to drive the metamorphosis of diffuse non-neuritic β-amyloid deposits to the characteristic and diagnostic neuritic plaques of Alzheimer's disease.

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© 1995 by the American Association of Neuropathologists, Inc.

Topic:

• amyloid
• cytokine
• alzheimer's disease
• interleukin-1
• polymorphism
• immune response
• biological metamorphosis
• microglia
• neurites
• senile plaques
• diagnosis
• neural development

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