Neuroinflammation in Alzheimer disease
Neuroinflammation in Alzheimer disease
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.
Heneka, Michael T.
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van der Flier, Wiesje M.
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Jessen, Frank
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Boche, Delphine
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Gomez-Nicola, Diego
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Heneka, Michael T.
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van der Flier, Wiesje M.
9829018f-eaf7-465d-b84c-e1e1d101ad8a
Jessen, Frank
053caca2-d254-4a74-94d4-8dd7b3f20547
Boche, Delphine
bdcca10e-6302-4dd0-919f-67218f7e0d61
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5
Heneka, Michael T., van der Flier, Wiesje M. and Jessen, Frank
,
et al.
(2024)
Neuroinflammation in Alzheimer disease.
Nature Reviews Immunology.
(doi:10.1038/s41577-024-01104-7).
Abstract
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.
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Accepted/In Press date: 9 October 2024
e-pub ahead of print date: 9 December 2024
Identifiers
Local EPrints ID: 496300
URI: http://eprints.soton.ac.uk/id/eprint/496300
ISSN: 1474-1733
PURE UUID: 82b6c0ee-b053-4bf1-a499-b66063e81a56
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Date deposited: 11 Dec 2024 17:37
Last modified: 14 Dec 2024 02:44
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Contributors
Author:
Michael T. Heneka
Author:
Wiesje M. van der Flier
Author:
Frank Jessen
Corporate Author: et al.
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