Abstract
Biochemical and neuropathological studies of brains from individuals with Alzheimer disease (AD) provide clear evidence for an activation of inflammatory pathways, and long-term use of anti-inflammatory drugs is linked with reduced risk to develop the disease. As cause and effect relationships between inflammation and AD are being worked out, there is a realization that some components of this complex molecular and cellular machinery are most likely promoting pathological processes leading to AD, whereas other components serve to do the opposite. The challenge will be to find ways of fine tuning inflammation to delay, prevent, or treat AD.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Alzheimer Disease / genetics
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Alzheimer Disease / pathology*
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Alzheimer Disease / prevention & control
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Animals
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Anti-Inflammatory Agents / therapeutic use
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Arachidonic Acid / metabolism
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Astrocytes / pathology
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Clinical Trials as Topic
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Complement Activation / physiology
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Complement System Proteins / physiology
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Cytokines / physiology
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Encephalitis / pathology*
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Humans
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Mice
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Microglia / pathology
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Neurons / pathology
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Oligodendroglia / pathology
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Polymorphism, Genetic / genetics
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Prostaglandin-Endoperoxide Synthases / physiology
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Toll-Like Receptors / physiology
Substances
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Anti-Inflammatory Agents
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Cytokines
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Toll-Like Receptors
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Arachidonic Acid
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Complement System Proteins
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Prostaglandin-Endoperoxide Synthases