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Glia as a Therapeutic Target: Selective Suppression of Human Amyloid-β-Induced Upregulation of Brain Proinflammatory Cytokine Production Attenuates Neurodegeneration
TLDR
Oral administration of brain-penetrant compound MW01-5-188WH suppressed the human amyloid-β (Aβ) 1-42-induced upregulation of interleukin-1β, tumor necrosis factor-α, and S100B in the hippocampus and attenuated deficits in Y maze behavior, a hippocampal-linked task.
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Aminopyridazines inhibit β-amyloid-induced glial activation and neuronal damage in vivo
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Enhanced susceptibility of S‐100B transgenic mice to neuroinflammation and neuronal dysfunction induced by intracerebroventricular infusion of human β‐amyloid
TLDR
Tg mice showed increased vulnerability to Aβ‐induced neuropathology relative to either WT or KO mice, consistent with a model in which S‐100B overexpression in AD enhances glial activation and leads to an augmented neuroinflammatory process that increases the severity of neuropathologic sequelae.
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A novel p38α MAPK inhibitor suppresses brain proinflammatory cytokine up-regulation and attenuates synaptic dysfunction and behavioral deficits in an Alzheimer's disease mouse model
TLDR
The p38α MAPK pathway is quantitatively important in the Aβ-induced production of proinflammatory cytokines in hippocampus, and brain p38 α MAPK is a viable molecular target for future development of potential disease-modifying therapeutics in AD and related neurodegenerative disorders.
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Mechanism of glial activation by S100B: involvement of the transcription factor NFκB
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Interleukin 1 receptor antagonist knockout mice show enhanced microglial activation and neuronal damage induced by intracerebroventricular infusion of human β-amyloid
TLDR
The data are consistent with the neuroinflammation hypothesis whereby increased IL-1 signaling in AD enhances glia activation and leads to an augmented neuroinflammatory process that increases the severity of neuropathologic sequelae.
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P4-428 Glia as a therapeutic target: Selective suppression of human amyloid-beta-induced upregulation of brain proinflammatory cytokine production attenuates neurodegeneration
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Human amyloid beta-induced neuroinflammation is an early event in neurodegeneration.
TLDR
Abeta-induced neuroinflammation is an early event associated with onset and progression of pathophysiology, can be suppressed by the glial inhibitor over a range of intervention start times, and is amenable to suppression without inhibiting peripheral tissue inflammatory responses.
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Increased susceptibility of S100B transgenic mice to perinatal hypoxia‐ischemia
TLDR
Measurement of glial fibrillary acidic protein and S100B levels showed a significant increase in the Tg mice, consistent with heightened glial activation and neuroinflammation in response to injury, the first demonstration to the authors' knowledge that overexpression of S 100B in vivo enhances pathological response to Injury.
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Neuroinflammation: a potential therapeutic target
TLDR
The focus is on Alzheimer’s disease, but the concepts are transferrable to other neurodegenerative disorders with an inflammatory component, as well as development of novel synthetic compounds that selectively downregulate neuroinflammatory responses.
View on Taylor & Francis
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