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Journal ArticleDOI

A Meta-Analysis of Cytokines in Alzheimer's Disease

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TLDR
The results strengthen the clinical evidence that AD is accompanied by an inflammatory response, particularly higher peripheral concentrations of IL-6, TNF-α, IL-1β, TGF-β,IL-12 and IL-18 and higher CSF concentrations of T GF-β.
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This article is published in Biological Psychiatry.The article was published on 2010-11-15. It has received 866 citations till now.

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Immune attack: the role of inflammation in Alzheimer disease

TL;DR: As inflammation in AD primarily concerns the innate immune system — unlike in 'typical' neuroinflammatory diseases such as multiple sclerosis and encephalitides — the concept of neuroinflammation in AD may need refinement.
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Inflammation as a central mechanism in Alzheimer's disease

TL;DR: An overview of inflammation in AD is provided and a detailed coverage of a number of microglia‐related signaling mechanisms that have been implicated in AD are reviewed.
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Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?

TL;DR: The interrelationships between Neuroinflammation and amyloid and tau pathologies as well as the effect of neuroinflammation on the disease trajectory in AD are discussed, focusing on microglia as major players in neuro inflammation and how these cells could be modulated as a therapeutic strategy for AD.
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Microglial priming in neurodegenerative disease.

TL;DR: The concept of microglial priming, and the subsequent exaggerated response of these cells to secondary systemic inflammation, opens the way to treat neurodegenerative diseases by targeting systemic disease or interrupting the signalling pathways that mediate the CNS response to systemic inflammation.
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Role of pro-inflammatory cytokines released from microglia in neurodegenerative diseases.

TL;DR: Current understanding of the involvement of cytokines in neurodegenerative disorders and their potential signaling mechanisms are summarized to suggest that microglial activation and pro-inflammatory cytokines merit interest as targets in the treatment of neurodegnerative disorders.
References
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Microglia as a source and target of cytokines.

TL;DR: Strong responses and modulatory influences can be demonstrated, adding to the emerging view that microglial behavior is highly dependent on the (cytokine) environment and that reactions to a challenge may vary with the stimulation context.
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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

TL;DR: Although there is still little evidence that inflammation triggers or promotes Alzheimer disease, increasing evidence from mouse models suggests that certain inflammatory mediators are potent drivers of the disease.
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