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Journal ArticleDOI

Inflammatory processes in Alzheimer's disease.

TLDR
While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate APP processing by upregulation of beta secretase 1 and therefore are able to establish a vicious cycle.
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This article is published in Journal of Neuroimmunology.The article was published on 2007-03-01. It has received 895 citations till now. The article focuses on the topics: Gamma secretase & Amyloid beta.

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Microglial physiology: unique stimuli, specialized responses

TL;DR: A wealth of data now demonstrate that the microglia have very diverse effector functions, in line with macrophage populations in other organs, and the term activatedmicroglia needs to be qualified to reflect the distinct and very different states of activation-associated effector function in different disease states.
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Clusters of hyperactive neurons near amyloid plaques in a mouse model of Alzheimer's disease.

TL;DR: It is suggested that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides a mechanism for the disturbed cortical function in Alzheimer's disease.
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A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease.

TL;DR: Results indicate that NPD1 promotes brain cell survival via the induction of antiapoptotic and neuroprotective gene-expression programs that suppress Abeta42-induced neurotoxicity.
References
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Journal ArticleDOI

Microglia: a sensor for pathological events in the CNS

TL;DR: An understanding of intercellular signalling pathways for microglia proliferation and activation could form a rational basis for targeted intervention on glial reactions to injuries in the CNS.
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Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo.

TL;DR: It is reported that natural oligomers of human Aβ are formed soon after generation of the peptide within specific intracellular vesicles and are subsequently secreted from the cell, indicating that synaptotoxic Aβ oligomers can be targeted therapeutically.
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Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction

TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.
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Chemokines — Chemotactic Cytokines That Mediate Inflammation

TL;DR: This review introduces the burgeoning family of cytokines, with special emphasis on their role in the pathophysiology of disease and their potential as targets for therapy.
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