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Neuroinflammation in Alzheimer's disease
TLDR
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. Expand
NLRP3 is activated in Alzheimer´s disease and contributes to pathology in APP/PS1 mice
Alzheimer’s disease is the world’s most common dementing illness. Deposition of amyloid-β peptide drives cerebral neuroinflammation by activating microglia. Indeed, amyloid-β activation of the NLRP3Expand
Innate immune activation in neurodegenerative disease
TLDR
How the activation of innate immune signalling pathways — in particular, the NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome — by aberrant host proteins may be a common step in the development of diverse neurodegenerative disorders is discussed. Expand
TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis
TLDR
It is reported that missense mutations associated with FTD and FTD-like syndrome reduce TREM2 maturation, abolish shedding by ADAM proteases, and impair the phagocytic activity of TREM1-expressing cells. Expand
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. Expand
Protective action of the peroxisome proliferator‐activated receptor‐γ agonist pioglitazone in a mouse model of Parkinson's disease
TLDR
There was little reduction of MPTP‐induced dopamine depletion, with no detectable effect on loss of TH immunoreactivity and glial response in the striatum of pioglitazone‐treated animals. Expand
Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine
TLDR
It is indicated that decrease of NE in locus ceruleus projection areas facilitates the inflammatory reaction of microglial cells in AD and impairs microglia migration and phagocytosis, thereby contributing to reduced Aβ clearance. Expand
Protection by pioglitazone in the MPTP model of Parkinson's disease correlates with I kappa B alpha induction and block of NF kappa B and iNOS activation.
TLDR
The results suggest that pioglitazone sequentially acts through PPARgamma activation, IkappaBalpha induction, block of NFkappaB activation, iNOS induction and NO-mediated toxicity, and may offer a treatment opportunity in PD to slow the progression of disease that is mediated by inflammation. Expand
η-Secretase processing of APP inhibits neuronal activity in the hippocampus
TLDR
A new physiological APP processing pathway is described, which generates proteolytic fragments capable of inhibiting neuronal activity within the hippocampus, and this finding may also indicate potential translational relevance for therapeutic strategies targeting APP processing. Expand
Protection by pioglitazone in the MPTP model of Parkinson's disease correlates with IκBα induction and block of NFκB and iNOS activation
TLDR
The results suggest that pioglitazone sequentially acts through PPARγ activation, IκBα induction, block of NFκB activation, iNOS induction and NO‐mediated toxicity, and may offer a treatment opportunity in PD to slow the progression of disease that is mediated by inflammation. Expand
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