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Neuroinflammation in Alzheimer's disease
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 NLRP3…
TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis
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.
Innate immune activation in neurodegenerative disease
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.
Inflammatory processes in Alzheimer's disease
Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine
- M. Heneka, Fabian Nadrigny, M. Kummer
- Biology, ChemistryProceedings of the National Academy of Sciences
- 15 March 2010
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.
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.
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.
η-Secretase processing of APP inhibits neuronal activity in the hippocampus
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.
Protection by pioglitazone in the MPTP model of Parkinson's disease correlates with IκBα induction and block of NFκB and iNOS activation
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.
Neuroinflammatory processes in Alzheimer’s disease
Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD and a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or in concert account for the epidemiologically observed protection.