Inhibition of Aβ production by NF-κB inhibitors

Paris, Daniel; Patel, Nikunj; Quadros, Amita; Linan, Monica; Bakshi, Pancham; Ait‐Ghezala, Ghania; Mullan, Michael

doi:10.1016/j.neulet.2006.12.029

Cited by 71 publications

(51 citation statements)

References 22 publications

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“…Interestingly, both RAGE and BACE-1 expression are regulated by NFκB (40)(41)(42)(43). In particular, inhibition of NFκB signaling decreases RAGE expression in endothelial cells (44) and reduces Aβ production and BACE-1 expression levels (21,45,46). The inhibition of NFκB by nilvadipine therefore may represent a plausible mechanism responsible for both the inhibition of Aβ production and for the increased clearance of Aβ across the BBB observed following nilvadipine treatment.…”

Section: Discussionmentioning

confidence: 99%

Selective Antihypertensive Dihydropyridines Lower Aβ Accumulation by Targeting both the Production and the Clearance of Aβ across the Blood-Brain Barrier

Paris

Bachmeier

Patel

et al. 2010

Mol Med

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107

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Section: Discussionmentioning

confidence: 99%

Selective Antihypertensive Dihydropyridines Lower Aβ Accumulation by Targeting both the Production and the Clearance of Aβ across the Blood-Brain Barrier

Paris

Bachmeier

Patel

et al. 2010

Mol Med

Self Cite

107

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“…An alternative possibility is that CR activates Sirt1, which then deacetylases components of the NF-κB complex (Yeung et al, 2004b;Ghosh et al, 2007;Salminen et al, 2008; but see Barger et al, 2008). Previous studies have indeed found that NF-κB signaling is inhibited by caloric restriction in both rodents and humans (Phillips and Leeuwenburgh, 2005;Dirks and Leeuwenburgh, 2006;Weiss et al, 2006;Ugochukwu and Figgers, 2007), and that inhibition of NF-κB blocks the accumulation of beta-amyloid plaques in Alzheimer's mice (Paris et al, 2007), as well as neoplastic transformation of cells during the initial stages of cancer (Karin, 2006). Such effects result from blocking NF-κB activation, which is a characteristic feature of normal aging, as demonstrated by a recent genomic study (Adler et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Genes regulated by caloric restriction have unique roles within transcriptional networks

Swindell

2008

Mechanisms of Ageing and Development

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Caloric restriction (CR) has received much interest as an intervention that delays age-related disease and increases lifespan. Whole-genome microarrays have been used to identify specific genes underlying these effects, and in mice, this has led to the identification of genes with expression responses to CR that are shared across multiple tissue types. Such CR-regulated genes represent strong candidates for future investigation, but have been understood only as a list, without regard to their broader role within transcriptional networks. In this study, co-expression and network properties of CR-regulated genes were investigated using data generated by more than 600 Affymetrix microarrays. This analysis identified groups of co-expressed genes and regulatory factors associated with the mammalian CR response, and uncovered surprising network properties of CR-regulated genes. Genes downregulated by CR were highly connected and located in dense network regions. In contrast, CR-upregulated genes were weakly connected and positioned in sparse network regions. Some network properties were mirrored by CR-regulated genes from invertebrate models, suggesting an evolutionary basis for the observed patterns. These findings contribute to a systems-level picture of how CR influences transcription within mammalian cells, and point towards a comprehensive understanding of CR in terms of its influence on biological networks.

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“…All experiments were performed at least in quadruplicate for each treatment dose. Additionally, sAPP␣ was detected by Western blot in the culture medium surrounding 7W CHO cells using the antibody 6E10 (Signet Laboratories Inc.), which recognizes amino acids 1-17 of A␤, and sAPP␤ was detected in the culture medium using an anti-human sAPP␤ antibody (Immuno-Biological Laboratories Co. Ltd., Gunma, Japan) as we described previously (30).…”

Section: Methodsmentioning

confidence: 99%

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation

Paris

Ait‐Ghezala

Bachmeier

et al. 2014

Journal of Biological Chemistry

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Background: Spleen tyrosine kinase (Syk) mediates microglial activation and neurotoxicity elicited by Alzheimer A␤ peptides. Results: Syk regulates A␤ production via NFB-dependent mechanisms and Tau phosphorylation by controlling the activation of glycogen synthase 3␤. Conclusion: Inhibition of Syk can interrupt the neuroinflammation, pathological A␤ accumulation, and Tau hyperphosphorylation in AD. Significance: Syk represents a therapeutic target for the key pathological lesions that define AD.

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Inhibition of Aβ production by NF-κB inhibitors

Cited by 71 publications

References 22 publications

Selective Antihypertensive Dihydropyridines Lower Aβ Accumulation by Targeting both the Production and the Clearance of Aβ across the Blood-Brain Barrier

Selective Antihypertensive Dihydropyridines Lower Aβ Accumulation by Targeting both the Production and the Clearance of Aβ across the Blood-Brain Barrier

Genes regulated by caloric restriction have unique roles within transcriptional networks

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation

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