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- W2742495135 abstract "Abundant neurochemical, neuropathological, and genetic evidence suggests that a critical number of proinfl ammatory and innate immune system-associated factors are involved in the underlying pathological pathways that drive the sporadic Alzheimer’s disease (AD) process. Most recently, a series of epigenetic factors – including a select family of inducible, proinfl ammatory, NF-кB-regulated small noncoding RNAs called miRNAs – have been shown to be signifi cantly elevated in abundance in AD brain. These upregulated miRNAs appear to be instrumental in reshaping the human brain transcriptome. This reorganization of mRNA speciation and complexity in turn drives proinfl ammatory and pathogenic gene expression programs. The ensuing, progressively altered immune and infl ammatory signaling patterns in AD brain support immunopathogenetic events and proinfl ammatory features of the AD phenotype. This report will briefl y review what is known concerning NF-кB-inducible miRNAs that are signifi cantly upregulated in AD-targeted anatomical regions of degenerating human brain cells and tissues. Quenching of NF-кB-sensitive infl ammatory miRNA signaling using NF-кB-inhibitors such as the polyphenolic resveratrol analog trans-3,5,4’-trihydroxystilbene (CAY10512) may have some therapeutic value in reducing infl ammatory neurodegeneration. Antagonism of NF-кB-inducing, and hence proinfl ammatory, epigenetic and environmental factors, such as the neurotrophic herpes simplex virus-1 and exposure to the potent neurotoxin aluminum, are briefl y discussed. Early reports further indicate that miRNA neutralization employing anti-miRNA (antagomir) strategies may hold future promise in the clinical management of this insidious neurological disorder and expanding healthcare concern." @default.
- W2742495135 created "2017-08-17" @default.
- W2742495135 creator A5034934480 @default.
- W2742495135 date "2012-01-01" @default.
- W2742495135 modified "2023-09-24" @default.
- W2742495135 title "NF-кB-regulated, proinfl ammatory miRNAs in Alzheimer's disease" @default.
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