“…Importantly, the sensitivity of a small pro-inflammatory microRNA family consisting of miRNA-30b, miRNA-34a, miRNA-146a, miRNA-155 and others to NF-kB (p50/p65) signaling appears to be in part be due to the presence of one-to-several NF-kB-DNA-binding sites in the immediate promoters of the genes encoding these miRNAs [ 35 , 38 , 39 , 40 , 49 , 50 , 53 , 54 , 55 , 56 ]. An improved understanding of LPS molecular genetic interactions along the GI tract–CNS axis involving GI-tract-derived microbial neurotoxins, AD and other related disorders should further support the hypothesis of altered LPS–miRNA–mRNA coupled signaling networks, and these concepts are currently supported by recently described experimental-findings in the scientific literature [ 29 , 30 , 34 , 35 , 36 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 53 , 54 , 55 , 56 , 57 ]. For example, targeting and/or modulating GI-tract-microbiome-LPS-mediated, miRNA-30b-regulated NF-L pathways and other miRNA-mediated gene expression circuitry could be valuable in the design of future therapeutic strategies that: (i) could support and maintain cytoarchitectural components essential for neuronal shape, axonal caliber, inter-neuronal signaling and synaptic plasticity; and (ii) may more effectively manage the many neurological diseases in which NF-L gene expression and abundance play a defining and/or determinant role [ 29 , 39 , 55 , 56 , 57 ].…”