Table 1.

Run-on transcription—impairment of neuronal transcriptional output by lipopolysaccharide (LPS).

LPS (nM)	n	Alu	NFL	GFAP
0 (control)	8	100	100	100
50	10	54 ± 9.3	27 ± 8.7	86 ± 9.1
100	5	41 ± 10.3	16 ± 9.8	81 ± 11.2
500	5	36 ± 11.3	15 ± 11.3	72 ± 11.3
1000	5	35 ± 11.3	12 ± 11.3	72 ± 11.3

HNG cells in primary culture (Figure 3) were used to program run-on gene transcription, a highly informative and sensitive method for monitoring the mRNA generating capacity of any cell system (Lukiw et al., 1998; Ricicová and Palková, 2003; Cui et al., 2005; Smale, 2009; http://www.genomics.agilent.com/en/Bioanalyzer-DNA-RNA-Kits/RNA-Analysis-Kits/?cid=AG-PT-105&tabId=AG-PR-1172). Effect of various doses of LPS (nM) on in vitro RNAP II [mRNA transcripts coding for heterogeneous nuclear RNA (Alu) or for protein neurofilament light (NFL, GFAP)] activities in isolated human neocortical nuclei using Alu, NFL, or GFAP probes and expressed as a mean of control values ± one standard deviation (SD); n, number of individual run-on transcription experiments; Alu = Alu repetitive element; NFL, neurofilament light chain (neuron-specific marker); GFAP, glial fibrillary acidic protein (glial specific marker); LPS association with neuronal nuclei may block mRNA trafficking through nuclear pores and/or provide a biophysical barrier to restrict mRNA exit from the nucleus generating a mRNA-mediated down-regulation in gene expression as is widely observed in AD brain (Colangelo et al., 2002; Ginsberg et al., 2012; Garcia-Esparcia et al., 2017; Itoh and Voskuhl, 2017).