Alzheimer’s disease (AD), characterized by memory loss, cognitive decline, and dementia, is a progressive neurodegenerative disease. Although the long noncoding RNAs (lncRNAs) have recently been identified to play a role in the pathogenesis of AD, the specific effects of lncRNAs in AD remain unclear. In present study, we have investigated the expression profiles of lncRNAs in hippocampal of intranasal LPS-mediated Alzheimer’s disease models in mice by microarray method. A total of 395 lncRNAs and 123 mRNAs was detected to express differently in AD models and controls (>2.0 folds,p<0.05). The microarray expression was validated by Quantitative Real-Time-PCR (qRT-PCR). The pathway analysis showed the mRNAs that correlated with lncRNAs were involved in inflammation, apoptosis, and nervous system related pathways. The lncRNA-TFs network analysis suggested the lncRNAs were mostly regulated by HMGA2, ONECUT2, FOXO1, and CDC5L. Additionally, lncRNA-target-TFs network analysis indicated the FOXL1, CDC5L, ONECUT2, and CDX1 to be the TFs most likely to regulate the production of these lncRNAs. This is the first study to investigate lncRNAs expression pattern in intranasal LPS-mediated Alzheimer’s disease model in mice. And these results may facilitate the understanding of the pathogenesis of AD targeting lncRNAs.

Objective: Although the relationship between apolipoprotein E (ApoE) gene polymorphisms and the risk of Parkinson disease (PD) has been established, the results were inconsistent and inconclusive. Methods: A comprehensive search examining the association between APOE polymorphisms and PD through PubMed, Embase, Chinese National Knowledge Infrastructure (CNKI), and Cochrane Library databases was performed without published year limited. Results: A total of 47 studies with 7533 cases and 14442 controls were included in present study. The results showed statistically significant association between risk factor ApoE ε4 allele and PD in Asian population (P = .003, odds ratio, OR [95% confidence interval, CI] = 1.43 [1.13,1.80]). Genotype ε2ε4 have significantly associated with PD in Asian population (P = .004, OR [95% CI] = 4.43 [1.62,12.10]). Genotype ε3ε4 was significantly associated with PD in Latin-American population (P = .01, OR [95% CI] = 1.44 [1.08,1.91]). In addition, the frequency of the genotype ε3ε4 is lower in PD group than that in the control group in Caucasian population, and the difference of genotype ε3ε4 is also statistically significant (P = .006, OR [95% CI] = 0.86 [0.77,0.96]). Although significant heterogeneity was observed among all studies, the results were shown to be stabilized by sensitive analysis. No publish bias was observed. Conclusions: This meta-analysis suggests that the APOE ε4, but no ε2, might be a risk factor for PD in Asian population. Furthermore, the genotype ε2ε4 may be a susceptible factor for PD in Asian population, and the genotype ε3ε4 may be a susceptible factor for PD in both Caucasian and Latin-American populations.

Alzheimer’s disease (AD) is acommon neurodegenerative disease in the aged population. Tripterygium glycoside (TG) has been reported to protect the nervous system. However, the effect of TG on AD is still unknown. We aimed to explore the effect of TG on AD. Thirty-two C57BL/6J mice were randomly selected and assigned to the normal control, AD model, AD+donepezil, and AD+TG groups. PC12 cells were assigned to the normal control, AD cell model, and AD+TG groups. The alterations in spatial memory and learning abilities of mice were measured by Morris water maze. Neuronal damage in mice was detected using Nissl staining. The expression levels of Aβ_25-35, p-Tau, and CD11b in brain tissues were detected using immunohistochemistry. The expression levels of IL-1β, TNF-α, NO, p-P38, P38, p-IκBα, Caspase1, COX2, and iNOS were measured using ELISAs, qRT–PCR, and western blotting.TG significantly improved the spatial memory and learning abilities of AD mice. Compared toAD model group, significantly lower expression levels of Aβ_25-35, p-Tau, and CD11b were observed in AD+TG group (p < 0.05). The neuron density significantly increased in AD+TG group (p < 0.05). Significantly lower expression levels of IL-1β, TNF-α, NO, caspase-1, COX2, iNOS, p-IκBα and p-P38 MAPK were detected in AD+TG group (p < 0.05). In summary, TG may exert aneuroprotective effect by suppressing the release of inflammatory factors and microglial activity and inhibiting the phosphorylation of IκBα and p38 MAPK. These findings may improve our understanding of the mechanism of TG intervention in AD.

The serotonin receptor gene (5-HT2A) has been reported to be a susceptible factor in behavioral and psychological symptoms of dementia (BPSD) in Alzheimer’s disease (AD). However, previous results were conflicting. We aim to investigate the association of 5-HT2A T102C with BPSD in AD using a meta-analysis. Studies were collected using PubMed, Web of Science, the Cochrane Library databases, Chinese National Knowledge Infrastructure (CNKI), and Embase. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess associations. Nine studies with 1899 AD patients with/without BPSD were included in this meta-analysis. The 102C and CC genotypes were associated with psychosis in AD (102C: p<0.00001, OR [95% CI] = 3.19 [2.12–4.79]; CC: p<0.00001, OR [95% CI] = 7.24 [3.60–14.59]). The TT genotype was significantly associated with hallucinations, aberrant motor behavior, and psychosis in AD (hallucinations: p=0.001, OR [95% CI] = 0.52 [0.36–0.77]; aberrant motor behavior: p=0.03, OR [95% CI] = 0.58 [0.35–0.95]; and psychosis: p=0.002, OR [95% CI] = 0.34 [0.17–0.67]). No association was observed between T102C alleles or genotypes and delusions, agitation/aggression, depression, and apathy (p>0.05). Thus, the 5HT2A T102C might be a susceptible factor for hallucinations, aberrant motor behavior, and psychosis in AD. The potential mechanism of this polymorphism in BPSD in AD requires further exploration.