Background: Many studies have reported on the role of statin therapy in dementia, but its efficacy remains controversial. We aimed to search for reliable and meaningful articles to assess the efficacy of statin therapy for dementia risk, cognitive items, and pathologic markers.Methods: Related literature for this study was published in the period from January 1, 1987 to January 1, 2018. Odds ratio (OR) and 95% confidence interval (95% CI) estimates were pooled in either fixed or random effects models.Results: A total of 23 relevant studies were included after the application of the search strategy. The pooled results showed that statin therapy would downregulate dementia risk according to an analysis of 1,314,431 dementia patients and 1,836,539 healthy controls (OR: 0.64, 95% CI: 0.50, 0.81). In addition, specific changes in mini-mental state examination (MMSE) score were observed in individuals with dementia with statin therapy (OR: 0.46, 95% CI: 0.17, 0.74). However, the results of this meta-analysis showed that statin therapy did not significantly modify the Alzheimer's Disease Assessment Scale (ADAS-cog) score (OR: −0.26, 95% CI: −1.13, 0.62). No significant association was found between statin therapy and activities of daily living performance (OR: −0.69, 95% CI: −4.12, 2.74). When investigating pathological markers, our results indicated a significant influence of statin therapy on plasma amyloid β 40 (Aβ 40

This paper was aimed to analyze the microRNA (miRNA) signatures in Alzheimer disease (AD) and find the significant expressions of miRNAs, their target genes, the functional enrichment analysis of the confirmed genes, and potential drug treatment. The miRNA expression information of the gene expression profile data was downloaded from the Gene Expression Omnibus database. The total data sample size is 1309, including 1021 AD samples and 288 normal samples. A total of 21 differentially expressed miRNAs were obtained, of which 16 (hsa-miR-6761-3p, hsa-miR-6747-3p, hsa-miR-6875-3p, hsa-miR-6754-3p, hsa-miR-6736-3p, hsa-miR-6762-3p, hsa-miR-6787-3p, hsa-miR-208a-5p, hsa-miR-6740-3p, hsa-miR-6778-3p, hsa-miR-595, hsa-miR-6753-3p, hsa-miR-4747-3p, hsa-miR-3646, hsa-miR-6716-3p and hsa-miR-4435) were up-regulated and 5 (hsa-miR-125a-3p, hsa-miR-22-3p, hsa-miR-24-3p, hsa-miR-6131 and hsa-miR-125b-1-3p) were down-regulated in AD. A total of 6 miRNAs (hsa-miR-595, hsa-miR-3646, hsa-miR-4435 hsa-miR-125a-3p, hsa-miR-22-3p and hsa-miR-24-3p) and 78 miRNA-disease-related gene sub-networks were predicted, and 116 ceRNA regulatory relationship pairs, and the ceRNA regulatory network were obtained. The results of enrichment analysis suggested that the main target pathways of several miRNAs differentially expressed in AD were mitogen-activated protein kinase signal pathway. According to the prediction results of Drug-Gene Interaction database 2.0, we obtained 53 pairs of drug-gene interaction, including 7 genes (PTGS2, EGFR, CALM1, PDE4D, FGFR2, HMGCR, cdk6) and 53 drugs. We hope our results are helpful to find a viable way to prevent, delay the onset, diagnose, and treat AD.

Background The complement component (3b/4b) receptor 1 gene (CR1) gene has been proved to affect the susceptibility of Alzheimer’s disease (AD) in different ethnic and districts groups. However, the effect of CR1 genetic variants on amyloid β (Aβ) metabolism of AD human is still unclear. Hence, the aim of this study was to investigate genetic influences of CR1 gene on Aβ metabolism. Methods All data of AD patients and normal controls (NC) were obtained from alzheimer’s disease neuroimaging initiative database (ADNI) database. In order to assess the effect of each single nucleotide polymorphism (SNP) of CR1 on Aβ metabolism, the PLINK software was used to conduct the quality control procedures to enroll appropriate SNPs. Moreover, the correlation between CR1 genotypes and Aβ metabolism in all participants were estimated with multiple linear regression models. Results After quality control procedures, a total of 329 samples and 83 SNPs were enrolled in our study. Moreover, our results identified five SNPs (rs10494884, rs11118322, rs1323721, rs17259045 and rs41308433), which were linked to Aβ accumulation in brain. In further analyses, rs17259045 was found to decrease Aβ accumulation among AD patients. Additionally, our study revealed the genetic variants in rs12567945 could increase CSF Aβ42 in NC population. Conclusions Our study had revealed several novel SNPs in CR1 genes which might be involved in the progression of AD via regulating Aβ accumulation. These findings will provide a new basis for the diagnosis and treatment AD.

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BackgroundAlzheimer's disease (AD) is an increasingly common type of dementia that presents a heavy economic and social burden. Apolipoprotein E (APOE) is a strong risk factor for AD. Here, we explored alterations in grey matter structure and networks in AD, as well as the effects of the ApoE ε 4 allele on neuroimaging regions based on structural magnetic resonance imaging (sMRI).MethodsPatients with AD and healthy controls who visited the Department of Neurology, the Second Affiliated Hospital of Nanjing Medical University, from July 2020 to March 2021 were enrolled and grouped according to ApoE ε 4 allele carrying status. All subjects underwent an sMRI scan. Grey matter volume (GMV) and cortical thickness were calculated using voxel-based morphological analysis, and structural networks were constructed based on graph theory analysis to compare differences between AD and normal controls.Results(1) Compared with the control group, the volumes of grey matter in the bilateral inferior temporal gyrus, right middle temporal gyrus, right inferior parietal lobule, right limbic lobe, right frontal lobe, left anterior cingulate gyrus, and bilateral olfactory cortex of patients with AD were significantly decreased. GMV was moderately correlated with MMSE scores in patients with AD and in controls. (2) Compared with the controls, the cortical thickness in patients with AD was significantly reduced in the left lateral occipital lobe, inferior parietal lobe, orbitofrontal region, precuneus, superior parietal gyrus, right precentral gyrus, middle temporal gyrus, pars opercularis gyrus, insular gyrus, superior marginal gyrus, bilateral fusiform gyrus, and superior frontal gyrus. The normal aging population having the ApoE ε 4(+) gene has more pronounced temporal lobe atrophy than non-carriers. (3) In terms of the global properties of the network, ApoE ε 4(+) AD shows a more random topology than ApoE ε 4(-) AD. In terms of local properties, there were significant differences between the AD and control groups in these areas, including the right bank, right temporalis pole, bilateral middle temporal gyrus, right transverse temporal gyrus, left postcentral gyrus, and left parahippocampal gyrus.ConclusionThere were significant differences in the morphological and structural covariate networks between patients with AD and healthy controls. The ApoE ε 4 allele has important effects on neuroimaging and cognitive function.

Background: Alzheimer’s disease (AD) is an increasingly common type of dementia. Apolipoprotein E (APOE) gene is a strong risk factor for AD. Objective: Here, we explored alterations in grey matter structure (GMV) and networks in AD, as well as the effects of the APOE ɛ4 allele on neuroimaging regions based on structural magnetic resonance imaging (sMRI). Methods: All subjects underwent an sMRI scan. GMV and cortical thickness were calculated using voxel-based morphological analysis, and structural networks were constructed based on graph theory analysis to compare differences between AD and normal controls. Results: The volumes of grey matter in the bilateral inferior temporal gyrus, right middle temporal gyrus, right inferior parietal lobule, right limbic lobe, right frontal lobe, left anterior cingulate gyrus, and bilateral olfactory cortex of patients with AD were significantly decreased. The cortical thickness in patients with AD was significantly reduced in the left lateral occipital lobe, inferior parietal lobe, orbitofrontal region, precuneus, superior parietal gyrus, right precentral gyrus, middle temporal gyrus, pars opercularis gyrus, insular gyrus, superior marginal gyrus, bilateral fusiform gyrus, and superior frontal gyrus. In terms of local properties, there were significant differences between the AD and control groups in these areas, including the right bank, right temporalis pole, bilateral middle temporal gyrus, right transverse temporal gyrus, left postcentral gyrus, and left parahippocampal gyrus. Conclusion: There were significant differences in the morphological and structural covariate networks between AD patients and healthy controls under APOE ɛ4 allele effects.

Background Complement component (3b/4b) receptor 1 (CR1) is an interesting candidate gene which has a close connection with Alzheimer's disease, and its polymorphisms have been reported to link to the lateonset Alzheimer's disease (LOAD) susceptibility. However, the findings of these related studies are inconsistent. Objective To explore the effect of CR1 genetic variants in LOAD susceptibility. MethodsWe searched relevant studies for the period up to 1 November 2020. And odds ratios (ORs) and their 95% confidence intervals (CIs) were utilized to assess the strength of the association. In addition, we carried out a case-control association study to assess their genetic association. ResultsFinally, a total of 30 articles with 30108 LOAD cases and 37895 controls were included. Significant allele frequency between LOAD patients and controls was observed in rs3818361 and rs6656401 (rs3818361,