IL-6, IL-8 and IL-10 polymorphisms may impact predisposition of Alzheimer’s disease: a meta-analysis

Yang, Rongmei; Duan, Jinfeng; Luo, Fugang; Tao, Pingyu; Hu, Chenling

doi:10.1007/s13760-020-01369-4

Cited by 8 publications

(5 citation statements)

References 19 publications

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“…Heatmaps showed a strong correlation between these hub genes and different immune factors. IL-10 single nucleotide polymorphisms were found to affect the susceptibility to AD pathology (Babić Leko et al, 2020 ; Yang et al, 2021 ). When stimulated by anti-inflammatory cytokines, macrophages are converted to the M2 phenotype.…”

Section: Discussionmentioning

confidence: 99%

Hub Genes, Diagnostic Model, and Predicted Drugs Related to Iron Metabolism in Alzheimer's Disease

Lai

Liu

et al. 2022

Front. Aging Neurosci.

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Alzheimer's disease (AD), the most common neurodegenerative disease, remains unclear in terms of its underlying causative genes and effective therapeutic approaches. Meanwhile, abnormalities in iron metabolism have been demonstrated in patients and mouse models with AD. Therefore, this study sought to find hub genes based on iron metabolism that can influence the diagnosis and treatment of AD. First, gene expression profiles were downloaded from the GEO database, including non-demented (ND) controls and AD samples. Fourteen iron metabolism-related gene sets were downloaded from the MSigDB database, yielding 520 iron metabolism-related genes. The final nine hub genes associated with iron metabolism and AD were obtained by differential analysis and WGCNA in brain tissue samples from GSE132903. GO analysis revealed that these genes were mainly involved in two major biological processes, autophagy and iron metabolism. Through stepwise regression and logistic regression analyses, we selected four of these genes to construct a diagnostic model of AD. The model was validated in blood samples from GSE63061 and GSE85426, and the AUC values showed that the model had a relatively good diagnostic performance. In addition, the immune cell infiltration of the samples and the correlation of different immune factors with these hub genes were further explored. The results suggested that these genes may also play an important role in immunity to AD. Finally, eight drugs targeting these nine hub genes were retrieved from the DrugBank database, some of which were shown to be useful for the treatment of AD or other concomitant conditions, such as insomnia and agitation. In conclusion, this model is expected to guide the diagnosis of patients with AD by detecting the expression of several genes in the blood. These hub genes may also assist in understanding the development and drug treatment of AD.

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Section: Discussionmentioning

confidence: 99%

Hub Genes, Diagnostic Model, and Predicted Drugs Related to Iron Metabolism in Alzheimer's Disease

Lai

Liu

et al. 2022

Front. Aging Neurosci.

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“…IL6 is also important in neuronal cell growth and differentiation [63]. Recently, rs1800796 in IL6 has been associated with increased AD risk in a meta-analysis [64]. Furthermore, multiple polymorphisms in gene coding for IL6 receptors (IL6R) were found in AD GWAS studies [65,66].…”

Section: Discussionmentioning

confidence: 99%

Systematic Search for Novel Circulating Biomarkers Associated with Extracellular Vesicles in Alzheimer’s Disease: Combining Literature Screening and Database Mining Approaches

Vogrinc

Goričar

Kunej

et al. 2021

JPM

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miRNAs play an important role in neurodegenerative diseases. Many miRNA-target gene interactions (MTI) have been experimentally confirmed and associated with Alzheimer’s disease (AD). miRNAs may also be contained within extracellular vesicles (EVs), mediators of cellular communication and a potential source of circulating biomarkers in body fluids. Therefore, EV-associated miRNAs (EV-miRNAs) in peripheral blood could support earlier and less invasive AD diagnostics. We aimed to prioritize EV-related miRNA with AD-related genes and to identify the most promising candidates for novel AD biomarkers. A list of unique EV-miRNAs from the literature was combined with a known set of AD risk genes and enriched for MTI. Additionally, miRNAs associated with the AD phenotype were combined with all known target genes in MTI enrichment. Expression in different sample types was analyzed to identify AD-associated miRNAs with the greatest potential as AD circulating biomarkers. Four common MTI were observed between EV-miRNAs and AD-associated miRNAs: hsa-miR-375–APH1B, hsa-miR-107–CDC42SE2, hsa-miR-375–CELF2, and hsa-miR-107–IL6. An additional 61 out of 169 unique miRNAs (36.1%) and seven out of 84 unique MTI (8.3%), observed in the body fluids of AD patients, were proposed as very strong AD-circulating biomarker candidates. Our analysis summarized several potential novel AD biomarkers, but further studies are needed to evaluate their potential in clinical practice.

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“…The inflammatory state induced by iron load regulates the synthesis of hepcidin, of which interleukin 6 (IL-6) is involved in the process of iron metabolism through hepcidin [ 126 ]. IL-6 is increased in the AD brain as a multifunctional cytokine, and high levels of IL-6 can cause memory impairment [ 139 ]. In contrast, regular physical exercise attenuates IL-6 expression in the brains of AD mice [ 140 ].…”

Section: Methodsmentioning

confidence: 99%

Brain metabolism in Alzheimer’s disease: biological mechanisms of exercise

Liu

Qin

et al. 2023

Transl Neurodegener

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Alzheimer’s disease (AD) is a major subtype of neurodegenerative dementia caused by long-term interactions and accumulation of multiple adverse factors, accompanied by dysregulation of numerous intracellular signaling and molecular pathways in the brain. At the cellular and molecular levels, the neuronal cellular milieu of the AD brain exhibits metabolic abnormalities, compromised bioenergetics, impaired lipid metabolism, and reduced overall metabolic capacity, which lead to abnormal neural network activity and impaired neuroplasticity, thus accelerating the formation of extracellular senile plaques and intracellular neurofibrillary tangles. The current absence of effective pharmacological therapies for AD points to the urgent need to investigate the benefits of non-pharmacological approaches such as physical exercise. Despite the evidence that regular physical activity can improve metabolic dysfunction in the AD state, inhibit different pathophysiological molecular pathways associated with AD, influence the pathological process of AD, and exert a protective effect, there is no clear consensus on the specific biological and molecular mechanisms underlying the advantages of physical exercise. Here, we review how physical exercise improves crucial molecular pathways and biological processes associated with metabolic disorders in AD, including glucose metabolism, lipid metabolism, Aβ metabolism and transport, iron metabolism and tau pathology. How metabolic states influence brain health is also presented. A better knowledge on the neurophysiological mechanisms by which exercise improves AD metabolism can contribute to the development of novel drugs and improvement of non-pharmacological interventions.

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IL-6, IL-8 and IL-10 polymorphisms may impact predisposition of Alzheimer’s disease: a meta-analysis

Cited by 8 publications

References 19 publications

Hub Genes, Diagnostic Model, and Predicted Drugs Related to Iron Metabolism in Alzheimer's Disease

Hub Genes, Diagnostic Model, and Predicted Drugs Related to Iron Metabolism in Alzheimer's Disease

Systematic Search for Novel Circulating Biomarkers Associated with Extracellular Vesicles in Alzheimer’s Disease: Combining Literature Screening and Database Mining Approaches

Brain metabolism in Alzheimer’s disease: biological mechanisms of exercise

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