Increased Glutaminyl Cyclase Expression in Peripheral Blood of Alzheimer's Disease Patients

2013 ◽  
Vol 34 (1) ◽  
pp. 263-271 ◽  
Author(s):  
Maria Teresa Valenti ◽  
Silvia Bolognin ◽  
Cristina Zanatta ◽  
Luca Donatelli ◽  
Giulio Innamorati ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Glutaminyl Cyclase

scholarly journals P4-264: Increased glutaminyl cyclase expression in peripheral blood of Alzheimer's disease patients

2012 ◽  
Vol 8 (4S_Part_20) ◽  
pp. S751-S751 ◽  
Author(s):  
Silvia Bolognin ◽  
Maria Teresa Valenti ◽  
Luca Dalle Carbonare
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Glutaminyl Cyclase

scholarly journals Association between methylation of BIN1 promoter in peripheral blood and preclinical Alzheimer’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hao Hu ◽  
Lan Tan ◽  
Yan-Lin Bi ◽  
Wei Xu ◽  
Lin Tan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Late Onset ◽  
Early Stage ◽  
Susceptibility Gene ◽  
Subjective Cognitive Decline ◽  
Preclinical Ad ◽  
T Tau ◽  
New Evidence

AbstractThe bridging integrator 1 (BIN1) gene is the second most important susceptibility gene for late-onset Alzheimer’s disease (LOAD) after apolipoprotein E (APOE) gene. To explore whether the BIN1 methylation in peripheral blood changed in the early stage of LOAD, we included 814 participants (484 cognitively normal participants [CN] and 330 participants with subjective cognitive decline [SCD]) from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) database. Then we tested associations of methylation of BIN1 promoter in peripheral blood with the susceptibility for preclinical AD or early changes of cerebrospinal fluid (CSF) AD-related biomarkers. Results showed that SCD participants with significant AD biological characteristics had lower methylation levels of BIN1 promoter, even after correcting for covariates. Hypomethylation of BIN1 promoter were associated with decreased CSF Aβ42 (p = 0.0008), as well as increased p-tau/Aβ42 (p = 0.0001) and t-tau/Aβ42 (p < 0.0001) in total participants. Subgroup analysis showed that the above associations only remained in the SCD subgroup. In addition, hypomethylation of BIN1 promoter was also accompanied by increased CSF p-tau (p = 0.0028) and t-tau (p = 0.0130) in the SCD subgroup, which was independent of CSF Aβ42. Finally, above associations were still significant after correcting single nucleotide polymorphic sites (SNPs) and interaction of APOE ɛ4 status. Our study is the first to find a robust association between hypomethylation of BIN1 promoter in peripheral blood and preclinical AD. This provides new evidence for the involvement of BIN1 in AD, and may contribute to the discovery of new therapeutic targets for AD.

scholarly journals Differential Expression of mRNAs in Peripheral Blood Related to Prodrome and Progression of Alzheimer’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Weishuang Xue ◽  
Jinwei Li ◽  
Kailei Fu ◽  
Weiyu Teng
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Bioinformatics Analysis ◽  
Gene Expression Omnibus ◽  
Venn Diagram ◽  
Ppi Network ◽  
Hub Genes ◽  
Protein Protein Interaction ◽  
Ppi Networks

Alzheimer’s disease (AD) is a chronic progressive neurodegenerative disease that affects the quality of life of elderly individuals, while the pathogenesis of AD is still unclear. Based on the bioinformatics analysis of differentially expressed genes (DEGs) in peripheral blood samples, we investigated genes related to mild cognitive impairment (MCI), AD, and late-stage AD that might be used for predicting the conversions. Methods. We obtained the DEGs in MCI, AD, and advanced AD patients from the Gene Expression Omnibus (GEO) database. A Venn diagram was used to identify the intersecting genes. Gene Ontology (GO) and Kyoto Gene and Genomic Encyclopedia (KEGG) were used to analyze the functions and pathways of the intersecting genes. Protein-protein interaction (PPI) networks were constructed to visualize the network of the proteins coded by the related genes. Hub genes were selected based on the PPI network. Results. Bioinformatics analysis indicated that there were 61 DEGs in both the MCI and AD groups and 27 the same DEGs among the three groups. Using GO and KEGG analyses, we found that these genes were related to the function of mitochondria and ribosome. Hub genes were determined by bioinformatics software based on the PPI network. Conclusions. Mitochondrial and ribosomal dysfunction in peripheral blood may be early signs in AD patients and related to the disease progression. The identified hub genes may provide the possibility for predicting AD progression or be the possible targets for treatments.

Innate phagocytosis by peripheral blood monocytes is altered in Alzheimer’s disease

2016 ◽  
Vol 132 (3) ◽  
pp. 377-389 ◽  
Author(s):  
Ben J. Gu ◽  
◽  
Xin Huang ◽  
Amber Ou ◽  
Alan Rembach ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes

Common Aging Signature in the Peripheral Blood of Vascular Dementia and Alzheimer’s Disease

2015 ◽  
Vol 53 (6) ◽  
pp. 3596-3605 ◽  
Author(s):  
Hongbo Luo ◽  
Guangchun Han ◽  
Jiajia Wang ◽  
Fan Zeng ◽  
Yuanming Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Peripheral Blood

scholarly journals Meta-Analysis of Peripheral Blood Apolipoprotein E Levels in Alzheimer’s Disease

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e89041 ◽  
Author(s):  
Chong Wang ◽  
Jin-Tai Yu ◽  
Hui-Fu Wang ◽  
Teng Jiang ◽  
Chen-Chen Tan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Peripheral Blood ◽  
Meta Analysis

P3-031: New mouse model to develop and test drugs against the human Glutaminyl Cyclase (hQC) for Alzheimer's disease research

2011 ◽  
Vol 7 ◽  
pp. S524-S524
Author(s):  
Annamaria Molnar ◽  
Stephan Kurat ◽  
Stephan Schilling ◽  
Stefanie Flunkert ◽  
Hans Demuth ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Glutaminyl Cyclase ◽  
Disease Research

Muscarinic Receptors Expression in the Peripheral Blood Cells Differentiate Dementia with Lewy Bodies from Alzheimer’s Disease

2021 ◽  
pp. 1-8
Author(s):  
Marcella Reale ◽  
Claudia Carrarini ◽  
Mirella Russo ◽  
Fedele Dono ◽  
Laura Ferri ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Dementia With Lewy Bodies ◽  
Mononuclear Cells ◽  
Lewy Bodies ◽  
Acetylcholinesterase Inhibitors ◽  
Operating Characteristics ◽  
Peripheral Blood Mononuclear

Background: Central nervous system disruption of cholinergic (ACh) signaling, which plays a major role in cognitive processes, is well documented in dementia with Lewy bodies (DLB) and Alzheimer’s disease (AD). The expression of muscarinic ACh receptors type 1 and 4 (CHRM1 and CHRM4) has been reported to be altered in the brain of DLB patients. Objective: We aim to assess the peripheral gene expression of CHRM1 and 4 in DLB as a possible marker as compared to AD and healthy control (HC) subjects. Methods: Peripheral blood mononuclear cells were collected from 21 DLB, 13 AD, and 8 HC matched subjects. RT-PCR was performed to estimate gene expression of CHRM1 and CHRM4. Results: Peripheral CHRM1 expression was higher and CHRM4 was lower in DLB and AD compared to HC, whereas both CHRM1 and CHRM4 levels were higher in AD compared to DLB patients. Receiver operating characteristics curves, with logistic regression analysis, showed that combining peripheral CHRM1 and CHRM4 levels, DLB and AD subjects were classified with an accuracy of 76.0%. Conclusion: Alterations of peripheral CHRM1 and CHRM4 was found in both AD and DLB patients as compared to HC. CHRM1 and CHRM4 gene expression resulted to be lower in DLB patients compared to AD. In the future, peripheral CHRM expression could be studied as a possible marker of neurodegenerative conditions associated with cholinergic deficit and a possible marker of response to acetylcholinesterase inhibitors.

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