scholarly journals Association of complement receptor 1 gene polymorphisms with cognitive function

2018 ◽  
Vol 50 (2) ◽  
pp. 102-103
Author(s):  
L. E. Zijlstra ◽  
J. W. Jukema ◽  
S. P. Mooijaart ◽  
M. A. de Vries ◽  
D. J. Stott ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Gene Polymorphisms ◽  
The Elderly ◽  
Genomic Region ◽  
Chromosome 1 ◽  
Complement Receptor ◽  
Nucleotide Polymorphisms ◽  
Complement Receptor 1

Previous evidence suggest involvement of the complement receptor 1 (CR1) in development of Alzheimer’s disease. We investigated the association of CR1 gene polymorphisms with cognitive function in older subjects. Single nucleotide polymorphisms (SNPs) within the CR1 region on chromosome 1 ( n = 73) were assessed in 5,244 participants in the PROspective Study of Pravastatin in the Elderly at Risk (51.9% female, mean age 75.3 yr). Linear regression, adjusted for age, sex, country, and use of pravastatin, was used to assess the association between the SNPs and cognitive function. All 73 SNPs within the genomic region of the CR1 gene on chromosome 1 were extracted. Eighteen were independent, according to a relatively stringent R2 threshold of >0.8 with LDlink. Twelve of the 18 investigated CR1 SNPs were significantly associated with a decline in cognitive function (all P < 0.05). These data indicate that genetic variation within the CR1 gene is associated not only with Alzheimer’s disease, but also with general cognitive function during late life.

Alzheimer's disease risk factor complement receptor 1 is associated with depression

2012 ◽  
Vol 510 (1) ◽  
pp. 6-9 ◽  
Author(s):  
Gillian Hamilton ◽  
Kathryn L. Evans ◽  
Donald J. MacIntyre ◽  
Ian J. Deary ◽  
Anna Dominiczak ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Complement Receptor ◽  
Disease Risk Factor ◽  
Complement Receptor 1

Complement receptor 1 coding variant p.Ser1610Thr in Alzheimer's disease and related endophenotypes

2013 ◽  
Vol 34 (9) ◽  
pp. 2235.e1-2235.e6 ◽  
Author(s):  
Caroline Van Cauwenberghe ◽  
Karolien Bettens ◽  
Sebastiaan Engelborghs ◽  
Mathieu Vandenbulcke ◽  
Jasper Van Dongen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement Receptor ◽  
Complement Receptor 1

scholarly journals Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: Polymorphisms, structure, and function of complement receptor 1

2018 ◽  
Vol 14 (11) ◽  
pp. 1438-1449 ◽  
Author(s):  
Jenny U. Johansson ◽  
William D. Brubaker ◽  
Harold Javitz ◽  
Andrew W. Bergen ◽  
Denise Nishita ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Structure And Function ◽  
Complement Receptor ◽  
Amyloid Β Peptide ◽  
Complement Receptor 1 ◽  
And Function

scholarly journals Complement receptor 1 gene (CR1) intragenic duplication and risk of Alzheimer’s disease

2018 ◽  
Vol 137 (4) ◽  
pp. 305-314 ◽  
Author(s):  
Ezgi Kucukkilic ◽  
◽  
Keeley Brookes ◽  
Imelda Barber ◽  
Tamar Guetta-Baranes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement Receptor ◽  
Complement Receptor 1 ◽  
Intragenic Duplication

Complement receptor 1 (CR1) and Alzheimer's disease

Immunobiology ◽  
2012 ◽  
Vol 217 (2) ◽  
pp. 244-250 ◽  
Author(s):  
Helen Crehan ◽  
Patrick Holton ◽  
Selina Wray ◽  
Jennifer Pocock ◽  
Rita Guerreiro ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement Receptor ◽  
Complement Receptor 1

scholarly journals Short-term resistance exercise inhibits neuroinflammation and attenuates neuropathological changes in 3xTg Alzheimer’s disease mice

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Yan Liu ◽  
John Man Tak Chu ◽  
Tim Yan ◽  
Yan Zhang ◽  
Ying Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Resistance Training ◽  
Resistance Exercise ◽  
The Elderly ◽  
Short Term ◽  
Neuroprotective Effects ◽  
Beneficial Effects

Abstract Background Both human and animal studies have shown beneficial effects of physical exercise on brain health but most tend to be based on aerobic rather than resistance type regimes. Resistance exercise has the advantage of improving both muscular and cardiovascular function, both of which can benefit the frail and the elderly. However, the neuroprotective effects of resistance training in cognitive impairment are not well characterized. Methods We evaluated whether short-term resistant training could improve cognitive function and pathological changes in mice with pre-existing cognitive impairment. Nine-month-old 3xTg mouse underwent a resistance training protocol of climbing up a 1-m ladder with a progressively heavier weight loading. Results Compared with sedentary counterparts, resistance training improved cognitive performance and reduced neuropathological and neuroinflammatory changes in the frontal cortex and hippocampus of mice. In line with these results, inhibition of pro-inflammatory intracellular pathways was also demonstrated. Conclusions Short-term resistance training improved cognitive function in 3xTg mice, and conferred beneficial effects on neuroinflammation, amyloid and tau pathology, as well as synaptic plasticity. Resistance training may represent an alternative exercise strategy for delaying disease progression in Alzheimer’s disease.

scholarly journals Multi-Modal Data Analysis for Alzheimer's Disease Diagnosis: An Ensemble Model Using Imagery and Genetic Features

2021 ◽  
Author(s):  
Qi Ying ◽  
Xin Xing ◽  
Gongbo Liang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genome Wide Association Study ◽  
Model Performance ◽  
Brain Magnetic Resonance Imaging ◽  
The Elderly ◽  
Disease Diagnosis ◽  
Future Research ◽  
Nucleotide Polymorphisms ◽  
Snp Data

Alzheimer's disease (AD) is a devastating neurological disorder primarily affecting the elderly. An estimated 6.2 million Americans age 65 and older are suffering from Alzheimer's dementia today. Brain magnetic resonance imaging (MRI) is widely used for the clinical diagnosis of AD. In the meanwhile, medical researchers have identified 40 risk locus using single-nucleotide polymorphisms (SNPs) information from Genome-wide association study (GWAS) in the past decades. However, existing studies usually treat MRI and GWAS separately. For instance, convolutional neural networks are often trained using MRI for AD diagnosis. GWAS and SNPs are frequently used to identify genomic traits. In this study, we propose a multi-modal AD diagnosis neural network that uses both MRIs and SNPs. The proposed method demonstrates a novel way to use GWAS findings by directly including SNPs in predictive models. We test the proposed methods on the Alzheimer's Disease Neuroimaging Initiative dataset. The evaluation results show that the proposed method improves the model performance on AD diagnosis and achieves 93.5% AUC and 96.1% AP, respectively, when patients have both MRI and SNP data. We believe this work brings exciting new insights to GWAS applications and sheds light on future research directions.

scholarly journals Inherited and Acquired Decrease in Complement Receptor 1 (CR1) Density on Red Blood Cells Associated with High Levels of Soluble CR1 in Alzheimer’s Disease

2018 ◽  
Vol 19 (8) ◽  
pp. 2175 ◽  
Author(s):  
Rachid Mahmoudi ◽  
Sarah Feldman ◽  
Aymric Kisserli ◽  
Valérie Duret ◽  
Thierry Tabary ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement Receptor ◽  
Low Density ◽  
Amyloid Deposits ◽  
Length Polymorphisms ◽  
Phenotype Data ◽  
Data Density ◽  
Hindiii Polymorphism ◽  
Complement Receptor 1

The complement receptor 1 (CR1) gene was shown to be involved in Alzheimer’s disease (AD). We previously showed that AD is associated with low density of the long CR1 isoform, CR1*2 (S). Here, we correlated phenotype data (CR1 density per erythrocyte (CR1/E), blood soluble CR1 (sCR1)) with genetic data (density/length polymorphisms) in AD patients and healthy controls. CR1/E was enumerated using flow cytometry, while sCR1 was quantified by ELISA. CR1 polymorphisms were assessed using restriction fragment length polymorphism (RFLP), pyrosequencing, and high-resolution melting PCR. In AD patients carrying the H allele (HindIII polymorphism) or the Q allele (Q981H polymorphism), CR1/E was significantly lower when compared with controls carrying the same alleles (p < 0.01), contrary to sCR1, which was significantly higher (p < 0.001). Using multivariate analysis, a reduction of 6.68 units in density was associated with an increase of 1% in methylation of CR1 (estimate −6.68; 95% confidence intervals (CIs) −12.37, −0.99; p = 0.02). Our data show that, in addition to inherited genetic factors, low density of CR1/E is also acquired. The involvement of CR1 in the pathogenesis of AD might be linked to insufficient clearance of amyloid deposits. These findings may open perspectives for new therapeutic strategies in AD.

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