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Article ; Online: Genome research in pre-dementia stages of Alzheimer's disease.

Moreno-Grau, Sonia / Ruiz, Agustín

Expert reviews in molecular medicine

2016 Volume 18, Page(s) e11

Abstract: Genetic characterization of individuals at risk of Alzheimer's disease (AD), i.e. people having amyloid deposits in the brain without symptoms, people suffering from subjective cognitive decline (SCD) or mild cognitive impairment (MCI), has spurred the ... ...

Abstract	Genetic characterization of individuals at risk of Alzheimer's disease (AD), i.e. people having amyloid deposits in the brain without symptoms, people suffering from subjective cognitive decline (SCD) or mild cognitive impairment (MCI), has spurred the interests of researchers. However, their pre-dementia genetic profile remains mostly unexplored. In this study, we reviewed the loci related to phenotypes of AD, MCI and SCD from literature and performed the first meta-analyses evaluating the role of apolipoprotein E (APOE) in the risk of conversion from a healthy status to MCI and SCD. For AD dementia risk, an increased number of loci have been identified; to date, 28 genes have been associated with Late Onset AD. In MCI syndrome, APOE is confirmed as a pheno-conversion factor leading from MCI to AD, and clusterin is a promising candidate. Additionally, our meta-analyses revealed APOE as genetic risk factor to convert from a healthy status to MCI [OR = 1.849 (1.587-2.153); P = 2.80 × 10-15] and to a lesser extent from healthy status to SCD [OR = 1.151 (1.015-1.304); P = 0.028]. Thus, we believe that genetic studies in longitudinal SCD and MCI series may provide new therapeutic targets and improve the existing knowledge of AD. This type of studies must be completed on healthy subjects to better understand the natural disease resistance to brain insults and neurodegeneration.
MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Alzheimer Disease/physiopathology ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Brain/physiopathology ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/physiopathology ; Dementia/diagnosis ; Dementia/genetics ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genomics/methods ; Humans ; Inheritance Patterns ; Phenotype ; Quantitative Trait Loci ; Risk Factors
Chemical Substances	Biomarkers
Language	English
Publishing date	2016-05-30
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/erm.2016.12
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Article: Mitochondrial DNA and Alzheimer’s disease: a first case–control study of the Tunisian population

Ben Salem, Nesrine / Boussetta, Sami / de Rojas, Itziar / Moreno-Grau, Sonia / Montrreal, Laura / Mokni, Narjes / Mahmoud, Imene / Younes, Samia / Daouassi, Nizar / Frih-Ayed, Mahbouba / Hammami, Afef / Ben Ammar Elgaaied, Amel / Ruiz, Agustín / Cherni, Lotfi

Molecular biology reports. 2022 Mar., v. 49, no. 3

2022

Abstract: BACKGROUND: Alzheimer’s disease (AD) is the most common neurodegenerative disorder in humans and presents a major health problem throughout the world. The etiology of AD is complex, and many factors are implicated, including mitochondria. Mitochondrial ... ...

Abstract	BACKGROUND: Alzheimer’s disease (AD) is the most common neurodegenerative disorder in humans and presents a major health problem throughout the world. The etiology of AD is complex, and many factors are implicated, including mitochondria. Mitochondrial alteration has been proposed as a possible cause of AD. Therefore, several studies have focused on finding an association between inherited mitochondrial DNA variants and AD onset. METHODS: In this study, we looked, for the first time, for a potential association between mitochondrial haplogroups or polymorphisms and AD in the Tunisian population. We also evaluated the distribution of the major genetic risk factor for AD, the apolipoprotein E epsilon 4 (APOE ε4), in this population. In total, 159 single-nucleotide polymorphisms (SNPs) of mitochondrial DNA haplogroups were genotyped in 254 individuals (58 patients and 196 controls). An additional genotyping of APOE ε4 was performed. RESULTS: No significant association between mitochondrial haplogroups and AD was found. However, two individual SNPs, A5656G (p = 0.03821, OR = 10.46) and A13759G (p = 0.03719, OR = 10.78), showed a significant association with AD. APOE 4 was confirmed as a risk factor for AD (p = 0.000014). CONCLUSION: Our findings may confirm the absence of a relation between mitochondrial haplogroups and AD and support the possible involvement of some inherited variants in the pathogenicity of AD.
Keywords	apolipoprotein E ; case-control studies ; etiology ; genotyping ; mitochondria ; mitochondrial DNA ; molecular biology ; neurodegenerative diseases ; pathogenicity ; risk factors
Language	English
Dates of publication	2022-03
Size	p. 1687-1700.
Publishing place	Springer Netherlands
Document type	Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-021-06978-7
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Article ; Online: Genetic architecture of neurodegenerative dementias.

Clarimon, Jordi / Moreno-Grau, Sonia / Cervera-Carles, Laura / Dols-Icardo, Oriol / Sánchez-Juan, Pascual / Ruiz, Agustín

Neuropharmacology

2020 Volume 168, Page(s) 108014

Abstract: Molecular genetics has been an invaluable tool to help understand the molecular basis of neurodegenerative dementias. In this review, we provide an overview of the genetic architecture underlying some of the most prevalent causes of dementia, including ... ...

Abstract	Molecular genetics has been an invaluable tool to help understand the molecular basis of neurodegenerative dementias. In this review, we provide an overview of the genetic architecture underlying some of the most prevalent causes of dementia, including Alzheimer's dementia, frontotemporal lobar degeneration, Lewy body dementia, and prion diseases. We also discuss the complexity of the human genome and how the novel technologies have revolutionized and accelerated the way we screen the variety of our DNA. Finally, we also provide some examples about how this genetic knowledge is being transferred into the clinic through personalized medicine. This article is part of the special issue entitled 'The Quest for Disease-Modifying Therapies for Neurodegenerative Disorders'.
MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Animals ; Dementia/diagnosis ; Dementia/genetics ; Frontotemporal Lobar Degeneration/diagnosis ; Frontotemporal Lobar Degeneration/genetics ; Genetic Testing/methods ; Genetic Testing/trends ; Humans ; Lewy Body Disease/diagnosis ; Lewy Body Disease/genetics ; Neurodegenerative Diseases/diagnosis ; Neurodegenerative Diseases/genetics ; Pharmacogenetics/methods ; Pharmacogenetics/trends ; Prion Diseases/diagnosis ; Prion Diseases/genetics
Language	English
Publishing date	2020-02-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2020.108014
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Article ; Online: Validating and automating learning of cardiometabolic polygenic risk scores from direct-to-consumer genetic and phenotypic data: implications for scaling precision health research.

Lopez-Pineda, Arturo / Vernekar, Manvi / Moreno-Grau, Sonia / Rojas-Muñoz, Agustin / Moatamed, Babak / Lee, Ming Ta Michael / Nava-Aguilar, Marco A / Gonzalez-Arroyo, Gilberto / Numakura, Kensuke / Matsuda, Yuta / Ioannidis, Alexander / Katsanis, Nicholas / Takano, Tomohiro / Bustamante, Carlos D

Human genomics

2022 Volume 16, Issue 1, Page(s) 37

Abstract: Introduction: A major challenge to enabling precision health at a global scale is the bias between those who enroll in state sponsored genomic research and those suffering from chronic disease. More than 30 million people have been genotyped by direct- ... ...

Abstract	Introduction: A major challenge to enabling precision health at a global scale is the bias between those who enroll in state sponsored genomic research and those suffering from chronic disease. More than 30 million people have been genotyped by direct-to-consumer (DTC) companies such as 23andMe, Ancestry DNA, and MyHeritage, providing a potential mechanism for democratizing access to medical interventions and thus catalyzing improvements in patient outcomes as the cost of data acquisition drops. However, much of these data are sequestered in the initial provider network, without the ability for the scientific community to either access or validate. Here, we present a novel geno-pheno platform that integrates heterogeneous data sources and applies learnings to common chronic disease conditions including Type 2 diabetes (T2D) and hypertension. Methods: We collected genotyped data from a novel DTC platform where participants upload their genotype data files and were invited to answer general health questionnaires regarding cardiometabolic traits over a period of 6 months. Quality control, imputation, and genome-wide association studies were performed on this dataset, and polygenic risk scores were built in a case-control setting using the BASIL algorithm. Results: We collected data on N = 4,550 (389 cases / 4,161 controls) who reported being affected or previously affected for T2D and N = 4,528 (1,027 cases / 3,501 controls) for hypertension. We identified 164 out of 272 variants showing identical effect direction to previously reported genome-significant findings in Europeans. Performance metric of the PRS models was AUC = 0.68, which is comparable to previously published PRS models obtained with larger datasets including clinical biomarkers. Discussion: DTC platforms have the potential of inverting research models of genome sequencing and phenotypic data acquisition. Quality control (QC) mechanisms proved to successfully enable traditional GWAS and PRS analyses. The direct participation of individuals has shown the potential to generate rich datasets enabling the creation of PRS cardiometabolic models. More importantly, federated learning of PRS from reuse of DTC data provides a mechanism for scaling precision health care delivery beyond the small number of countries who can afford to finance these efforts directly. Conclusions: The genetics of T2D and hypertension have been studied extensively in controlled datasets, and various polygenic risk scores (PRS) have been developed. We developed predictive tools for both phenotypes trained with heterogeneous genotypic and phenotypic data generated outside of the clinical environment and show that our methods can recapitulate prior findings with fidelity. From these observations, we conclude that it is possible to leverage DTC genetic repositories to identify individuals at risk of debilitating diseases based on their unique genetic landscape so that informed, timely clinical interventions can be incorporated.
MeSH term(s)	Cardiovascular Diseases ; Diabetes Mellitus, Type 2/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Hypertension/genetics ; Multifactorial Inheritance/genetics ; Phenotype ; Precision Medicine ; Risk Factors
Language	English
Publishing date	2022-09-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2147618-4
ISSN	1479-7364 ; 1479-7364
ISSN (online)	1479-7364
ISSN	1479-7364
DOI	10.1186/s40246-022-00406-y
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Article ; Online: Mitochondrial DNA and Alzheimer's disease: a first case-control study of the Tunisian population.

Molecular biology reports

2021 Volume 49, Issue 3, Page(s) 1687–1700

Abstract: Background: Alzheimer's disease (AD) is the most common neurodegenerative disorder in humans and presents a major health problem throughout the world. The etiology of AD is complex, and many factors are implicated, including mitochondria. Mitochondrial ... ...

Abstract	Background: Alzheimer's disease (AD) is the most common neurodegenerative disorder in humans and presents a major health problem throughout the world. The etiology of AD is complex, and many factors are implicated, including mitochondria. Mitochondrial alteration has been proposed as a possible cause of AD. Therefore, several studies have focused on finding an association between inherited mitochondrial DNA variants and AD onset. Methods: In this study, we looked, for the first time, for a potential association between mitochondrial haplogroups or polymorphisms and AD in the Tunisian population. We also evaluated the distribution of the major genetic risk factor for AD, the apolipoprotein E epsilon 4 (APOE ε4), in this population. In total, 159 single-nucleotide polymorphisms (SNPs) of mitochondrial DNA haplogroups were genotyped in 254 individuals (58 patients and 196 controls). An additional genotyping of APOE ε4 was performed. Results: No significant association between mitochondrial haplogroups and AD was found. However, two individual SNPs, A5656G (p = 0.03821, OR = 10.46) and A13759G (p = 0.03719, OR = 10.78), showed a significant association with AD. APOE 4 was confirmed as a risk factor for AD (p = 0.000014). Conclusion: Our findings may confirm the absence of a relation between mitochondrial haplogroups and AD and support the possible involvement of some inherited variants in the pathogenicity of AD.
MeSH term(s)	Alleles ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; Case-Control Studies ; DNA, Mitochondrial/genetics ; Genetic Predisposition to Disease ; Genotype ; Humans ; Mitochondria/genetics ; Polymorphism, Single Nucleotide/genetics ; Tunisia/epidemiology
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E ; DNA, Mitochondrial
Language	English
Publishing date	2021-12-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-021-06978-7
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Article ; Online: Author Correction: Interaction of neuropsychiatric symptoms with APOE ε4 and conversion to dementia in MCI patients in a Memory Clinic.

Valero, Sergi / Marquié, Marta / De Rojas, Itziar / Espinosa, Ana / Moreno-Grau, Sonia / Orellana, Adelina / Montrreal, Laura / Hernández, Isabel / Mauleón, Ana / Rosende-Roca, Maiteé / Alegret, Montse / Pérez-Cordón, Alba / Ortega, Gemma / Roberto, Natalia / Sanabria, Angela / Abdelnour, Carla / Gil, Silvia / Tartari, Juan Pablo / Vargas, Liliana /

Antonio, Ester Esteban-De / Benaque, Alba / Tárraga, Lluís / Boada, Mercè / Ruíz, Agustín

Scientific reports

2021 Volume 11, Issue 1, Page(s) 4762

Language	English
Publishing date	2021-02-22
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-84389-1
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Article ; Online: Genetic markers of lipid metabolism genes associated with low susceptibility to HCV infection.

Real, Luis Miguel / Macías, Juan / Rivero-Juárez, Antonio / Téllez, Francisco / Merino, Dolores / Moreno-Grau, Sonia / Orellana, Adelina / Gómez-Salgado, Juan / Sáez, María E / Frías, Mario / Corma-Gómez, Anaïs / Merchante, Nicolás / Ruiz, Agustín / Caruz, Antonio / Pineda, Juan A

Scientific reports

2019 Volume 9, Issue 1, Page(s) 9054

Abstract: Due to the relation between lipids and Hepatitis C virus (HCV) life-cycle, we aimed to explore the existence of single nucleotide polymorphisms (SNPs) associated with low susceptibility to HCV-infection within lipid metabolism genes. This was a case- ... ...

Abstract	Due to the relation between lipids and Hepatitis C virus (HCV) life-cycle, we aimed to explore the existence of single nucleotide polymorphisms (SNPs) associated with low susceptibility to HCV-infection within lipid metabolism genes. This was a case-control study in three phases: (I) allelic frequencies of 9 SNPs within 6 genes were compared in 404 HCV-infected patients and 801 population controls; (II) results were validated in 602 HCV-infected individuals and 1352 controls; (III) results were confirmed in 30 HCV-exposed uninfected (EU) individuals. In phase I, only the LDLRAP1-rs4075184-A allele was differentially distributed in patients and controls (358 of 808 alleles [44.3%] and 807 of 1602 alleles [50.3%], respectively) (p = 0.004). In phase II, the A allele frequency was 547 of 1204 alleles (45.4%) in patients and 1326 of 2704 alleles (49.0%) in controls (p = 0.037). This frequency in EU was 36 of 60 alleles (60%), which was higher than that observed in patients from phase I (p = 0.018) and phase II (p = 0.027). The LDLRAP1-mRNA expression was lower in AA carriers than in non-AA carriers (median [Q1-Q3]: 0.85 [0.17-1.75] relative-units [ru] versus 1.71 [1.00-2.73] ru; p = 0.041). Our results suggest that LDLRAP1-rs4075184-A allele is associated with lower susceptibility to HCV-infection and with reduced expression of LDLRAP1-mRNA.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adult ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Hepatitis C/genetics ; Humans ; Lipid Metabolism/genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide
Chemical Substances	Adaptor Proteins, Signal Transducing ; LDLRAP1 protein, human
Language	English
Publishing date	2019-06-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-45389-4
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Article ; Online: A genome-wide association study on low susceptibility to hepatitis C virus infection (GEHEP012 study).

Real, Luis M / Fernández-Fuertes, Marta / Sáez, María E / Rivero-Juárez, Antonio / Frías, Mario / Téllez, Francisco / Santos, Jesús / Merino, Dolores / Moreno-Grau, Sonia / Gómez-Salgado, Juan / González-Serna, Alejandro / Corma-Gómez, Anais / Ruiz, Agustín / Macías, Juan / Pineda, Juan A

Liver international : official journal of the International Association for the Study of the Liver

2019 Volume 39, Issue 10, Page(s) 1918–1926

Abstract: Background: A low proportion of individuals repeatedly exposed to the hepatitis C virus (HCV) remain uninfected. This condition could have a genetic basis but it is not known whether or not it is mainly driven by a high-penetrance common allele.: ... ...

Abstract	Background: A low proportion of individuals repeatedly exposed to the hepatitis C virus (HCV) remain uninfected. This condition could have a genetic basis but it is not known whether or not it is mainly driven by a high-penetrance common allele. Objective: To explore whether low susceptibility to HCV infection is mainly driven by a high-penetrance common allele. Methods: In this genome-wide association study (GWAS), a total of 804 HCV-seropositive individuals and 27 high-risk HCV-seronegative (HRSN) subjects were included. Plink and Magma software were used to carry out single nucleotide polymorphism (SNP)-based and gene-based association analyses respectively. Results: No SNP nor any gene was associated with low susceptibility to HCV infection after multiple testing correction. However, SNPs previously associated with this trait and allocated within the LDLR gene, rs5925 and rs688, were also associated with this condition in our study under a dominant model (24 out of 27 [88.9%] rs5925-C carriers in the HRSN group vs 560 of 804 [69.6%] rs5925-C carriers in the HCV-seropositive group, P = 0.031, odds ratio [OR] = 3.48; 95% confidence interval [CI] = 1.04-11.58; and 24 out of 27 [88.9%] rs688-T carriers in the HRSN group vs 556 of 804 [69.1%] rs688-T carriers in the HCV-seropositive group, P = 0.028, OR = 3.57, 95% CI = 1.65-11.96). Conclusions: Low susceptibility to HCV infection does not seem to be mainly driven by a high-penetrant common allele. By contrast, it seems a multifactorial trait where genes such as LDLR could be involved.
MeSH term(s)	Adult ; Alleles ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Hepacivirus ; Hepatitis C/genetics ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Receptors, LDL/genetics ; Spain
Chemical Substances	LDLR protein, human ; Receptors, LDL
Language	English
Publishing date	2019-07-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/liv.14177
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Article ; Online: Real-world response of COVID-19 patients in Mexico

Gonzalez-Arroyo, Gilberto / Gomez Garcia, Salvador / Gomez Garcia, Anel / Pacifuentes Orozco, Adan / Gonzalez Orozco, Jorge Gustavo / Garcia Arreola, Maricela / Lopez Lopez, Karla Guadalupe / Ortiz Castillo, Tonatihu / Or-Geva, Noga / Moreno-Grau, Sonia / Alvarez Aguilar, Cleto / Bustamante, Carlos D / Lopez Pineda, Arturo

medRxiv

Abstract: Currently in Mexico, the available clinical guidelines published for COVID-19 treatment recommend symptom treatment and home isolation for mild forms; and other medications for severe and acute forms. The effectiveness of how real-world treatment ... ...

Abstract	Currently in Mexico, the available clinical guidelines published for COVID-19 treatment recommend symptom treatment and home isolation for mild forms; and other medications for severe and acute forms. The effectiveness of how real-world treatment patterns impact mortality and recovery is still unknown. In this retrospective observational study, we investigated 5,575 medicated patients with COVID-19 treated at two Mexican states seen in the largest healthcare system in Mexico. A survival analysis was performed using death and discharge as primary and secondary outcomes (respectively). Machine learning models were built to predict mortality and discharge. The higher prevalence of obesity, diabetes, and heart disease comorbidities is consistent with Mexico9s epidemiological profile. Mortality occurs around 15-20 days from the start of symptoms. Antivirals in combination with antibiotics present lower survival rates, with patients undertaking neuraminidase inhibitors (NAIs) being the most affected. Our findings recommend against using specific treatment combinations with NAIs, and should help improve the country9s clinical guidelines.
Keywords	covid19
Language	English
Publishing date	2021-12-17
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2021.12.16.21267866
Database	COVID19

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Article ; Online: Interaction of neuropsychiatric symptoms with APOE ε4 and conversion to dementia in MCI patients in a Memory Clinic.

Valero, Sergi / Marquié, Marta / De Rojas, Itziar / Espinosa, Ana / Moreno-Grau, Sonia / Orellana, Adelina / Montrreal, Laura / Hernández, Isabel / Mauleón, Ana / Rosende-Roca, Maitée / Alegret, Montse / Pérez-Cordón, Alba / Ortega, Gemma / Roberto, Natalia / Sanabria, Angela / Abdelnour, Carla / Gil, Silvia / Tartari, Juan Pablo / Vargas, Liliana /

Esteban-De Antonio, Ester / Benaque, Alba / Tárraga, Lluís / Boada, Mercè / Ruíz, Agustín

Scientific reports

2020 Volume 10, Issue 1, Page(s) 20058

Abstract: To date, very few studies have been focused on the impact of the convergence of neuropsychiatric symptoms (NPS) and APOE ε4 on the conversion to dementia in patients with Mild Cognitive Impairment patients (MCI), and none has been based in a clinical ... ...

Abstract	To date, very few studies have been focused on the impact of the convergence of neuropsychiatric symptoms (NPS) and APOE ε4 on the conversion to dementia in patients with Mild Cognitive Impairment patients (MCI), and none has been based in a clinical setting. The objective of the study is to determine the predictive value of additive and multiplicative interactions of NPS and APOE ε4 status on the prediction of incident dementia among MCI patients monitored in a Memory Clinic. 1512 patients (aged 60 and older) with prevalent MCI were followed for a mean of 2 years. Neuropsychiatric symptoms were assessed at baseline using the Neuropsychiatric Inventory Questionnaire. Cox proportional hazards models were calculated. Additive interactions for depression, apathy, anxiety, agitation, appetite, or irritability and a positive ε4 carrier status were obtained, significantly increasing the hazard ratios of incident dementia (HR range 1.3-2.03). Synergistic interactions between NPS and APOE ε4 are identified among MCI patients when predicting incident dementia. The combination of the behavioral status and the genetic trait could be considered a useful strategy to identify the most vulnerable MCI patients to dementia conversion in a Memory Clinic.
MeSH term(s)	Aged ; Aged, 80 and over ; Apolipoprotein E4/genetics ; Cognitive Dysfunction/complications ; Dementia/etiology ; Dementia/pathology ; Female ; Heterozygote ; Humans ; Male ; Memory Disorders/etiology ; Memory Disorders/pathology ; Neuropsychological Tests ; Psychotic Disorders/physiopathology
Chemical Substances	Apolipoprotein E4
Language	English
Publishing date	2020-11-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-77023-z
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