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Article ; Online: Step by step: towards a better understanding of the genetic architecture of Alzheimer's disease.

Lambert, Jean-Charles / Ramirez, Alfredo / Grenier-Boley, Benjamin / Bellenguez, Céline

2023 Volume 28, Issue 7, Page(s) 2716–2727

Abstract: Alzheimer's disease (AD) is considered to have a large genetic component. Our knowledge of this component has progressed over the last 10 years, thanks notably to the advent of genome-wide association studies and the establishment of large consortia that ...

Abstract	Alzheimer's disease (AD) is considered to have a large genetic component. Our knowledge of this component has progressed over the last 10 years, thanks notably to the advent of genome-wide association studies and the establishment of large consortia that make it possible to analyze hundreds of thousands of cases and controls. The characterization of dozens of chromosomal regions associated with the risk of developing AD and (in some loci) the causal genes responsible for the observed disease signal has confirmed the involvement of major pathophysiological pathways (such as amyloid precursor protein metabolism) and opened up new perspectives (such as the central role of microglia and inflammation). Furthermore, large-scale sequencing projects are starting to reveal the major impact of rare variants - even in genes like APOE - on the AD risk. This increasingly comprehensive knowledge is now being disseminated through translational research; in particular, the development of genetic risk/polygenic risk scores is helping to identify the subpopulations more at risk or less at risk of developing AD. Although it is difficult to assess the efforts still needed to comprehensively characterize the genetic component of AD, several lines of research can be improved or initiated. Ultimately, genetics (in combination with other biomarkers) might help to redefine the boundaries and relationships between various neurodegenerative diseases.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Genome-Wide Association Study ; Risk Factors ; Biomarkers ; Apolipoproteins E/genetics
Chemical Substances	Biomarkers ; Apolipoproteins E
Language	English
Publishing date	2023-05-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-023-02076-1
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Article ; Online: Genetics of Alzheimer's disease: where we are, and where we are going.

Bellenguez, Céline / Grenier-Boley, Benjamin / Lambert, Jean-Charles

Current opinion in neurobiology

2019 Volume 61, Page(s) 40–48

Abstract: Alzheimer's disease (AD) has a very strong genetic component, whose characterization has become an essential part of efforts to understand the pathophysiological processes of the disease. Thanks to the systematic use of high-throughput approaches over ... ...

Abstract	Alzheimer's disease (AD) has a very strong genetic component, whose characterization has become an essential part of efforts to understand the pathophysiological processes of the disease. Thanks to the systematic use of high-throughput approaches over the last 10 years, more than 40 genes/loci have been linked to the AD risk. Although some of these signals are likely to be false positives, this genetic knowledge has shed new light on the pathogenesis of AD and, in particular, the major role of microglia. However, our knowledge of the genetics of AD is far from complete, and larger and more diverse genetic studies are required. Lastly, post-GWAS analyses will be needed to make sense of this genetic information without focusing too much on what we think we know about the disease.
MeSH term(s)	Alzheimer Disease ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Microglia
Language	English
Publishing date	2019-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2019.11.024
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Article ; Online: Modifications of the endosomal compartment in fibroblasts from sporadic Alzheimer's disease patients are associated with cognitive impairment.

Xicota, Laura / Lagarde, Julien / Eysert, Fanny / Grenier-Boley, Benjamin / Rivals, Isabelle / Botté, Alexandra / Forlani, Sylvie / Landron, Sophie / Gautier, Clément / Gabriel, Cecilia / Bottlaender, Michel / Lambert, Jean-Charles / Chami, Mounia / Sarazin, Marie / Potier, Marie-Claude

Translational psychiatry

2023 Volume 13, Issue 1, Page(s) 54

Abstract: Morphological alterations of the endosomal compartment have been widely described in post-mortem brains from Alzheimer's disease (AD) patients and subjects with Down syndrome (DS) who are at high risk for AD. Immunostaining with antibodies against ... ...

Abstract	Morphological alterations of the endosomal compartment have been widely described in post-mortem brains from Alzheimer's disease (AD) patients and subjects with Down syndrome (DS) who are at high risk for AD. Immunostaining with antibodies against endosomal markers such as Early Endosome Antigen 1 (EEA1) revealed increased size of EEA1-positive puncta. In DS, peripheral cells such as peripheral blood mononuclear cells (PBMCs) and fibroblasts, share similar phenotype even in the absence of AD. We previously found that PBMCs from AD patients have larger EEA1-positive puncta, correlating with brain amyloid load. Here we analysed the endosomal compartment of fibroblasts from a very well characterised cohort of AD patients (IMABio3) who underwent thorough clinical, imaging and biomarkers assessments. Twenty-one subjects were included (7 AD with mild cognitive impairment (AD-MCI), 7 AD with dementia (AD-D) and 7 controls) who had amyloid-PET at baseline (PiB) and neuropsychological tests at baseline and close to skin biopsy. Fibroblasts isolated from skin biopsies were immunostained with anti-EEA1 antibody and imaged using a spinning disk microscope. Endosomal compartment ultrastructure was also analysed by electron microscopy. All fibroblast lines were genotyped and their AD risk factors identified. Our results show a trend to an increased EEA1-positive puncta volume in fibroblasts from AD-D as compared to controls (p.adj = 0.12) and reveal enhanced endosome area in fibroblasts from AD-MCI and AD-AD versus controls. Larger puncta size correlated with PiB retention in different brain areas and with worse cognitive scores at the time of biopsy as well as faster decline from baseline to the time of biopsy. Finally, we identified three genetic risk factors for AD (ABCA1, COX7C and MYO15A) that were associated with larger EEA1 puncta volume. In conclusion, the endosomal compartment in fibroblasts could be used as cellular peripheral biomarker for both amyloid deposition and cognitive decline in AD patients.
MeSH term(s)	Humans ; Alzheimer Disease ; Amyloid ; Amyloid beta-Peptides ; Cognitive Dysfunction ; Endosomes/pathology ; Fibroblasts ; Leukocytes, Mononuclear ; Positron-Emission Tomography
Chemical Substances	Amyloid ; Amyloid beta-Peptides
Language	English
Publishing date	2023-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-023-02355-z
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Article ; Online: Genetically downregulated Interleukin-6 signalling is associated with a lower risk of frailty.

Mourtzi, Niki / Georgakis, Mariosk / Ntanasi, Eva / Hatzimanolis, Alexandros / Ramirez, Alfredo / Heilmann-Heimbach, Stephanie / Grenier-Boley, Benjamin / Lambert, Jeanc / Yannakoulia, Mary / Kosmidis, Mary / Dardiotis, Efthimios / Hadjigeorgiou, Giorgos / Sakka, Paraskevi / Scarmeas, Nikolaos

Age and ageing

2023 Volume 52, Issue 1

Abstract: Background: numerous studies point towards a critical role of Interleukin 6 (IL-6) pathway in frailty pathogenesis yet the causal relationship between the two remains elusive.: Methods: we selected genetic variants near the IL-6 receptor locus (IL-6R) ...

Abstract	Background: numerous studies point towards a critical role of Interleukin 6 (IL-6) pathway in frailty pathogenesis yet the causal relationship between the two remains elusive. Methods: we selected genetic variants near the IL-6 receptor locus (IL-6R) associated with reduced C-reactive protein (CRP) levels, a downstream effector of IL-6 pathway, and we used them as genetic proxies of IL-6 signalling downregulation. We then performed a two-sample Mendelian randomisation (MR) to investigate the association with frailty status, as defined by the Frailty Index (FI) in 11,171 individuals from the Hellenic Longitudinal Investigation of Ageing and Diet (HELIAD) study. MR analysis was repeated after excluding depression or cognition-related FI items as well as following age or sex stratification. Association with frailty was also examined using an alternative instrument, weighted on s-IL-6R levels. Replication was attempted in UK Biobank dataset. Results: genetic predisposition to IL-6 signalling downregulation, weighted on CRP levels, was associated with lower risk of frailty, inserted either as categorical (odds ratio [95% confidence interval] = 0.15 [-3.39, -0.40], P = 0.013) or continuous variable (beta [se] = -0.09 [0.003], P = 0.0009). Sensitivity analyses revealed similar estimates across different MR methods with no evidence for horizontal pleiotropy or heterogeneity. Results remained robust after exclusion of depression or cognition-related FI items and following sex or age stratification. Genetically increased s-IL-6R levels were negatively correlated with frailty and this finding remained significant in a meta-analysis of UK Biobank and HELIAD cohorts. Conclusion: our results support a potential causal effect of IL-6 signalling on frailty and further suggest that downregulation of IL-6 levels may reduce frailty risk.
MeSH term(s)	Humans ; Frailty/diagnosis ; Frailty/genetics ; Interleukin-6/genetics ; Longitudinal Studies ; Aging/genetics ; Mendelian Randomization Analysis/methods
Chemical Substances	Interleukin-6
Language	English
Publishing date	2023-12-15
Publishing country	England
Document type	Meta-Analysis ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186788-x
ISSN	1468-2834 ; 0002-0729
ISSN (online)	1468-2834
ISSN	0002-0729
DOI	10.1093/ageing/afac318
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Zs.A 877: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 448: Show issues

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Article ; Online: Primary brain cell infection by

Mouveaux, Thomas / Roger, Emmanuel / Gueye, Alioune / Eysert, Fanny / Huot, Ludovic / Grenier-Boley, Benjamin / Lambert, Jean-Charles / Gissot, Mathieu

Open biology

2021 Volume 11, Issue 10, Page(s) 210053

Abstract: Toxoplasma ... ...

Abstract	Toxoplasma gondii
MeSH term(s)	Animals ; Cells, Cultured ; Disease Models, Animal ; Fibroblasts/cytology ; Fibroblasts/parasitology ; Foreskin/cytology ; Foreskin/parasitology ; Gene Expression Profiling/methods ; Gene Regulatory Networks ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Mice ; Neurons/cytology ; Neurons/parasitology ; Primary Cell Culture ; Protozoan Proteins/genetics ; Rats ; Sequence Analysis, RNA ; Toxoplasma/genetics ; Toxoplasma/pathogenicity ; Toxoplasmosis, Cerebral/genetics ; Toxoplasmosis, Cerebral/pathology
Chemical Substances	Protozoan Proteins
Language	English
Publishing date	2021-10-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2630944-0
ISSN	2046-2441 ; 2046-2441
ISSN (online)	2046-2441
ISSN	2046-2441
DOI	10.1098/rsob.210053
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Article ; Online: Genetic propensity for cerebral amyloidosis and risk of mild cognitive impairment and Alzheimer's disease within a cognitive reserve framework.

Mourtzi, Niki / Charisis, Sokratis / Tsapanou, Angeliki / Ntanasi, Eva / Hatzimanolis, Alexandros / Ramirez, Alfredo / Heilmann-Heimbach, Stefanie / Grenier-Boley, Benjamin / Lambert, Jean-Charles / Yannakoulia, Mary / Kosmidis, Mary / Dardiotis, Efthimios / Hadjigeorgiou, Georgiios / Sakka, Paraskevi / Georgakis, Marios / Yaakov, Stern / Scarmeas, Nikolaos

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19, Issue 9, Page(s) 3794–3805

Abstract: Introduction: We constructed a polygenic risk score (PRS) for β-amyloid (PRSAβ42) to proxy AD pathology and investigated its association with incident Alzheimer's disease (AD)/amnestic mild cognitive impairment (aMCI) and the influence of cognitive ... ...

Abstract	Introduction: We constructed a polygenic risk score (PRS) for β-amyloid (PRSAβ42) to proxy AD pathology and investigated its association with incident Alzheimer's disease (AD)/amnestic mild cognitive impairment (aMCI) and the influence of cognitive reserve (CR), proxied by educational years, on the relationship between PRSAβ42 and AD/aMCI risk. Methods: A total of 618 cognitive-normal participants were followed-up for 2.92 years. The association of PRSAβ42 and CR with AD/aMCI incidence was examined with COX models. Then we examined the additive interaction between PRSAβ42 and CR and the CR effect across participants with different PRSAβ42 levels. Results: Higher PRSAβ42 and CR were associated with a 33.9% higher risk and 8.3% less risk for AD/aMCI, respectively. An additive interaction between PRSAβ42 and CR was observed. High CR was associated with 62.6% less risk of AD/aMCI incidence only in the high-PRSAβ42 group. Discussion: A super-additive effect of PRSAβ42 and CR on AD/aMCI risk was observed. CR influence was evident in participants with high PRSAβ42.
MeSH term(s)	Humans ; Alzheimer Disease/complications ; Cognitive Reserve ; Neuropsychological Tests ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/complications ; Amyloidosis
Language	English
Publishing date	2023-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.12980
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Zs.MO 540: Show issues

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Article ; Online: Vascular burden and genetic risk in association with cognitive performance and dementia in a population-based study.

Georgakis, Marios K / Ntanasi, Eva / Ramirez, Alfredo / Grenier-Boley, Benjamin / Lambert, Jean-Charles / Sakka, Paraskevi / Yannakoulia, Mary / Kosmidis, Mary H / Dardiotis, Efthimios / Hadjigeorgiou, Georgios M / Charissis, Sokratis / Mourtzi, Niki / Hatzimanolis, Alexandros / Scarmeas, Nikolaos

Cerebral circulation - cognition and behavior

2022 Volume 3, Page(s) 100145

Abstract: Background and purpose: Vascular risk factors may influence cognitive function and thus represent possible targets for preventive approaches against dementia. Yet it remains unknown, if they associate with cognition independently of the individual ... ...

Abstract	Background and purpose: Vascular risk factors may influence cognitive function and thus represent possible targets for preventive approaches against dementia. Yet it remains unknown, if they associate with cognition independently of the individual genetic risk for dementia. Methods: In a population-based study of 1172 community-dwelling individuals aged ≥65 years in Greece, we constructed a vascular burden score (VBS; based on presence of hypertension, diabetes, hyperlipidemia, heart disease, and cerebrovascular disease, range 0-5) and a polygenic risk score (PRS) for clinically-diagnosed Alzheimer's disease (AD) based on 23 genetic variants. We then explored in joint models the associations of the PRS for AD and VBS with global cognitive performance, cognitive performance across multiple cognitive domains, and odds of dementia. Results: The mean age of study participants was 73.9 ± 5.2 years (57.1% females). Both the PRS for AD and VBS were associated with worse global cognitive performance (beta per-SD-increment in PRS: -0.06, 95%CI: -0.10 to -0.02, beta per-point-increment in VBS: -0.05, 95%CI: -0.09 to -0.02), worse performance across individual cognitive domains (memory, executive function, attention, language, visuospatial ability), and higher odds of dementia (OR per-SD increment in PRS: 1.56, 95%CI: 1.17-2.09, OR per-point increment in VBS: 1.38, 95%CI: 1.05-1.81). There was no evidence of an interaction between the two scores. Higher VBS was associated with worse cognitive performance equally across tertiles of the PRS for AD, even among individuals at the highest tertile. Conclusions: Both genetic risk and vascular burden are independently and additively associated with worse cognitive performance and higher odds of dementia.
Language	English
Publishing date	2022-05-05
Publishing country	Netherlands
Document type	Journal Article
ISSN	2666-2450
ISSN (online)	2666-2450
DOI	10.1016/j.cccb.2022.100145
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Article ; Online: Association of

Xicota, Laura / Gyorgy, Beata / Grenier-Boley, Benjamin / Lecoeur, Alexandre / Fontaine, Gaëlle / Danjou, Fabrice / Gonzalez, Jorge Samper / Colliot, Olivier / Amouyel, Philippe / Martin, Garance / Levy, Marcel / Villain, Nicolas / Habert, Marie-Odile / Dubois, Bruno / Lambert, Jean-Charles / Potier, Marie-Claude

Neurology

2022 Volume 99, Issue 5, Page(s) e462–e475

Abstract: Background and objectives: Brain amyloid deposition, a major risk factor for Alzheimer disease (AD), is currently estimated by measuring CSF or plasma amyloid peptide levels or by PET imaging. Assessing genetic risks relating to amyloid deposition ... ...

Abstract	Background and objectives: Brain amyloid deposition, a major risk factor for Alzheimer disease (AD), is currently estimated by measuring CSF or plasma amyloid peptide levels or by PET imaging. Assessing genetic risks relating to amyloid deposition before any accumulation has occurred would allow for earlier intervention in persons at increased risk for developing AD. Previous work linking amyloid burden and genetic risk relied almost exclusively on Methods: We included 291 asymptomatic older participants from the INveStIGation of AlzHeimer's PredicTors (INSIGHT pre-AD) cohort who underwent amyloid imaging, including 83 amyloid-positive (+) participants. We used an Alzheimer's (A) PRS composed of 33 AD risk variants excluding Results: A-PRS was not significantly associated with amyloid burden in the INSIGHT or ADNI cohorts with or without correction for the Discussion: PRSs relying on AD genetic risk factors excluding
MeSH term(s)	Aged ; Humans ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid/metabolism ; Amyloid beta-Peptides/metabolism ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; Brain/diagnostic imaging ; Brain/metabolism ; Genetic Risk Score
Chemical Substances	Amyloid ; Amyloid beta-Peptides ; Apolipoprotein E4 ; Apolipoproteins E ; ApoE protein, human
Language	English
Publishing date	2022-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000200544
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Article ; Online: miRNA-dependent target regulation: functional characterization of single-nucleotide polymorphisms identified in genome-wide association studies of Alzheimer's disease.

Delay, Charlotte / Grenier-Boley, Benjamin / Amouyel, Philippe / Dumont, Julie / Lambert, Jean-Charles

Alzheimer's research & therapy

2016 Volume 8, Issue 1, Page(s) 20

Abstract: Background: A growing body of evidence suggests that microRNAs (miRNAs) are involved in Alzheimer's disease (AD) and that some disease-associated genetic variants are located within miRNA binding sites. In the present study, we sought to characterize ... ...

Abstract	Background: A growing body of evidence suggests that microRNAs (miRNAs) are involved in Alzheimer's disease (AD) and that some disease-associated genetic variants are located within miRNA binding sites. In the present study, we sought to characterize functional polymorphisms in miRNA target sites within the loci defined in earlier genome-wide association studies (GWAS). The main objectives of this study were to (1) facilitate the identification of the gene or genes responsible for the GWAS signal within a locus of interest and (2) determine how functional polymorphisms might be involved in the AD process (e.g., by affecting miRNA-mediated variations in gene expression). Methods: Stringent in silico analyses were developed to select potential polymorphisms susceptible to impairment of miRNA-mediated repression, and subsequent functional assays were performed in HeLa and HEK293 cells. Results: Two polymorphisms were identified and further analyzed in vitro. The AD-associated rs7143400-T allele (located in 3' untranslated region [3'-UTR] of FERMT2) cotransfected with miR-4504 resulted in lower protein levels relative to the rs7143400-G allele cotransfected with the same miRNA. The AD-associated rs9909-C allele in the 3'-UTR of NUP160 abolished the miR-1185-1-3p-regulated expression observed for the rs9909-G allele. Conclusions: When considered in conjunction with the findings of previous association studies, our results suggest that decreased expression of FERMT2 might be a risk factor in the etiopathology of AD, whereas increased expression of NUP160 might protect against the disease. Our data therefore provide new insights into AD by highlighting two new proteins putatively involved in the disease process.
MeSH term(s)	3' Untranslated Regions ; Alzheimer Disease/genetics ; Binding Sites ; Computer Simulation ; Gene Expression Regulation ; Genome-Wide Association Study ; HEK293 Cells ; HeLa Cells ; Humans ; MicroRNAs/genetics ; Polymorphism, Single Nucleotide
Chemical Substances	3' Untranslated Regions ; MicroRNAs
Language	English
Publishing date	2016-05-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-016-0186-x
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Article: Association of the Polygenic Risk Score With the Probability of Prodromal Parkinson's Disease in Older Adults.

Maraki, Maria I / Hatzimanolis, Alexandros / Mourtzi, Niki / Stefanis, Leonidas / Yannakoulia, Mary / Kosmidis, Mary H / Dardiotis, Efthimios / Hadjigeorgiou, Georgios M / Sakka, Paraskevi / Ramirez, Alfredo / Grenier-Boley, Benjamin / Lambert, Jean-Charles / Heilmann-Heimbach, Stefanie / Stamelou, Maria / Scarmeas, Nikolaos / Xiromerisiou, Georgia

Frontiers in molecular neuroscience

2021 Volume 14, Page(s) 739571

Abstract: Several studies have investigated the association of the Parkinson's disease (PD) polygenic risk score (PRS) with several aspects of well-established PD. We sought to evaluate the association of PRS with the prodromal stage of PD. We calculated PRS in a ... ...

Abstract	Several studies have investigated the association of the Parkinson's disease (PD) polygenic risk score (PRS) with several aspects of well-established PD. We sought to evaluate the association of PRS with the prodromal stage of PD. We calculated PRS in a longitudinal sample (
Language	English
Publishing date	2021-12-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2021.739571
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