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Article ; Online: Génétique de la schizophrénie - Le complément, facteur de risque ?

Campion, Dominique

2016 Volume 32, Issue 6-7, Page(s) 556–557

Title translation	Genetics of schizophrenia: is the complement component 4 a risk factor?.
MeSH term(s)	Adolescent ; Adult ; Complement C4/genetics ; Genetic Predisposition to Disease ; Humans ; Nerve Net/growth & development ; Nerve Net/physiology ; Neurogenesis/genetics ; Risk Factors ; Schizophrenia/genetics ; Young Adult
Chemical Substances	Complement C4
Language	French
Publishing date	2016-06
Publishing country	France
Document type	News
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20163206009
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Article ; Online: Moderate Overexpression of Tau in Drosophila Exacerbates Amyloid-β-Induced Neuronal Phenotypes and Correlates with Tau Oligomerization.

Miguel, Laetitia / Frebourg, Thierry / Campion, Dominique / Lecourtois, Magalie

Journal of Alzheimer's disease : JAD

2020 Volume 74, Issue 2, Page(s) 637–647

Abstract: Alzheimer's disease (AD) is neuropathologically defined by two key hallmarks: extracellular senile plaques composed primarily of amyloid-β (Aβ) peptide and intraneuronal neurofibrillary tangles, containing abnormally hyperphosphorylated tau protein. The ... ...

Abstract	Alzheimer's disease (AD) is neuropathologically defined by two key hallmarks: extracellular senile plaques composed primarily of amyloid-β (Aβ) peptide and intraneuronal neurofibrillary tangles, containing abnormally hyperphosphorylated tau protein. The tau protein is encoded by the MAPT gene. Recently, the H1 and H2 haplotypes of the MAPT gene were associated with AD risk. The minor MAPT H2 haplotype has been linked with a decreased risk of developing late-onset AD (LOAD). MAPT haplotypes show different levels of MAPT/Tau expression with H1 being ∼1.5-fold more expressed than H2, suggesting that MAPT expression level could be related to LOAD risk. In this study, we investigated whether this moderate difference in MAPT/Tau expression could influence Aβ-induced toxicity in vivo. We show that modest overexpression of tau protein in Drosophila exacerbates neuronal phenotypes in AβPP/BACE1 flies. The exacerbation of neuronal defects correlates with the accumulation of insoluble dTau oligomers, suggesting that the moderate difference in level of tau expression observed between H1 and H2 haplotypes could influence Aβ toxicity through the production of oligomeric tau insoluble species.
MeSH term(s)	Amyloid beta-Peptides/toxicity ; Animals ; Animals, Genetically Modified ; Drosophila ; Gene Expression ; Neurons/drug effects ; Neurons/metabolism ; Phenotype ; tau Proteins/biosynthesis ; tau Proteins/genetics
Chemical Substances	Amyloid beta-Peptides ; tau Proteins
Language	English
Publishing date	2020-02-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-190906
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Article ; Online: SORL1 genetic variants and Alzheimer disease risk: a literature review and meta-analysis of sequencing data.

Campion, Dominique / Charbonnier, Camille / Nicolas, Gaël

Acta neuropathologica

2019 Volume 138, Issue 2, Page(s) 173–186

Abstract: Massive parallel sequencing recently allowed the identification of three genes carrying a higher burden of rare, protein-truncating and missense predicted damaging variants in Alzheimer disease (AD) cases as compared to controls: TREM2, SORL1, and ABCA7. ...

Abstract	Massive parallel sequencing recently allowed the identification of three genes carrying a higher burden of rare, protein-truncating and missense predicted damaging variants in Alzheimer disease (AD) cases as compared to controls: TREM2, SORL1, and ABCA7. SORL1 encodes SorLA, a key protein involved in the processing of the amyloid-beta (Aβ) precursor protein (APP) and the secretion of the Aβ peptide, the aggregation of which triggers AD pathophysiology. Common SORL1 single nucleotide polymorphisms had originally been associated with AD with modest odds ratios (ORs). The association of AD with rare SORL1 coding variants has been demonstrated at the gene level by aggregating protein-truncating (PTV) and rare predicted damaging missense variants. In addition to the loss of SorLA function induced by PTVs, a few missense variants were studied in vitro, showing diverse degrees of decreased SorLA function and leading to increased Aβ secretion. However, the exact functional consequences of most of the missense variants remain to be determined as well as corresponding levels of AD risk. Hereby we review the evidence of the association of SORL1 common and rare variants with AD risk and conduct a meta-analysis of published data on SORL1 rare variants in five large sequencing studies. We observe a significant enrichment in PTVs with ORs of 12.29 (95% confidence interval = [4.22-35.78]) among all AD cases and 27.50 [7.38-102.42] among early-onset cases. Rare [minor allele frequency (MAF) < 1%] and ultra-rare (MAF < 10
MeSH term(s)	ATP-Binding Cassette Transporters/genetics ; Alzheimer Disease/genetics ; Apolipoprotein E4/genetics ; Case-Control Studies ; Codon/genetics ; Female ; Gene Frequency ; Genes, Dominant ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; LDL-Receptor Related Proteins/genetics ; Male ; Membrane Transport Proteins/genetics ; Mutation, Missense ; Pedigree ; Polymorphism, Single Nucleotide ; Protein Domains ; Risk ; Sequence Analysis, DNA ; Whole Genome Sequencing
Chemical Substances	ABCA7 protein, human ; ATP-Binding Cassette Transporters ; Apolipoprotein E4 ; Codon ; LDL-Receptor Related Proteins ; Membrane Transport Proteins ; SORL1 protein, human
Language	English
Publishing date	2019-03-25
Publishing country	Germany
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-019-01991-4
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Article: A Connected Network of Interacting Proteins Is Involved in Human-Tau Toxicity in

Feuillette, Sébastien / Charbonnier, Camille / Frebourg, Thierry / Campion, Dominique / Lecourtois, Magalie

Frontiers in neuroscience

2020 Volume 14, Page(s) 68

Abstract: Tauopathies are neurodegenerative diseases characterized by the presence of aggregates of abnormally phosphorylated Tau. Deciphering the pathophysiological mechanisms that lead from the alteration of Tau biology to neuronal death depends on the ... ...

Abstract	Tauopathies are neurodegenerative diseases characterized by the presence of aggregates of abnormally phosphorylated Tau. Deciphering the pathophysiological mechanisms that lead from the alteration of Tau biology to neuronal death depends on the identification of Tau cellular partners. Combining genetic and transcriptomic analyses in
Language	English
Publishing date	2020-02-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2020.00068
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Article ; Online: From Common to Rare Variants: The Genetic Component of Alzheimer Disease.

Nicolas, Gaël / Charbonnier, Camille / Campion, Dominique

Human heredity

2016 Volume 81, Issue 3, Page(s) 129–141

Abstract: Alzheimer disease (AD) is a remarkable example of genetic heterogeneity. Extremely rare variants in the APP, PSEN1, or PSEN2 genes, or duplications of the APP gene cause autosomal dominant forms, generally with complete penetrance by the age of 65 years. ...

Abstract	Alzheimer disease (AD) is a remarkable example of genetic heterogeneity. Extremely rare variants in the APP, PSEN1, or PSEN2 genes, or duplications of the APP gene cause autosomal dominant forms, generally with complete penetrance by the age of 65 years. Nonautosomal dominant forms are considered as a complex disorder with a high genetic component, whatever the age of onset. Although genetically heterogeneous, AD is defined by the same neuropathological criteria in all configurations. According to the amyloid cascade hypothesis, the Aβ peptide, which aggregates in AD brains, is a key player. APP, PSEN1, or PSEN2 gene mutations increase the production of more aggregation-prone forms of the Aβ peptide, triggering the pathological process. Several risk factors identified in association studies hit genes involved in Aβ production/secretion, aggregation, clearance, or toxicity. Among them, the APOE ε4 allele is a rare example of a common allele with a large effect size, the ORs ranging from 4 to 11-14 for heterozygous and homozygous carriers, respectively. In addition, genome-wide association studies have identified more than two dozen loci with a weak but significant association, the OR of the at-risk allele ranging from 1.08 to 1.30. Recently, the use of massive parallel sequencing has enabled the analysis of rare variants in a genome-wide manner. Two rare variants have been nominally associated with AD risk or protection (TREM2 p.R47H, MAF approximately 0.002, OR approximately 4 and APP p.A673T, MAF approximately 0.0005, OR approximately 0.2). Association analyses at the gene level identified rare loss-of-function and missense, predicted damaging, variants (MAF <0.01) in the SORL1 and ABCA7 genes associated with a moderate relative risk (OR approximately 5 and approximately 2.8, respectively). Although the latter analyses revealed association signals with moderately rare variants by collapsing them, the power to detect genes hit by extremely rare variants is still limited. An alternative approach is to consider the de novo paradigm, stating that de novo variants may contribute to AD genetics in sporadic patients. Here, we critically review AD genetics reports with a special focus on rare variants.
MeSH term(s)	Alleles ; Alzheimer Disease/genetics ; Amyloid beta-Peptides/metabolism ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Heterozygote ; Humans ; Membrane Glycoproteins/genetics ; Mutation ; Receptors, Immunologic/genetics
Chemical Substances	Amyloid beta-Peptides ; Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human
Language	English
Publishing date	2016
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2424-7
ISSN	1423-0062 ; 0001-5652
ISSN (online)	1423-0062
ISSN	0001-5652
DOI	10.1159/000452256
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Article ; Online: Copy number variations involving the microtubule-associated protein tau in human diseases.

Rovelet-Lecrux, Anne / Campion, Dominique

Biochemical Society transactions

2012 Volume 40, Issue 4, Page(s) 672–676

Abstract: Mutations of the MAPT (microtubule-associated protein tau) gene are associated with FTLD (frontotemporal lobar degeneration) with tau pathology. These mutations result in a decreased ability of tau to bind MTs (microtubules), an increased production of ... ...

Abstract	Mutations of the MAPT (microtubule-associated protein tau) gene are associated with FTLD (frontotemporal lobar degeneration) with tau pathology. These mutations result in a decreased ability of tau to bind MTs (microtubules), an increased production of tau with four MT-binding repeats or enhanced tau aggregation. In two FTLD patients, we recently described CNVs (copy number variations) affecting the MAPT gene, consisting of a partial deletion and a complete duplication of the gene. The partial deletion resulted in a truncated protein lacking the first MT-binding domain, which had a dramatic decrease in the binding to MTs but acquired the ability to bind MAP (microtubule-associated protein) 1-B. In this case, tauopathy probably resulted from both a loss of normal function and a gain of function by which truncated tau would sequester another MAP. In the other FTLD patient, the complete duplication might result in the overexpression of tau, which in the mouse model induces axonopathy and tau aggregates reminiscent of FTLD-tau pathology. Interestingly, the same rearrangement was also described in several children with mental retardation, autism spectrum disorders and dysmorphic features, as well as in a schizophrenic patient. Finally, complete deletions of the MAPT gene have been associated with mental retardation, hypotonia and facial dysmorphism.
MeSH term(s)	DNA Copy Number Variations/genetics ; Humans ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Schizophrenia/genetics ; Schizophrenia/metabolism ; tau Proteins/genetics ; tau Proteins/metabolism
Chemical Substances	Microtubule-Associated Proteins ; tau Proteins
Language	English
Publishing date	2012-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20120045
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Article ; Online: Estimation of minimal disease prevalence from population genomic data: Application to primary familial brain calcification.

Nicolas, Gaël / Charbonnier, Camille / Campion, Dominique / Veltman, Joris A

American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics

2017 Volume 177, Issue 1, Page(s) 68–74

Abstract: Primary Familial Brain Calcification (PFBC) is a rare calcifying disorder of the brain with autosomal dominant inheritance, of unknown prevalence. Four causal genes have been identified so far: SLC20A2, PDGFB, PDGFRB, and XPR1, with pathogenic, probably ... ...

Abstract	Primary Familial Brain Calcification (PFBC) is a rare calcifying disorder of the brain with autosomal dominant inheritance, of unknown prevalence. Four causal genes have been identified so far: SLC20A2, PDGFB, PDGFRB, and XPR1, with pathogenic, probably pathogenic or missense variants of unknown significance found in 27.7% probands in the French PFBC series. Estimating PFBC prevalence from a clinical input is arduous due to a large diversity of symptoms and ages of onset and to incomplete clinical penetrance. Abnormal calcifications on CT scan can be used as a reliable diagnostic biomarker whatever the clinical status, but differential diagnoses should be ruled out including the challenging exclusion of common basal ganglia calcifications. Our primary aim was to estimate the minimal prevalence of PFBC due to a variant in one of the known genes. We extracted variants from the four known genes present in the gnomAD database gathering genomic data from 138,632 individuals. We interpreted all variants based on their predicted effect, their frequency, and previous studies on PFBC patients. Using the most conservative estimate, the minimal prevalence of PFBC related to a variant in one of the four known genes was 4.5 p. 10,000 (95%CI [3.4-5.5] p. 10,000). We then used variant detection rates in patients to extrapolate an overall minimal prevalence of PFBC to 2.1 p. 1,000 (95%CI [1.9-2.4] p. 1,000). The population-based genomic analysis indicates that PFBC is not an exceptionally rare disorder, still underestimated and underdiagnosed.
MeSH term(s)	Brain/pathology ; Brain Diseases/genetics ; Brain Diseases/metabolism ; Calcinosis/genetics ; Cross-Sectional Studies ; Databases, Genetic ; Genetics, Population/methods ; Humans ; Metagenomics/methods ; Pedigree ; Prevalence ; Proto-Oncogene Proteins c-sis/genetics ; Receptor, Platelet-Derived Growth Factor beta/genetics ; Sodium-Phosphate Cotransporter Proteins, Type III/genetics
Chemical Substances	Proto-Oncogene Proteins c-sis ; SLC20A2 protein, human ; Sodium-Phosphate Cotransporter Proteins, Type III ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1)
Language	English
Publishing date	2017-11-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2143866-3
ISSN	1552-485X ; 1552-4841
ISSN (online)	1552-485X
ISSN	1552-4841
DOI	10.1002/ajmg.b.32605
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Article ; Online: Generation of 17q21.31 duplication iPSC-derived neurons as a model for primary tauopathies.

Miguel, Laetitia / Rovelet-Lecrux, Anne / Chambon, Pascal / Joly-Helas, Géraldine / Rousseau, Stéphane / Wallon, David / Epelbaum, Stéphane / Frébourg, Thierry / Campion, Dominique / Nicolas, Gaël / Lecourtois, Magalie

Stem cell research

2022 Volume 61, Page(s) 102762

Abstract: Tau proteins belong to the microtubule associated protein family and are mainly expressed in neurons. Tau accumulates in patients' brain in several neurodegenerative diseases, including Fronto-temporal dementia and Alzheimer's disease. Recently, we ... ...

Abstract	Tau proteins belong to the microtubule associated protein family and are mainly expressed in neurons. Tau accumulates in patients' brain in several neurodegenerative diseases, including Fronto-temporal dementia and Alzheimer's disease. Recently, we described a 17q21.31 duplication in patients presenting different cognitive or motor symptoms and characterized by the accumulation of different Tau isoforms. This duplication involves four genes, including the MAPT gene that encodes the Tau protein. The main pathophysiological consequence associated with this duplication was a 1.6-1.9-fold increase in the MAPT messenger RNA as measured in blood samples of duplication carriers. However, the pathophysiological consequences of this duplication in a cell type relevant for neurodegenerative diseases have never been explored so far. In this study, we developed the first model of primary tauopathy linked to a 17q21.31 duplication in iPSC-induced neurons from 2 unrelated carriers. As in patients' blood, we demonstrated that this duplication was associated with an increase in MAPT mRNA resulting in elevated Tau protein levels in iPSC-derived cortical neurons. We believe that these iPSC lines will be a pertinent tool to elucidate how a same genetic cause could lead to distinct types of tauopathies and the pathophysiological mechanisms associated with Tau-mediated neurodegeneration in the 17q21.31 duplication context.
MeSH term(s)	Humans ; Induced Pluripotent Stem Cells/metabolism ; Neurodegenerative Diseases/metabolism ; Neurons/metabolism ; Tauopathies/genetics ; Tauopathies/metabolism ; tau Proteins/genetics ; tau Proteins/metabolism
Chemical Substances	tau Proteins
Language	English
Publishing date	2022-03-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2393143-7
ISSN	1876-7753 ; 1873-5061
ISSN (online)	1876-7753
ISSN	1873-5061
DOI	10.1016/j.scr.2022.102762
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Article ; Online: Penetrance estimation of Alzheimer disease in SORL1 loss-of-function variant carriers using a family-based strategy and stratification by APOE genotypes.

Schramm, Catherine / Charbonnier, Camille / Zaréa, Aline / Lacour, Morgane / Wallon, David / Boland, Anne / Deleuze, Jean-François / Olaso, Robert / Alarcon, Flora / Campion, Dominique / Nuel, Grégory / Nicolas, Gaël

Genome medicine

2022 Volume 14, Issue 1, Page(s) 69

Abstract: Background: Alzheimer disease (AD) is a common complex disorder with a high genetic component. Loss-of-function (LoF) SORL1 variants are one of the strongest AD genetic risk factors. Estimating their age-related penetrance is essential before putative ... ...

Abstract	Background: Alzheimer disease (AD) is a common complex disorder with a high genetic component. Loss-of-function (LoF) SORL1 variants are one of the strongest AD genetic risk factors. Estimating their age-related penetrance is essential before putative use for genetic counseling or preventive trials. However, relative rarity and co-occurrence with the main AD risk factor, APOE-ε4, make such estimations difficult. Methods: We proposed to estimate the age-related penetrance of SORL1-LoF variants through a survival framework by estimating the conditional instantaneous risk combining (i) a baseline for non-carriers of SORL1-LoF variants, stratified by APOE-ε4, derived from the Rotterdam study (N = 12,255), and (ii) an age-dependent proportional hazard effect for SORL1-LoF variants estimated from 27 extended pedigrees (including 307 relatives ≥ 40 years old, 45 of them having genotyping information) recruited from the French reference center for young Alzheimer patients. We embedded this model into an expectation-maximization algorithm to accommodate for missing genotypes. To correct for ascertainment bias, proband phenotypes were omitted. Then, we assessed if our penetrance curves were concordant with age distributions of APOE-ε4-stratified SORL1-LoF variant carriers detected among sequencing data of 13,007 cases and 10,182 controls from European and American case-control study consortia. Results: SORL1-LoF variants penetrance curves reached 100% (95% confidence interval [99-100%]) by age 70 among APOE-ε4ε4 carriers only, compared with 56% [40-72%] and 37% [26-51%] in ε4 heterozygous carriers and ε4 non-carriers, respectively. These estimates were fully consistent with observed age distributions of SORL1-LoF variant carriers in case-control study data. Conclusions: We conclude that SORL1-LoF variants should be interpreted in light of APOE genotypes for future clinical applications.
MeSH term(s)	Alzheimer Disease/genetics ; Apolipoproteins E/genetics ; Case-Control Studies ; Genotype ; Humans ; LDL-Receptor Related Proteins/genetics ; Membrane Transport Proteins/genetics ; Penetrance
Chemical Substances	ApoE protein, human ; Apolipoproteins E ; LDL-Receptor Related Proteins ; Membrane Transport Proteins ; SORL1 protein, human
Language	English
Publishing date	2022-06-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-022-01070-6
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Article ; Online: Publisher Correction: Penetrance estimation of Alzheimer disease in SORL1 loss-of-function variant carriers using a family-based strategy and stratification by APOE genotypes.

Genome medicine

2022 Volume 14, Issue 1, Page(s) 83

Language	English
Publishing date	2022-08-03
Publishing country	England
Document type	Published Erratum
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-022-01091-1
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