Portrait de Guillaume Dumas

Guillaume Dumas

Membre académique associé
Professeur agrégé, Université de Montréal, Département de psychiatrie et d’addictologie
Professeur adjoint, McGill University, Département de psychiatrie

Biographie

Guillaume Dumas est professeur agrégé de psychiatrie computationnelle à la Faculté de médecine de l'Université de Montréal et chercheur principal du laboratoire de psychiatrie de précision et de physiologie sociale du Centre de recherche du CHU Sainte-Justine. Il est titulaire de la chaire IVADO IA en santé mentale et chercheur-boursier junior 1 du Fonds de recherche du Québec - Santé (FRQS) dans le domaine de l’ IA en santé et de la santé numérique. En 2023, il a été retenu dans le cadre du Programme des chercheurs mondiaux CIFAR-Azrieli pour le programme de recherche Cerveau, esprit et conscience. Il a également été nommé parmi les Futurs leaders canadiens de la recherche sur le cerveau par la Fondation Brain Canada.

Il a auparavant été chercheur permanent en neurosciences et en biologie computationnelle à l'Institut Pasteur (Paris, France), ainsi que chercheur postdoctoral au Center for Complex Systems and Brain Sciences à l’Université Florida Atlantic (FAU), aux États-Unis. Il est titulaire d'un diplôme d'ingénieur en ingénierie avancée et informatique (École centrale Paris), de deux masters (physique théorique, Université Paris-Saclay; sciences cognitives, ENS/EHESS/Paris 5) et d'un doctorat en neurosciences cognitives (Sorbonne Université).

Ses recherches visent à combiner l’intelligence artificielle, les neurosciences cognitives et la médecine numérique à travers un programme interdisciplinaire suivant deux axes principaux :

- L’intelligence artificielle en santé mentale, par la création de nouveaux algorithmes pour étudier le développement de l'architecture cognitive humaine et pour fournir une médecine personnalisée en neuropsychiatrie grâce à des données allant du génome à celles des téléphones intelligents;

- Les neurosciences sociales en intelligence artificielle, par la traduction de la recherche fondamentale sur le cerveau et le formalisme des systèmes dynamiques en des modèles hybrides neurocomputationnels et d’apprentissage automatique (NeuroML) et de nouvelles architectures présentant des capacités d'apprentissage social (NeuroIA Sociale et IHM).

Étudiants actuels

Visiteur de recherche indépendant - Université de Montréal
Maîtrise recherche - Université de Montréal
Maîtrise recherche - Université de Montréal
Postdoctorat - Université de Montréal

Publications

Dark control: The default mode network as a reinforcement learning agent
Elvis Dohmatob
Differential neural circuitry behind autism subtypes with imbalanced social-communicative and restricted repetitive behavior symptoms
Natasha Bertelsen
Isotta Landi
Richard A.I. Bethlehem
Jakob Seidlitz
Elena Maria Busuoli
Veronica Mandelli
Eleonora Satta
Stavros Trakoshis
Bonnie Auyeung
Prantik Kundu
Eva Loth
Sarah Baumeister
Christian Beckmann
Sven Bölte
Thomas Bourgeron
Tony Charman
Sarah Durston
Christine Ecker
Rosemary Holt … (voir 15 de plus)
Mark Johnson
Emily J. H. Jones
Luke Mason
Andreas Meyer-Lindenberg
Carolin Moessnang
Marianne Oldehinkel
Antonio Persico
Julian Tillmann
Steven C. R. Williams
Will Spooren
Declan Murphy
Jan K. Buitelaar
Simon Baron-Cohen
Meng-Chuan Lai
Michael V. Lombardo
Social-communication (SC) and restricted repetitive behaviors (RRB) are autism diagnostic symptom domains. SC and RRB severity can markedly … (voir plus)differ within and between individuals and may be underpinned by different neural circuitry and genetic mechanisms. Modeling SC-RRB balance could help identify how neural circuitry and genetic mechanisms map onto such phenotypic heterogeneity. Here we developed a phenotypic stratification model that makes highly accurate (97-99%) out-of-sample SC=RRB, SC>RRB, and RRB>SC subtype predictions. Applying this model to resting state fMRI data from the EU-AIMS LEAP dataset (n=509), we find that while the phenotypic subtypes share many commonalities in terms of intrinsic functional connectivity, they also show subtype-specific qualitative differences compared to a typically-developing group (TD). Specifically, the somatomotor network is hypoconnected with perisylvian circuitry in SC>RRB and visual association circuitry in SC=RRB. The SC=RRB subtype also showed hyperconnectivity between medial motor and anterior salience circuitry. Genes that are highly expressed within these subtype-specific networks show a differential enrichment pattern with known ASD associated genes, indicating that such circuits are affected by differing autism-associated genomic mechanisms. These results suggest that SC-RRB imbalance subtypes share some commonalities but also express subtle differences in functional neural circuitry and the genomic underpinnings behind such circuitry.
Atypical brain asymmetry in autism – a candidate for clinically meaningful stratification
Dorothea L. Floris
Thomas Wolfers
Mariam Zabihi
Nathalie E. Holz
Christine Ecker
Flavio Dell’Acqua
Simon Baron-Cohen
Rosemary Holt
Sarah Durston
Eva Loth
Andre Marquand
Christian Beckmann
Jumana Ahmad
Sara Ambrosino
Bonnie Auyeung
Tobias Banaschewski
Sarah Baumeister
Sven Bölte
Thomas Bourgeron
Carsten Bours … (voir 51 de plus)
Michael Brammer
Daniel Brandeis
Claudia Brogna
Yvette de Bruijn
Jan K. Buitelaar
Bhismadev Chakrabarti
Tony Charman
Ineke Cornelissen
Daisy Crawley
Jessica Faulkner
Vincent Frouin
Pilar Garcés
David Goyard
Lindsay Ham
Hannah Hayward
Joerg F. Hipp
Mark Johnson
Emily J. H. Jones
Prantik Kundu
Meng-Chuan Lai
Xavier Liogier D’ardhuy
Michael V. Lombardo
David J. Lythgoe
René Mandl
Luke Mason
Maarten Mennes
Andreas Meyer-Lindenberg
Carolin Moessnang
Nico Mueller
Declan Murphy
Beth Oakley
Laurence O’Dwyer
Marianne Oldehinkel
Bob Oranje
Gahan Pandina
Antonio Persico
Barbara Ruggeri
Amber N. V. Ruigrok
Jessica Sabet
Roberto Sacco
Antonia San José Cáceres
Emily Simonoff
Will Spooren
Julian Tillmann
Roberto Toro
Heike Tost
Jack Waldman
Steve C. R. Williams
Caroline Wooldridge
Marcel P. Zwiers
Dissecting the phenotypic heterogeneity in sensory features in autism spectrum disorder: a factor mixture modelling approach
Julian Tillmann
M. Uljarevic
Daisy Crawley
G. Dumas
Eva Loth
D. Murphy
J. Buitelaar
Tony Charman
Jumana Sara Bonnie Sarah Christian Thomas Carsten Michael Daniel Claudia Yvette Bhismadev Ineke Flavio Dell’ Guillaume Christine Jessica Vincent Pilar David Hannah Joerg Mark H. Emily J. H. Prantik Meng-Chuan Xavier Liogier Michael David J. René Luke Andreas Carolin Nico Laurence Marianne Bob Gahan Antonio M. Barbara Amber Jessica Roberto Roberto Heike Jack Steve C. R. Caroline Marcel P. Ahmad
Jumana Sara Bonnie Sarah Christian Thomas Carsten Michael Ahmad Ambrosino Auyeung Baumeister Beckmann Bourge
Jumana Ahmad
Sara Ambrosino
Bonnie Auyeung
Sarah Baumeister
Christian Beckmann
Thomas Bourgeron
Carsten Bours
Michael Brammer
Daniel Brandeis
Claudia Brogna … (voir 39 de plus)
Yvette de Bruijn
Bhismadev Chakrabarti
Ineke Cornelissen
Flavio Dell’ Acqua
Christine Ecker
Jessica Faulkner
Vincent Frouin
Pilar Garcés
David Goyard
Hannah Hayward
Joerg F. Hipp
Mark Johnson
Emily J. H. Jones
Prantik Kundu
Meng-Chuan Lai
Xavier Liogier D’ardhuy
Michael V. Lombardo
David J. Lythgoe
René Mandl
Luke Mason
Andreas Meyer-Lindenberg
Carolin Moessnang
Nico Mueller
Laurence O’Dwyer
Marianne Oldehinkel
Bob Oranje
Gahan Pandina
Antonio Persico
Barbara Ruggeri
Amber N. V. Ruigrok
Jessica Sabet
Roberto Sacco
Roberto Toro
Heike Tost
Jack Waldman
Steve C. R. Williams
Caroline Wooldridge
Marcel P. Zwiers
Autism spectrum disorder
Catherine Lord
Traolach S. Brugha
Tony Charman
James Cusack
Thomas Frazier
Emily J. H. Jones
Rebecca M. Jones
Andrew Pickles
Matthew W. State
Julie Lounds Taylor
Jeremy Veenstra-VanderWeele
Divergent protein-coding genes and brain size in primates
Malesys Bourgeron Dumas
Simon Malesys
Thomas Bourgeron
17 The human brain differs from that of other primates, but the genetic basis of these differences 18 remains unclear. We investigated the e… (voir plus)volutionary pressures acting on almost all human 19 protein-coding genes ( N =11,667; 1:1 orthologs in primates) on the basis of their divergence 20 from those of early hominins, such as Neanderthals, and non-human primates. We confirm 21 that genes encoding brain-related proteins are among the most strongly conserved protein- 22 coding genes in the human genome. Combining our evolutionary pressure metrics for the 23 protein-coding genome with recent datasets, we found that this conservation applied to genes 24 functionally associated with the synapse and expressed in brain structures such as the 25 prefrontal cortex and the cerebellum. Conversely, several of the protein-coding genes that 26 diverge most in hominins relative to other primates are associated with brain-associated 27 diseases, such as micro/macrocephaly, dyslexia, and autism. We also showed that cerebellum 28 granule neurons express a set of divergent protein-coding genes that may have contributed to 29 the emergence of fine motor skills and social cognition in humans. This resource is available 30 from http://neanderthal.pasteur.fr and can be used to estimate evolutionary constraints acting 31 on a set of genes and to explore their relative contributions to human traits. 32
Title : Differential functional neural circuitry behind autism subtypes with marked imbalance between social-communicative and restricted repetitive behavior symptom domains
Natasha Bertelsen
Isotta Landi
Richard A.I. Bethlehem
Jakob Seidlitz
Elena
Maria Busuoli
Veronica Mandelli
Eleonora Satta
Stavros Trakoshis
Bonnie Auyeung
Prantik Kundu
Eva Loth
Sarah Baumeister
Christian Beckmann
Sven Bölte
Thomas Bourgeron
Tony Charman
Sarah Durston
Christine Ecker … (voir 22 de plus)
Rosemary Holt
Mark Johnson
Emily J. H. Jones
Luke Mason
-. AndreasMeyer
Lindenberg
Carolin
Moessnang
Marianne
Oldehinkel
Antonio
Persico
Julian
Tillmann
Steven C. R. Williams
Will Spooren
Declan Murphy
Katherine Jan
Buitelaar
Simon Baron-Cohen
Meng-Chuan Lai
Michael V. Lombardo
Social-communication (SC) and restricted repetitive behaviors (RRB) are autism diagnostic symptom domains. SC and RRB severity can markedly … (voir plus)differ within and between individuals and is underpinned by different neural circuitry and genetic mechanisms. Modeling SC-RRB balance could help identify how neural circuitry and genetic mechanisms map onto such phenotypic heterogeneity. Here we developed a phenotypic stratification model that makes highly accurate (96-98%) out-of-sample SC=RRB, SC>RRB, and RRB>SC subtype predictions. Applying this model to resting state fMRI data from the EU-AIMS LEAP dataset (n=509), we find replicable somatomotor-perisylvian hypoconnectivity in the SC>RRB subtype versus a typically-developing (TD) comparison group. In contrast, replicable motor-anterior salience hyperconnectivity is apparent in the SC=RRB subtype versus TD. Autism-associated genes affecting astrocytes, excitatory, and inhibitory neurons are highly expressed specifically within SC>RRB hypoconnected networks, but not SC=RRB hyperconnected networks. SC-RRB balance subtypes may indicate different paths individuals take from genome, neural circuitry, to the clinical phenotype. (CIMH). Procedures were undertaken to optimize the MRI sequences for the best scanner-specific options, and phantoms and travelling heads were employed to assure standardization and quality assurance of the multisite image-acquisition 20 . Structural images were obtained using a 5.5 minute MPRAGE sequence (TR=2300ms, TE=2.93ms, T1=900ms, voxels size=1.1x1.1x1.2mm, flip angle=9°, matrix size=256x256, FOV=270mm, 176 slices). An eight-to-ten minute resting-state fMRI (rsfMRI) scan was acquired using a multi-echo planar imaging (ME-EPI) sequence 65,66 ; TR=2300ms, TE~12ms, 31ms, and 48ms (slight variations are present across centers), flip angle=80°, matrix size=64x64, (UMCU), 215 (KCL, CIMH), 265 (RUMC, UCAM). were to relax, with eyes open and fixate on a cross presented on the screen for the duration of the rsfMRI scan.
Towards robust and replicable sex differences in the intrinsic brain 1 function of autism 2 3
Dorothea L. Floris
José O. A. Filho
Meng-Chuan Lai
Steve
Giavasis
Marianne Oldehinkel
Maarten Mennes
Tony Charman
Julian
Tillmann
Christine Ecker
Flavio Dell’Acqua
Tobias Banaschewski
Carolin Moessnang
Simon Baron-Cohen
Sarah
Durston
Eva Loth
Declan Murphy … (voir 4 de plus)
Jan K. Buitelaar
Christian Beckmann
Michael P. Milham
A. Martino
84 Background: Marked sex differences in autism prevalence accentuate the need to understand 85 the role of biological sex-related factors i… (voir plus)n autism. Efforts to unravel sex differences in the 86 brain organization of autism have, however, been challenged by the limited availability of 87 female data. Methods: We addressed this gap by using a large sample of males and females 88 with autism and neurotypical (NT) control individuals (ABIDE; Autism: 362 males, 82 89 females; NT: 409 males, 166 females; 7-18 years). Discovery analyses examined main effects 90 of diagnosis, sex and their interaction across five resting-state fMRI (R-fMRI) metrics 91 (voxel-level Z > 3.1, cluster-level P 0.01, gaussian random field corrected). Secondary 92 analyses assessed the robustness of the results to different pre-processing approaches and 93 their replicability in two independent samples: the EU-AIMS Longitudinal European Autism 94 Project (LEAP) and the Gender Explorations of Neurogenetics and Development to Advance 95 Autism Research (GENDAAR). Results: Discovery analyses in ABIDE revealed significant 96 main effects across the intrinsic functional connectivity (iFC) of the posterior cingulate 97 cortex, regional homogeneity and voxel-mirrored homotopic connectivity (VMHC) in several 98 cortical regions, largely converging in the default network midline. Sex-by-diagnosis 99 interactions were confined to the dorsolateral occipital cortex, with reduced VMHC in 100 females with autism. All findings were robust to different pre-processing steps. Replicability 101 in independent samples varied by R-fMRI measures and effects with the targeted sex-by102 diagnosis interaction being replicated in the larger of the two replication samples – EU-AIMS 103 LEAP. Limitations: Given the lack of a priori harmonization among the discovery and 104 replication datasets available to date, sample-related variation remained and may have 105 affected replicability. Conclusions: Atypical cross-hemispheric interactions are 106 neurobiologically relevant to autism. They likely result from the combination of sex107
Interactive Psychometrics for Autism with the Human Dynamic Clamp: Interpersonal Synchrony from Sensory-motor to Socio-cognitive Domains
Florence Baillin
Aline Lefebvre
Amandine Pedoux
Yann Beauxis
Denis-Alexander Engemann
Anna Maruani
Frederique Amsellem
Thomas Bourgeron
Richard Delorme
Neuropsychiatric mutations delineate functional brain connectivity dimensions contributing to autism and schizophrenia
Clara A. Moreau
Sebastian Urchs
Pierre Orban
Catherine Schramm
Aurélie Labbe
Guillaume Huguet
Elise Douard
Pierre-Olivier Quirion
Amy Lin
Leila Kushan
Stephanie Grot
David Luck
Adrianna Mendrek
Stephane Potvin
Emmanuel Stip
Thomas Bourgeron
Alan C. Evans
Carrie E. Bearden
Sébastien Jacquemont
16p11.2 and 22q11.2 Copy Number Variants (CNVs) confer high risk for Autism Spectrum Disorder (ASD), schizophrenia (SZ), and Attention-Defic… (voir plus)it-Hyperactivity-Disorder (ADHD), but their impact on functional connectivity (FC) remains unclear. We analyzed resting-state functional magnetic resonance imaging data from 101 CNV carriers, 755 individuals with idiopathic ASD, SZ, or ADHD and 1,072 controls. We used CNV FC-signatures to identify dimensions contributing to complex idiopathic conditions. CNVs had large mirror effects on FC at the global and regional level. Thalamus, somatomotor, and posterior insula regions played a critical role in dysconnectivity shared across deletions, duplications, idiopathic ASD, SZ but not ADHD. Individuals with higher similarity to deletion FC-signatures exhibited worse cognitive and behavioral symptoms. Deletion similarities identified at the connectivity level could be related to the redundant associations observed genome-wide between gene expression spatial patterns and FC-signatures. Results may explain why many CNVs affect a similar range of neuropsychiatric symptoms.
Patterns of autism symptoms: hidden structure in the ADOS and ADI-R instruments
Jeremy Lefort-Besnard
Kai Vogeley
Leonhard Schilbach
Gael Varoquaux
Bertrand Thirion