
Laura Roberts, MD, MA
· Katharine Dexter McCormick and Stanley McCormick Memorial ProfessorStanford University · Psychology
Active 1977–2026
About
Dr. Laura Roberts, MD, MA, is the Katharine Dexter McCormick and Stanley McCormick Memorial Professor in the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine. She serves as Chairman of the department and is a nationally recognized scholar and leader in ethics, psychiatry, medicine, and medical education. Her early work focused on elevating the perspectives of key stakeholders in psychiatric research, including individuals with lived experience of mental and physical disorders, investigators, community members, and policymakers. Over more than two decades, Dr. Roberts has received scientific, peer-reviewed funding from the National Institutes of Health, the Department of Energy, and private foundations to conduct empirical studies on modern ethical issues in research, clinical care, and health policy, with a particular emphasis on vulnerable and special populations. She has authored hundreds of peer-reviewed articles and scholarly works, and has written or edited numerous books in professionalism and ethics in medicine, professional development for physicians, and clinical psychiatry. Dr. Roberts is also the Editor-in-Chief of the journal Academic Medicine and has served as Editor-in-Chief for the journal Academic Psychiatry. Her academic background includes a Bachelor of Arts in History and a Master of Arts in the Conceptual Foundations of Science from the University of Chicago, as well as a medical degree and fellowship in clinical medical ethics from the University of Chicago Pritzker School of Medicine. She completed her residency in psychiatry at the University of New Mexico School of Medicine, where she also received additional training in child and adolescent psychiatry. Her prior academic appointments include faculty positions at the University of New Mexico and the Medical College of Wisconsin, where she served as department chair and held the title of Charles E. Kubly Professor of Psychiatry and Behavioral Medicine. Her clinical focus encompasses psychiatry, psychosomatic medicine, adult, child, and adolescent psychiatry, clinical ethics, physician well-being, and collaborative care. Dr. Roberts has received numerous awards and honors for her contributions to psychiatry and medical ethics, including the Vestermark Award from the American Psychiatric Association, the Ethics Prize from the International College of Neuropsychopharmacology, and the MacLean Center Prize in Clinical Ethics from the University of Chicago. She is actively involved in teaching, research, and leadership roles at Stanford University, contributing to the advancement of ethics and psychiatry in academic medicine.
Research topics
- Biology
- Medicine
- Immunology
- Internal medicine
- Genetics
- Bioinformatics
- Cell biology
- Cancer research
- Pathology
Selected publications
Journal of Pharmaceutical Sciences · 2026-01-31
articleOpen accessSomatic mutations reveal the ontogeny of human microglia
bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-20
articleOpen accessAbstract Microglia are the resident hematopoietic cells of the central nervous system 1 . In mice, microglia seed the brain during embryogenesis and can be maintained throughout life with minimal input from adult hematopoiesis 2–4 . The origins of human microglia are less clear, but recent evidence suggests that marrow-derived cells may be able to supplement the human microglial pool in certain individuals 5,6 . Here, to investigate the ontogeny of human microglia, we develop a method that uses the collection of accumulated somatic mutations which uniquely labels each clone of cells to track the infiltration of marrow-derived cells into the human brain. Applying this method to 20 aged individuals, we find evidence of an influx of marrow-derived cells into the brain in all examined individuals. Single cell analysis, including single cell lineage tracing using mitochondrial DNA variants, demonstrates that these infiltrating cells are nearly identical to microglia and can comprise a large fraction of the microglial pool. Analysis of large-scale sequencing cohorts demonstrates a protective association between most types of clonal hematopoiesis and Alzheimer’s disease. In sum, this work uncovers a widespread influx of myeloid cells into the healthy human brain which serves to reinforce the pool of human microglia and becomes common with aging.
Journal of Pharmaceutical Sciences · 2025-03-31 · 2 citations
article1st authorCorrespondingSingle cell RNA sequencing of haematopoietic cells in fresh and frozen human atheroma tissue
Cardiovascular Research · 2025-02-01 · 4 citations
articleAIMS: Single-cell RNA sequencing (scRNA-seq) is a powerful method for exploring the cellular heterogeneity within human atheroma but typically requires fresh tissue to preserve cell membrane integrity, limiting the feasibility of large-scale biobanking for later analysis. The aim of this study was to determine whether cryopreservation of fragile and necrotic atheroma tissue affects the viability and transcriptomic profiles of haematopoietic cells in subsequent scRNA-seq analysis, enabling the use of cryopreserved atheroma samples for future research. METHODS AND RESULTS: We performed scRNA-seq on five paired fresh and cryopreserved atheroma samples-three from coronary arteries and two from carotid arteries. Each sample was enzymatically digested, sorted for CD45+ haematopoietic cells, and processed using the 10× Genomics scRNA-seq workflow. Half of each sample was processed immediately, while the other half was cryopreserved in liquid nitrogen for an average of 5 weeks before thawing and processing. In carotid artery samples, we noted the absence of LYVE1+ macrophages, likely due to the loss of the adventitial layer during endarterectomy procedures. Our results indicated that cryopreservation modestly affected cellular integrity, leading to an increase in the relative abundance of mitochondrial RNA in frozen samples. Minimal differences were observed between fresh and cryopreserved samples in uniquely detected transcripts, cell clustering, or transcriptional profiles within haematopoietic populations. CONCLUSIONS: Our study demonstrates that cryopreserved human atheroma samples can be successfully profiled using scRNA-seq, with comparable transcriptomic data to that obtained from fresh samples. These findings suggest that cryopreservation is a viable method for biobanking atheroma tissues, facilitating large-scale studies without the need for immediate sample processing.
Distributed Quantum Computing in Silicon
arXiv (Cornell University) · 2024-06-03 · 12 citations
preprintOpen accessCommercially impactful quantum algorithms such as quantum chemistry and Shor's algorithm require a number of qubits and gates far beyond the capacity of any existing quantum processor. Distributed architectures, which scale horizontally by networking modules, provide a route to commercial utility and will eventually surpass the capability of any single quantum computing module. Such processors consume remote entanglement distributed between modules to realize distributed quantum logic. Networked quantum computers will therefore require the capability to rapidly distribute high fidelity entanglement between modules. Here we present preliminary demonstrations of some key distributed quantum computing protocols on silicon T centres in isotopically-enriched silicon. We demonstrate the distribution of entanglement between modules and consume it to apply a teleported gate sequence, establishing a proof-of-concept for T centres as a distributed quantum computing and networking platform.
Research Square · 2024-11-07
preprintOpen access1st authorCorrespondingClonal hematopoiesis is associated with protection from Alzheimer’s disease
Nature Medicine · 2023 · 144 citations
- Biology
- Immunology
- Medicine
), and Mendelian randomization analyses supported a potential causal association. We observed that the same mutations found in blood were also detected in microglia-enriched fraction of the brain in seven of eight CHIP carriers. Single-nucleus chromatin accessibility profiling of brain-derived nuclei in six CHIP carriers revealed that the mutated cells comprised a large proportion of the microglial pool in the samples examined. While additional studies are required to validate the mechanistic findings, these results suggest that CHIP may have a role in attenuating the risk of AD.
Journal of Pharmaceutical Sciences · 2023-08-28 · 3 citations
articleOpen accessBlood · 2023-11-02 · 4 citations
articleIntroduction Clonal Hematopoiesis of Indeterminate Potential (CHIP) is a source of age-associated inflammation, caused by somatic mutations in bone marrow stem cells that promote clonal expansion. The functional impact of CHIP mutations on macrophages derived from these stem cells is linked to increased cardiovascular disease risk among other diseases. Interestingly, CHIP-associated mutations frequently occur in genes with opposing functions: DNMT3A and TET2, enzymes responsible for DNA methylation and demethylation, respectively. While it is known that DNMT3A KO and TET2 KO in macrophages lead to hyperinflammatory responses, the underlying mechanism remains poorly understood how opposing mutations lead to a similar phenotype. Methods To evaluate how DNMT3A and TET2 contribute to inflammatory responses in the context of CHIP, we exposed bone marrow derived macrophages from Dnmt3a KO, Tet2 KO, and C57BL/6 Vav1-Cre wild type (WT) control mice to 0.5 ng/mL of the inflammatory stimuli lipopolysaccharide (LPS). We then measured gene responses with RNA-seq replicates across 12 time points from 0 to 24 hours, paired with single cell RNA-seq (scRNA-seq), ATAC-seq, and 50x-coverage whole genome enzymatic methyl-seq (EM-seq) for multiple time points. Results Although the composition and kinetics of the LPS-induced expression program were similar in all genotypes, Dnmt3a KO and Tet2 KO had significantly greater changes in gene expression and chromatin accessibility by 2 hours compared to WT, particularly for a large subset of inflammatory response genes, like Il1b, Il6, Cxcl1, Tnfsf9, and Il23a. The promoter regions of the 278 genes significantly overexpressed (adjusted p < 0.05) for both KOs at 2 hours compared to WT were enriched with binding sites of the inflammatory pioneer factor AP-1 (p = 0.001). Inflammatory signals were observed even before stimulation, suggesting altered DNA methylation in each KO predisposed cells to hyperinflammatory states. Bulk RNA-seq found the gene set ‘IFNA response’ from MSigDB Hallmarks collection to be most enriched at baseline in both KOs compared to WT (FDR < 0.0007). At baseline Dnmt3a KO and Tet2 KO had 1,566 and 441 over-expressed genes, respectively (adjusted p < 0.05). scRNA-seq similarly showed a baseline inflammatory population enriched with type 1 IFN response gene expression that contained more cells with measurable baseline expression of inflammatory genes for both KOs. ATAC-seq identified highly significant enrichment of AP-1 binding sites at baseline and at 2 hours in the 2,270 regions more accessible in Dnmt3a KO compared to WT (p = 1x10 -40), as well as the 2,148 regions less accessible in Tet2 KO compared to WT (p = 1x10 -41). Although LPS stimulation did not lead to sites with altered CpG methylation using a genome-wide significance threshold, methylation globally differed between genotypes at baseline especially for promoter and enhancer regions, and this differential methylation directly explained some of the hyper-responsive chromatin accessibility and gene expression. For example, the promoter region of Cxcl1 for both KOs was significantly hypomethylated and more accessible at baseline, with these chromatin accessibility and associated expression differences becoming even larger at 2 hours of LPS stimulation. In general, DNA methylation and chromatin accessibility were rarely concordantly altered in both KOs at regions near genes with differential expression. For adjusted p-value < 0.05, Dnmt3a KO had 236,062 differentially hypomethylated CpG segments and 1,023 hypermethylated, while Tet2 KO had 7,488 hypomethylated and 4,482 hypermethylated segments. Conclusions Our integrative multi-omic analysis demonstrates that Dnmt3a and Tet2 modulate DNA methylation to limit inflammatory gene expression in healthy macrophages. We find loss of Dnmt3a or Tet2 activity in macrophages alters baseline DNA methylation at different regions, separately influencing the transcription factor binding landscape of AP-1, and inducing similar baseline over-expression of type 1 interferon response genes. Upon stimulation, these differences lead to higher inflammatory gene expression, possibly through more cooperation with transcription factors NF-κB and IRFs. Targeting AP-1 and type 1 interferon may be a therapeutic avenue for blocking the pathogenic role of CHIP for many inflammatory diseases of aging.
Journal of Pharmaceutical Sciences · 2023-01-07 · 12 citations
articleOpen access
Frequent coauthors
- 49 shared
Daniel A. Arber
- 41 shared
Stanley L. Schrier
Stanford University
- 20 shared
Pornpan Sirankapracha
Mahidol University
- 20 shared
Rawiprapa Kumbunlue
Mahidol University
- 20 shared
Surai Hemsorach
Mahidol University
- 20 shared
Anong Piangitjagum
Stanford University
- 20 shared
Prawase Wasi
- 20 shared
Wanna Moungsub
Mahidol University
Labs
Vice Provost for Student AffairsPI
Education
B.A., History
University of Chicago
M.A., Conceptual Foundations of Science
University of Chicago
M.D.
University of Chicago Pritzker School of Medicine
Other, Clinical Medical Ethics
University of Chicago Pritzker School of Medicine
Other, Psychiatry
University of New Mexico School of Medicine
Other, Child and Adolescent Psychiatry
University of New Mexico School of Medicine
Awards & honors
- Vestermark Award, American Psychiatric Association (2023)
- Ethics Prize, The International College of Neuropsychopharma…
- Lifetime Service Award, American Association of Directors of…
- Carol Davis Ethics Award, American Psychiatric Association (…
- MacLean Center Prize in Clinical Ethics, University of Chica…
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