About

Dr. Monica Driscoll is a Distinguished Professor in the Department of Molecular Biology and Biochemistry at Rutgers University. Her research focuses on the basic biology of aging, with particular emphasis on the molecular mechanisms of healthspan extension through genetic, chemical, and exercise interventions. She investigates neuronal proteostasis and anti-neurodegeneration mechanisms, aiming to develop molecular, cellular, and trans-tissue strategies that promote healthy maintenance and protect against age-associated decline. Her work involves studying aging, disease genetics, neurological disease, neuroscience, and organelle biology, utilizing techniques such as cell biology, genetic engineering, genetics, and imaging. Dr. Driscoll's research is conducted using the model organism C. elegans, and she is dedicated to understanding the biological processes underlying aging and age-related diseases.

Research topics

• Biology
• Genetics
• Medicine
• Endocrinology
• Cell biology
• Biochemistry
• Physiology
• Chemistry

Selected publications

• Bone morphogenetic protein receptor 2 signaling mediates mitochondrial Ca2+ transport through its regulation of TAK1 splice variant

  Cell Communication and Signaling · 2026-02-11

  articleOpen access

  Bone morphogenetic proteins (BMPs) are highly conserved multifunctional signaling proteins with pleotropic effects throughout embryonic development. BMPs are aberrantly expressed in many diseases including cancer and Alzheimer’s disease. Recent studies suggested that BMP signaling negatively regulates mitochondrial bioenergetics. The mechanisms by which BMP signaling regulates bioenergetics and cell survival are not known. We utilized BMP type 2 receptor (BMPR2) inhibitor (JL189), BMPR2 kinase domain KO, BMPR2 siRNA, and BMP loss of function mutants in C. elegans to inhibit BMP signaling (BMPR2i). The effects of BMPR2i on mitochondrial bioenergetics were examined by measuring differences in TCA cycle intermediates (mass spectrometer), mitochondrial respiration (Agilent Seahorse), and mitochondrial mass (MitoTracker Green/TFAM). Fluorescent mitochondrial Ca2+ sensors Rhod-2AM and LAR-GECO were used to detect changes in mitochondrial Ca2+ levels in cell culture and C elegans respectively. The KO and siRNA of the mitochondria uniporter (MCU) were used to determine the mechanisms BMPR2i regulates the uptake of Ca2+ into the mitochondria. We compared the responses of BMPR2i in non-small cell lung cancer (NSCLC) cell lines, leukemia cells, breast cancer cells, and HT-22 mouse hippocampal cells to assess whether the biological response varied depending on the cell type. BMPR2i increased mitochondrial Ca2+ (mtCa2+) levels in all cells lines and in C. elegans, suggesting its regulation of Ca2+ transport is conserved. BMPR2i induced increase in mtCa2+ levels were dependent on the MCU, which effected mitochondrial bioenergetics and cell survival. In addition, our data suggests that BMPR2 regulation of mtCa2+ transport is mediated by TAK1-d splice variant. In leukemia cells, BMPR2i induced significant cell death that was attenuated by MCU KO. In NSCLC and HT-22 cells, BMPR2i increased mitochondrial bioenergetics and induced minimal cell death. These studies reveal that BMPR2 signaling regulates TAK1-d splice variant to mediate mitochondrial Ca2+ transport, which is dependent on the MCU. Our studies suggest that BMPR2 signaling utilizes mtCa2+ transport to regulate both mitochondrial bioenergetics and/or cell survival. Our studies provide novel insight into how aberrant BMPR2 signaling is pathogenic and suggests that the response could vary depending on the cell type.

  PublisherDOI

• Abstract 6790 Large Extracellular Vesicle Production by Proteo-Stressed Neurons: Throwing Out the Trash as a Facet of Proteostasis

  Journal of Biological Chemistry · 2026-05-01

  articleOpen access1st authorCorresponding
  PublisherDOI

• Defining Microbiome Impact on Host Physiology During Spaceflight Using Caenorhabditis elegans

  Methods in molecular biology · 2026-01-01

  book-chapter
  PublisherDOI

• Analysis of categorical data from biological experiments with logistic regression and CMH tests

  PLoS ONE · 2025-11-17

  articleOpen accessCorresponding

  The choice of appropriate statistical tests in experimental biology is critical for scientific rigor and can be challenging in the case of categorical data analysis. Using example datasets from Caenorhabditis elegans research, we conduct statistical analysis of (1) a rare cellular event involving the formation of a neuronal extrusion called an exopher and (2) a variable behavioral response across time. We employ the Cochran-Mantel-Haenszel (CMH) test and logistic regression for analysis. Recognizing there are potential accessibility issues using logistic regression, we provide step-by-step tutorials and example code. We emphasize that logistic regression can handle both simple and complex multivariable datasets; logistic regression can also provide more comprehensive insights into experimental outcomes when compared to simpler tests like CMH. By analyzing real biological examples and demonstrating their analysis with R code, we provide a practical guide for biologists to enhance the rigor and reproducibility of categorical data analysis in experimental studies.

  PublisherDOI

• Computer prediction and genetic analysis identifies retinoic acid modulation as a driver of conserved longevity pathways in genetically-diverse Caenorhabditis nematodes

  eLife · 2025-08-06

  articleOpen access

  Abstract Aging is a pan-metazoan process with significant consequences for human health and society—discovery of new compounds that ameliorate the negative health impacts of aging promise to be of tremendous benefit across a number of age-based comorbidities. One method to prioritize a testable subset of the nearly infinite universe of potential compounds is to use computational prediction of their likely anti-aging capacity. Here we present a survey of longevity effects for 16 compounds suggested by a previously published computational prediction set, capitalizing upon the comprehensive, multi-species approach utilized by the Caenorhabditis Intervention Testing Program (CITP). While eleven compounds (aldosterone, arecoline, bortezomib, dasatinib, decitabine, dexamethasone, erlotinib, everolimus, gefitinib, temsirolimus, and thalidomide) either had no effect on median lifespan or were toxic, five compounds (all-trans retinoic acid, berberine, fisetin, propranolol, and ritonavir) extended lifespan in Caenorhabditis elegans. These computer predictions yield a remarkable positive hit rate of 30%. Deeper genetic characterization of the longevity effects of one of the most efficacious compounds, the endogenous signaling ligand all-trans retinoic acid (atRA, designated tretinoin in medical products), which is widely prescribed for treatment of acne, skin photoaging and acute promyelocytic leukemia, demonstrated a requirement for the regulatory kinases AKT-1 and AKT-2. While the canonical Akt-target FOXO/DAF-16 was largely dispensable, other conserved Akt-targets (Nrf2/SKN-1 and HSF1/HSF-1), as well as the conserved catalytic subunit of AMPK AAK-2, were all necessary for longevity extension by atRA. Evolutionary conservation of retinoic acid as a signaling ligand and the structure of the downstream effector network of retinoic acid combine to suggest that the all-trans retinoic acid pathway is an ancient metabolic regulatory system that can modulate lifespan. Our results highlight the potential of combining computational prediction of longevity interventions with the power of nematode functional genetics and underscore that the manipulation of a conserved metabolic regulatory circuit by co-opting endogenous signaling molecules is a powerful approach for discovering aging interventions.

  PublisherDOI

• Author response: Computer prediction and genetic analysis identifies retinoic acid modulation as a driver of conserved longevity pathways in genetically diverse Caenorhabditis nematodes

  2025-12-23

  peer-reviewOpen access
  PublisherDOI

• Author response: Computer prediction and genetic analysis identifies retinoic acid modulation as a driver of conserved longevity pathways in genetically-diverse Caenorhabditis nematodes

  2025-08-06

  peer-reviewOpen access

  Aging is a pan-metazoan process with significant consequences for human health and society—discovery of new compounds that ameliorate the negative health impacts of aging promise to be of tremendous benefit across a number of age-based comorbidities. One method to prioritize a testable subset of the nearly infinite universe of potential compounds is to use computational prediction of their likely anti-aging capacity. Here we present a survey of longevity effects for 16 compounds suggested by a previously published computational prediction set, capitalizing upon the comprehensive, multi-species approach utilized by the Caenorhabditis Intervention Testing Program (CITP). While eleven compounds (aldosterone, arecoline, bortezomib, dasatinib, decitabine, dexamethasone, erlotinib, everolimus, gefitinib, temsirolimus, and thalidomide) either had no effect on median lifespan or were toxic, five compounds (all-trans retinoic acid, berberine, fisetin, propranolol, and ritonavir) extended lifespan in Caenorhabditis elegans. These computer predictions yield a remarkable positive hit rate of 30%. Deeper genetic characterization of the longevity effects of one of the most efficacious compounds, the endogenous signaling ligand all-trans retinoic acid (atRA, designated tretinoin in medical products), which is widely prescribed for treatment of acne, skin photoaging and acute promyelocytic leukemia, demonstrated a requirement for the regulatory kinases AKT-1 and AKT-2. While the canonical Akt-target FOXO/DAF-16 was largely dispensable, other conserved Akt-targets (Nrf2/SKN-1 and HSF1/HSF-1), as well as the conserved catalytic subunit of AMPK AAK-2, were all necessary for longevity extension by atRA. Evolutionary conservation of retinoic acid as a signaling ligand and the structure of the downstream effector network of retinoic acid combine to suggest that the all-trans retinoic acid pathway is an ancient metabolic regulatory system that can modulate lifespan. Our results highlight the potential of combining computational prediction of longevity interventions with the power of nematode functional genetics and underscore that the manipulation of a conserved metabolic regulatory circuit by co-opting endogenous signaling molecules is a powerful approach for discovering aging interventions.

  PublisherDOI

• The broccoli derivative sulforaphane extends lifespan by slowing the transcriptional aging clock

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-15 · 2 citations

  preprintOpen access

  Abstract Sulforaphane, an organosulfur isothiocyanate derived from cruciferous vegetables, has been shown to inhibit inflammation, oxidative stress, and cancer cell growth. To explore the potential of sulforaphane as a candidate natural compound for promoting longevity more generally, we tested the dose and age-specific effects of sulforaphane on C. elegans longevity, finding that it can extend lifespan by more than 50% at the most efficacious doses, but that treatment must be initiated early in life to be effective. We then created a novel, gene-specific, transcriptional aging clock, which demonstrated that sulforaphane-treated individuals exhibited a “transcriptional age” that was approximately four days younger than age-matched controls, representing a nearly 20% reduction in biological age. The clearest transcriptional responses were detoxification pathways, which, together with the shape of the dose-response curve, indicates a likely hormetic response to sulforaphane. These results support the idea that robust longevity-extending interventions can act via global effects across the organism, as revealed by systems level changes in gene expression.

  PublisherOA PDFDOI

• NIA Caenorhabditis Intervention Testing Program: identification of robust and reproducible pharmacological interventions that promote longevity across experimentally accessible, genetically diverse populations

  GeroScience · 2025-04-03 · 10 citations

  reviewOpen access1st authorCorresponding

  A core facet of the National Institute on Aging's mission is to identify pharmacological interventions that can promote human healthy aging and long life. As part of the comprehensive effort toward that goal, the NIA Division of Biology of Aging established the Caenorhabditis Intervention Testing Program (CITP) in 2013. The C. elegans model (with an ~ 21 day lifespan) has led the field in dissection of longevity genetics and offers features that allow for relatively rapid testing and for the potential elaboration of biological mechanisms engaged by candidate geroprotectants. CITP builds on this foundation by utilizing a genetically diverse set of intervention test strains so that "subjects" represent genetic diversity akin to that that between mouse and humans. Another distinctive aspect of the CITP is a dedicated focus on reproducibility of longevity outcomes as labs at three independent test sites confirm positive outcomes. The overall goal of the Caenorhabditis Intervention Testing Program (CITP) is to identify robust and reproducible pro-longevity interventions affecting genetically diverse cohorts in the Caenorhabditis genus. A strong Data Collection Center supports data collection and dissemination. Pharmacological interventions tested by CITP can be nominated by the general public, directed by in-house screens, or supported by published scientific literature. As of December 2024, CITP tested > 75 compounds and conducted > 725,000 animal assays over 891 trials. We identified 12 compounds that confer a ≥ 20% increase in median lifespan to reproducibly and robustly extend lifespan across multiple strains and labs. Five of these interventions have pro-longevity impact reported in the mouse literature (most CITP positive interventions are not tested yet in mouse). As part of the celebration of the 50th Anniversary of the NIA, we review the development history and accomplishments of the CITP program, and we comment on translation and the promise of advancing understanding of fundamental aging biology that includes the pharmacological intervention/health interface.

  PublisherOA PDFDOI

• Stress-associated High Production of Large Extracellular Vesicles in the Parent Generation is Not Inherited by C. elegans F1 Progeny

  PubMed · 2025-11-18

  articleOpen accessSenior author

   neurons, proteostress can induce the extrusion of aggregates and organelles in large extracellular vesicles called exophers. Under mild proteostress, ~20% of ALMR neurons produce exophers. We tested if the high exopher production trait is heritable. Offspring of parents that produced exophers (both under standard growth conditions and after 6-hour food withdrawal) displayed similar exopher production levels compared to offspring of parents that didn't produce ALMR exophers and the exopher level changes in response to fasting remained the same. Our data suggest that the high exopher production trait is not heritable.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21AG027513

  NIH · $290k · 2008

• Caenorhabditis Intervention Testing Program: Interventions That Modulate Health, Longevity and Aging Hallmarks

  NIH · $7.5M · 2013–2027

• Defining roles of genetic and age in extracellular elimination of neurotoxic aggregates

  NIH · $5.3M · 2017–2027

• NIH Grant R01AG024882

  NIH · $1.9M · 2010

• Genetic Dissection of Mechanisms by Which Exercise Promotes Systemic Health

  NIH · $2.0M · 2016–2022

Frequent coauthors

• Barth D. Grant

  Rutgers, The State University of New Jersey

  53 shared

• David H. Hall

  43 shared

• Meghan Lee Arnold

  Rutgers, The State University of New Jersey

  35 shared

• Anna J Smart

  Rutgers, The State University of New Jersey

  34 shared

• Nektarios Tavernarakis

  University of Crete

  34 shared

• Guoqiang Wang

  Rutgers, The State University of New Jersey

  33 shared

• Ken C. Q. Nguyen

  Albert Einstein College of Medicine

  33 shared

• Jason Cooper

  Van Andel Institute

  31 shared

Education

• PhD, Biochemistry & Molecular Biology

  Harvard University

  1985