About

Catherine Cahill is a Professor-in-Residence in the Department of Psychiatry and Biobehavioral Sciences at the University of California Los Angeles. Her research interests include cannabis constituents for pain management, new medication development, chronic and persistent pain, and opioid addiction. She has a distinguished academic background with a PhD in Pharmacology from Dalhousie University, an MS in Pharmacology from Dalhousie University, and a BS in Chemistry from Mount Allison University. Cahill has received numerous awards for her research and mentorship, including the Outstanding Research Mentor Award at UCLA in 2024 and the Editor Performance Award from the British Journal of Pharmacology in 2023. Her work has significantly contributed to understanding the neuropharmacology of pain and addiction, with a focus on opioid systems, endogenous opioids, and the development of safer pain therapies. She has authored numerous publications advancing the field of pain and addiction research.

Research topics

• Artificial Intelligence
• Computer Science
• Neuroscience
• Anatomy
• Psychiatry
• Internal medicine
• Biology
• Pharmacology
• Anesthesia
• Psychology
• Medicine

Selected publications

• A peripherally restricted cannabinoid 1 receptor agonist provides analgesic benefit from neuropathic pain and a lack of addiction-related behavior

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-15

  articleOpen accessSenior authorCorresponding

  Introduction: Cannabis is increasingly used for pain management, with many patients reporting relief from chronic pain that did not respond to conventional treatments. However, cannabis is also associated with unwanted side effects including psychomimetic effects and the potential of developing a cannabis use disorder. To circumvent the central nervous system effects, we investigated whether a peripherally restricted cannabinoid receptor (CB1) agonist, PrNMI [(4-{2-[-(1E)-1[(4-propylnaphthalen-1-yl)methylidene]-1H-inden-3yl]ethyl}morpholine] attenuated pain hypersensitivity associated with nerve injury and profiled its' abuse potential. Materials and Methods: Mice with chronic constriction injury (CCI) of the sciatic nerve developed hypersensitivity to mechanical stimulation. Paw withdrawal thresholds were assessed following administration of PrNMI (i.p. 0.3 mg/kg and 0.6 mg/kg) or vehicle in CCI and sham mice. The conditioned place preference model was used to measure drug-reward to 0.6 mg/kg i.p. PrNMI in CCI and sham-injury control animals. We further assessed abuse potential to determine if PrNMI (0.5 mg/kg) would reinstate drug-seeking behavior in mice trained to self-administer intravenous fentanyl (10 μg/kg/infusion). Results: PrNMI administration transiently increased paw withdrawal thresholds in mice with CCI-induced allodynia in a dose-dependent manner. PrNMI conditioning did not produce a conditioned place preference in mice with either CCI or sham injury. Mice who had learned to self-administer fentanyl and went through extinction training did not reinstate drug-seeking behavior when administered PrNMI. Discussion: The systemic CB1 receptor agonist PrNMI demonstrated analgesic benefit in alleviating mechanical allodynia associated with chronic constriction injury of the sciatic nerve without increasing addiction related behaviors associated with the establishment of addiction.

  PublisherOA PDFDOI

• C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1

  Nature Communications · 2025-12-11

  articleOpen access

  C1q levels in the CNS are elevated by inflammation and neurovascular trauma, yet the consequence of this increase for neural stem cell (NSC) regeneration response remain unknown. We have recently identified C1q receptor candidates that regulate NSC behavior. One of these is Brain Angiogenesis Inhibitor 1 (BAI1, ADGRB1), which has no previously discovered role in NSC. Here, we show that C1q acts in a BAI1-dependent manner to modulate NSC quiescence via two parallel mechanisms. First, negative regulation of MDM2, driving cell cycle suppression through p53. Second, endocytic internalization of C1q-BAI1-complex, driving regulation of p32 (C1qBP) and metabolic reprogramming towards aerobic glycolysis. We validated the biological significance of BAI1 in a male hNSC line in vivo using a female mouse model of acute spinal cord injury (SCI). These findings are relevant for a multiplicity of CNS disorders, and illuminate complex connections between C1q, cell cycle, and metabolism. Together, these data provide valuable insight into C1q-mediated regulation of NSC transition between activation and quiescence, processes fundamental for tissue development and repair.

  PublisherDOI

• Elucidating interplay between myrcene and cannabinoid receptor 1 receptors to produce antinociception in mouse models of neuropathic pain

  Pain · 2025-03-17 · 3 citations

  articleOpen accessSenior authorCorresponding

  ABSTRACT: The need for nonaddictive and effective treatments for chronic pain are at an all-time high. Historical precedence, and now clinical evidence, supports the use of cannabis for alleviating chronic pain. A plethora of research on delta-9-tetrahydrocannabinol exists, yet cannabis is comprised of a multitude of constituents, some of which possess analgesic potential, that have not been systematically investigated, including the terpene myrcene. Myrcene attenuates pain hypersensitivity in preclinical models and is one of the most abundant terpenes found in cannabis. Despite these findings, it remains unclear how myrcene elicits these effects on nociceptive systems. The present study uses a male and female mouse model of neuropathic pain as well as in vitro experiments with HEK293T cells to explore these questions. We first demonstrate myrcene (1-200 mg/kg i.p.) dose-dependently increases mechanical nociceptive thresholds, where potency was greater in female compared with male pain mice. Testing canonical tetrad outcomes, mice were tested for hypolocomotion and hypothermia after myrcene administration. Myrcene did not alter locomotion or temperature, but female pain mice showed a conditioned place aversion to myrcene. A cannabinoid receptor 1 (CB1) antagonist inhibited myrcene's anti-allodynia. By contrast, in vitro cell culture experiments using a TRUPATH assay revealed myrcene does not directly activate CB1 receptors nor alter CB1 receptor activity elicited by CB1 agonist (CP 55,940) or endocannabinoids (anandamide or 2-arachidonoylglycerol). Understanding engagement of CB1 receptors in pain modulation and myrcene's mechanism of action warrants further study to understand the diversity of cannabis pharmacology and to further the frontier of pain research.

  PublisherDOI

• Safety in treatment: Classical pharmacotherapeutics and new avenues for addressing maternal depression and anxiety during pregnancy

  Pharmacological Reviews · 2025-02-10 · 5 citations

  reviewOpen access

  We aimed to review clinical research on the safety profiles of antidepressant drugs and associations with maternal depression and neonatal outcomes. We focused on neuroendocrine changes during pregnancy and their effects on antidepressant pharmacokinetics. Pregnancy-induced alterations in drug disposition and metabolism impacting mothers and their fetuses are discussed. We considered evidence for the risks of antidepressant use during pregnancy. Teratogenicity associated with ongoing treatment, new prescriptions during pregnancy, or pausing medication while pregnant was examined. The Food and Drug Administration advises caution regarding prenatal exposure to most drugs, including antidepressants, largely owing to a dearth of safety studies caused by the common exclusion of pregnant individuals in clinical trials. We contrasted findings on antidepressant use with the lack of treatment where detrimental effects to mothers and children are well researched. Overall, drug classes such as selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors appear to have limited adverse effects on fetal health and child development. In the face of an increasing prevalence of major mood and anxiety disorders, we assert that individuals should be counseled before and during pregnancy about the risks and benefits of antidepressant treatment given that withholding treatment has possible negative outcomes. Moreover, newer therapeutics, such as ketamine and κ-opioid receptor antagonists, warrant further investigation for use during pregnancy. SIGNIFICANCE STATEMENT: The safety of antidepressant use during pregnancy remains controversial owing to an incomplete understanding of how drug exposure affects fetal development, brain maturation, and behavior in offspring. This leaves pregnant people especially vulnerable, as pregnancy can be a highly stressful experience for many individuals, with stress being the biggest known risk factor for developing a mood or anxiety disorder. This review focuses on perinatal pharmacotherapy for treating mood and anxiety disorders, highlighting the current knowledge and gaps in our understanding of consequences of treatment.

  PublisherDOI

• PROTEIMERs as catalytic inhibitors of APP mRNA translation: Toward a new therapeutic for Alzheimer's disease

  Journal of Alzheimer s Disease · 2025-11-19

  article

  BackgroundThe rising prevalence of Alzheimer's disease (AD) highlights the urgent need for novel therapeutic approaches capable of suppressing further neurodegeneration. Aberrant aggregation of the amyloid-β peptide fragment of the amyloid-β protein precursor (APP) has long been considered to be a central feature of AD pathology. However, directly targeting the amyloid-β peptide is complicated by its conformational flexibility. Instead, reducing APP expression at the translational level represents a promising alternative. The highly structured 5' untranslated region (UTR) of APP mRNA provides a targetable element for selective inhibition using RNA-binding therapeutics.ObjectiveTo develop and evaluate engineered protein-based RNA binders (PROTEIMERs) that selectively target the APP 5'-UTR to inhibit translation.MethodsWe applied high-throughput phage display screening techniques to identify two PROTEIMERs with high affinity for the APP 5'-UTR, confirmed via surface plasmon resonance. Domain engineering enabled the fusion of these binders to an RNase domain to facilitate catalytic degradation of APP mRNA.ResultsPROTEIMERs bound the APP 5'-UTR with nanomolar affinity. Structural modeling of the PROTEIMER-RNA complexes revealed that the engineered mutations within the binding pocket predominantly interact with the 5'-AGA-3' cleft of the APP mRNA. RNase-fused PROTEIMERs mediated sequence-specific APP mRNA cleavage in vitro, demonstrating robust target engagement and degradation. The PROTEIMER ProAPPS3-11 effectively inhibited APP translation in SH-SY5Y cells, reducing protein levels by up to 60% in a dose-dependent manner.ConclusionsThese findings establish the feasibility of PROTEIMERs as novel RNA-targeting biologics with therapeutic potential to reduce APP mRNA and protein levels, mitigating downstream AD-related neurodegeneration.

  PublisherDOI

• Chronic pain selectively reduces the motivation to work for remifentanil but not food reward

  Pain · 2025-05-13 · 3 citations

  articleOpen accessSenior authorCorresponding

  ABSTRACT: Currently, preclinical research has reported conflicting evidence as to whether chronic pain imparts resilience or vulnerability to opioid drug seeking. Here, we investigated the impact of chronic pain on the intravenous self-administration (IVSA) profile of the short-acting opioid analgesic remifentanil in a mouse model. Using a chronic constriction injury model of chronic neuropathic pain, 7 days after injury, male and female C57Bl/6J mice began remifentanil IVSA. During the acquisition phase, there were no differences in the total number of reinforcers earned but an increase in the number of active nose pokes in pain mice. An increase in the rate of acquisition within sessions was observed in male but not female mice. When work effort increased (fixed ratio 3 and progressive ratio), pain mice unexpectedly showed a reduction in the number of reinforcers earned and their breakpoint. This change in motivational state was specific to the willingness to work for remifentanil, as these changes were not observed with higher effort for a food reward. We hypothesized that chronic pain altered the dopaminergic state of the striatum, which would impact the motivation to work for a reward. We found that pain mice had significantly decreased phasic dopamine release assessed via fast-scan cyclic voltammetry and reduced potassium-evoked extracellular dopamine measured by microdialysis. Future studies will investigate the causal relationship between this hypo-dopaminergic state and decreased behavioral motivation associated with a chronic pain state.

  PublisherDOI

• A Miniaturized Batteryless and Wireless Biopotential Recorder With Dynamic Bandwidth and Data Rate Update for Power Optimization

  2025-07-14

  article

  This work presents a miniaturized, low-power, batteryless, and wireless biopotential recorder capable of dynamic bandwidth and data rate update for efficient operation. Since human biopotential signals have a wide range of bandwidths, tunability in sensing bandwidth and data transmission rate are required. Our proposed automated tuning approach allows for 0.25-10 kHz bandwidth in the analog front-end and 10.5-420 kbps data rate in the transmitter. The nominal power consumption of the SoC at 21 kbps is 32 µW. Furthermore, this setup facilitates adaptive adjustments to the sensing bandwidths and data rates, enabling multi-band sensing when the signal of interest changes over time. Detailed chip verification and in-vivo rodent electrocardiogram (ECG) measurement validate the performance of the sensing node.Clinical relevance- The tight external control over the data rate and sampling frequency in the sensing node not only enhances energy efficiency but also allows for adaptive adjustments in amplifier bandwidths. Such adaptability is particularly advantageous in neural recording applications, where different neural signals-such as local field potentials (LFPs) and action potentials (APs)-require distinct bandwidths for optimal capture. By dynamically tuning the amplifier characteristics, the system can selectively focus on specific neural signals of interest over time, facilitating high-fidelity recordings while minimizing power consumption.

  PublisherDOI

• Exploring Novel Pharmacotherapy Candidates for Cannabis Use Disorder: Uncovering Promising Agents on the Horizon by Mechanism of Action

  Drugs · 2024-10-10 · 5 citations

  reviewOpen access

  With rapid expansion of cannabis legalization worldwide, rates of cannabis use and cannabis use disorder (CUD) are increasing; the need for safe and effective medications to treat CUD is urgent. This narrative review evaluates evidence for promising pharmacotherapies to treat CUD from randomized, placebo-controlled trials. Pharmacotherapies for CUD are categorized based on compound targets (e.g., cannabinoid receptor 1 [CB1] agonists such as nabilone, serotonergic compounds such as bupropion, GABAergic compounds such as zolpidem) and outcomes are organized by predetermined withdrawal symptoms, cannabis craving, and cannabis relapse/use. Most promising pharmacotherapies for CUD are drugs that act on the endocannabinoid system and specifically at the CB1 receptor. Priority populations such as females, certain racial/ethnic groups, and age groups experience a different course of CUD progression, symptoms, and drug effects that are important to consider when evaluating outcomes related to CUD. Possible explanations for these disparities are explored, along with the clinical trials that explore these demographics in treating CUD with pharmacotherapies.

  PublisherOA PDFDOI

• Unveiling the link between chronic pain and misuse of opioids and cannabis

  Journal of Neural Transmission · 2024-04-03 · 9 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Neuroprotective Strategies and Cell-Based Biomarkers for Manganese-Induced Toxicity in Human Neuroblastoma (SH-SY5Y) Cells

  Biomolecules · 2024-05-31 · 7 citations

  articleOpen access1st author

  Manganese (Mn) is an essential heavy metal in the human body, while excess Mn leads to neurotoxicity, as observed in this study, where 100 µM of Mn was administered to the human neuroblastoma (SH-SY5Y) cell model of dopaminergic neurons in neurodegenerative diseases. We quantitated pathway and gene changes in homeostatic cell-based adaptations to Mn exposure. Utilizing the Gene Expression Omnibus, we accessed the GSE70845 dataset as a microarray of SH-SY5Y cells published by Gandhi et al. (2018) and applied statistical significance cutoffs at p < 0.05. We report 74 pathway and 10 gene changes with statistical significance. ReactomeGSA analyses demonstrated upregulation of histones (5 out of 10 induced genes) and histone deacetylases as a neuroprotective response to remodel/mitigate Mn-induced DNA/chromatin damage. Neurodegenerative-associated pathway changes occurred. NF-κB signaled protective responses via Sirtuin-1 to reduce neuroinflammation. Critically, Mn activated three pathways implicating deficits in purine metabolism. Therefore, we validated that urate, a purine and antioxidant, mitigated Mn-losses of viability in SH-SY5Y cells. We discuss Mn as a hypoxia mimetic and trans-activator of HIF-1α, the central trans-activator of vascular hypoxic mitochondrial dysfunction. Mn induced a 3-fold increase in mRNA levels for antioxidant metallothionein-III, which was induced 100-fold by hypoxia mimetics deferoxamine and zinc.

  PublisherOA PDFDOI

Frequent coauthors

• Jack T. Rogers

  University of Alabama at Birmingham

  81 shared

• Xudong Huang

  Anhui Jiyuan Software

  40 shared

• Debomoy K. Lahiri

  Indiana University School of Medicine

  28 shared

• Gary Ruvkun

  Brandeis University

  13 shared

• Maria Alexander-Bridges

  Amgen (United States)

  13 shared

• Justin Dore

  National Institute of Arthritis and Musculoskeletal and Skin Diseases

  13 shared

• Scott Ogg

  13 shared

• Nargis Nasrin

  Novartis (Switzerland)

  13 shared

Labs

• Cahill Pain and Addiction LabPI

Awards & honors

• Outstanding Research Mentor Award, UCLA, 2024
• Editor Performance Award, British Journal of Pharmacology, 2…
• Undergraduate Research Week Faculty Mentor Award, UCLA, 2022
• Hugill Anaesthesiology Award, University of Alberta, 2016
• Environment of Inquiry Award, UC Irvine, 2014