Andrew S. Fox
· Assistant ProfessorVerifiedUniversity of California, Davis · Neurology
Active 1994–2026
About
Andrew S. Fox joined the Foxlab in July 2016 and is an Associate Professor in the Psychology Department at UC Davis. He is also a Core Scientist in Neuroscience and Behavior and affiliated with the California National Primate Research Center. The Fox lab focuses on understanding the neuroscience of social and emotional behavior in both humans and nonhuman primates. Professor Fox's research employs modern neuroscientific approaches and computational modeling to investigate emotion-related decision-making and the development of social anxiety disorder.
Research topics
- Computer Science
- Psychology
- Neuroscience
- Psychiatry
- Evolutionary biology
- Biology
- Cognitive psychology
- Clinical psychology
- Cognitive science
Selected publications
46. Large-Scale Behavioral Monitoring of Non-Human Primates to Quantify Disorder-Relevant Behaviors
Biological Psychiatry · 2026-04-25
articleSenior author51. Unexpected Danger: Neural Computations of Aversive Prediction Errors
Biological Psychiatry · 2026-04-25
articleSenior author419. The Hidden Burden of Anxiety Disorders
Biological Psychiatry · 2026-04-25
articleSenior author63. Parvalbumin Neurons in Prelimbic Cortex Are Activated During Anticipation of Social Defeat
Biological Psychiatry · 2026-04-25
articleBiological Psychiatry · 2026-04-25
article21. Quantifying Behaviors in Non-Human Primates Using Deep Learning
Biological Psychiatry · 2025-04-09
articleSenior authorZenodo (CERN European Organization for Nuclear Research) · 2025-12-19
datasetOpen accessSupplementary files from snRNAseq experiments appearing in the original manuscript "Prenatal Maternal Immune Activation Triggers Lasting Cell-Specific Transcriptomic Dysregulation in the Amygdala of Primate Offspring" accepted to Molecular Psychiatry on December 2, 2025 (published December 19, 2025). Full experimental and technical details are available at https://doi.org/10.1038/s41380-025-03403-4.
Zenodo (CERN European Organization for Nuclear Research) · 2025-12-19
datasetOpen accessSupplementary files from snRNAseq experiments appearing in the original manuscript "Prenatal Maternal Immune Activation Triggers Lasting Cell-Specific Transcriptomic Dysregulation in the Amygdala of Primate Offspring" accepted to Molecular Psychiatry on December 2, 2025 (published December 19, 2025). Full experimental and technical details are available at https://doi.org/10.1038/s41380-025-03403-4.
Molecular Psychiatry · 2025-12-19 · 3 citations
articleOpen accessPrenatal exposure to a heightened maternal immune response, such as that triggered by viral infection in the mother, can alter fetal brain development and increase risk of neurodevelopmental disorders in offspring, including autism (ASD) and schizophrenia. However, the cellular and molecular mechanisms linking early inflammatory signals to long-term changes in brain function remain unclear. While rodent models of maternal immune activation (MIA) display brain and behavioral disruptions, their translational relevance to humans is limited. To address this gap, we utilized a nonhuman primate (NHP) MIA model to examine how transient maternal immune responses in early gestation alter gene expression in the amygdala-a brain region essential for socioemotional behavior and implicated many neurodevelopmental disorders. Pregnant macaques were administered the viral mimic Poly(I:C) during the late first trimester, and amygdala samples were collected from 4-year-old male offspring for single-nucleus RNA sequencing (>71,000 nuclei). We identified 2768 unique differentially expressed genes (DEGs), concentrated in excitatory and inhibitory neurons of the lateral nucleus and microglia of the central nucleus. These DEGs converge on synaptic structure, neurotransmission, and neuroimmune signaling-core processes in circuit assembly and behavioral regulation. MIA-associated DEGs significantly overlap with high-confidence ASD- and psychosis-risk gene sets, directly linking prenatal immune events to human disease pathways. This study provides the first region- and cell-type-specific evidence in a primate model that transient prenatal maternal immune responses lead to lasting transcriptomic dysregulation. These findings reveal how early immune insults may alter neurodevelopment and offer a translational framework for identifying molecular targets for early intervention.
Biological Psychiatry · 2025-04-09
articleSenior author
Recent grants
Frequent coauthors
- 62 shared
Ned H. Kalin
University of Wisconsin–Madison
- 47 shared
Alexander J. Shackman
- 42 shared
Jonathan A. Oler
University of Wisconsin–Madison
- 40 shared
J. Rick Turner
- 30 shared
Richard J. Davidson
University of Wisconsin–Madison
- 26 shared
Lillian J. Campos
University of California, Davis
- 22 shared
Patrick H. Roseboom
University of Wisconsin–Madison
- 20 shared
Cynthia M. Arokiaraj
California Institute of Technology
Labs
Fox LabPI
Understanding the neuroscience of social and emotional behavior in both humans and nonhuman primates.
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