Audrey Evers
Casual - Non-Exempt, Psych/General Psychiatry and Psychology (Adult)
Current Role at Stanford
Clinical Psychology Doctoral Student, PGSP-Stanford PsyD Consortium
Clinical Research Coordinator, Depression Research Clinic
All Publications
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Media hype regarding psychedelic treatments for depression and PTSD from 2017 to 2024.
Scientific reports
2026
View details for DOI 10.1038/s41598-026-50186-x
View details for PubMedID 42034826
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Insights from changes in NDEV biomarkers of metabolism: Effects of PPARγ and GLP1 receptor agonists on brain metabolism.
The Journal of clinical endocrinology and metabolism
2026
Abstract
Insulin resistance (IR) is implicated in central nervous system disorders, including depression and Alzheimer's disease (AD).We analyzed biological samples from two cohorts of clinical trial participants: 1) participants with unremitted depression after six months of treatment as usual who received pioglitazone (PPARγ agonist, N = 12) or placebo and 2) middle-aged participants at genetic risk for AD who received liraglutide (glucagon-like peptide 1 [GLP1] receptor agonist, N = 15) or placebo. These cohorts, which previously showed treatment-related improvements in peripheral IR, were used to assess the effects of pioglitazone and liraglutide on CNS insulin signaling using neuron-derived extracellular vesicles (NDEVs) as biomarkers. We utilized biological samples to measure biomarkers of IR in NDEVs. Eleven Akt-mTOR pathway proteins were measured before and after 12 weeks of treatment in both groups.Participants who received pioglitazone experienced broader changes, with significant increases in GSK3β (Ser9), mTOR (Ser2448), and RPS6 (Ser235/Ser236; all p ≤ 0.02) compared to placebo, and 77% of participants showed mTOR (Ser2448) response. Participants who received liraglutide demonstrated significantly increased NDEV-associated phosphorylated Akt (Ser473) and mTOR (Ser2448; p = 0.04 and p = 0.025, respectively) compared to placebo, with 40% and 30% of participants in the liraglutide group showing biomarker response in both Akt (Ser473) and mTOR (Ser2448), respectively. These effects appeared relatively independent from changes in fasting plasma insulin and glucose concentration at 120-minutes during the oral glucose tolerance test.Our findings demonstrate CNS-specific biomarker responses to both PPARγ agonists and GLP1 receptor agonists.
View details for DOI 10.1210/clinem/dgag176
View details for PubMedID 41992726
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LOW DOSE BUPRENORPHINE ENHANCES THE ANTISUICIDAL EFFECTS OF KETAMINE IN MAJOR DEPRESSIVE DISORDER: A RANDOMIZED CONTROLLED TRIAL
SPRINGERNATURE. 2026
View details for Web of Science ID 001665758000727
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Central Insulin Resistance in Bipolar Disorder Subtypes
WILEY. 2025: S40
View details for Web of Science ID 001578710100011
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CENTRAL AND PERIPHERAL SIGNATURES OF INSULIN RESISTANCE AS BIOMARKERS OF ACCELERATED COGNITIVE AGING
SPRINGERNATURE. 2024: 453-454
View details for Web of Science ID 001421429900063
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A randomized pilot study of the prophylactic effect of ketamine on laboratory-induced stress in healthy adults
NEUROBIOLOGY OF STRESS
2023; 22: 100505
Abstract
Stress exposure is a key risk factor for the development of major depressive disorder and posttraumatic stress disorder. Enhancing stress resilience in at-risk populations could potentially protect against stress-induced disorders. The administration of ketamine one week prior to an acute stressor prevents the development of stress-induced depressive-like behavior in rodents. This study aimed to test if the prophylactic effect of ketamine against stress also applies to humans.We conducted a double-blind, placebo-controlled study wherein 24 healthy subjects (n = 11 males) were randomized to receive either ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg) intravenously one week prior to an acute stress [Trier Social Stress Test (TSST)]. The primary endpoint was the anxious-composed subscale of the Profile of Mood States Bipolar Scale (POMS-Bi) administered immediately after the TSST. Salivary and plasma cortisol and salivary alpha amylase were also measured at 15-min intervals for 60 min following the stressor, as proxies of hypothalamic pituitary adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axis activity, respectively.Compared to the midazolam group (n = 12), the ketamine group (n = 12) showed a moderate to large (Cohen's d = 0.7) reduction in levels of anxiety immediately following stress, although this was not significant (p = 0.06). There was no effect of group on change in salivary cortisol or salivary alpha amylase following stress. We conducted a secondary analysis excluding one participant who did not show an expected correlation between plasma and salivary cortisol (n = 23, ketamine n = 11). In this subgroup, we observed a significant reduction in the level of salivary alpha amylase in the ketamine group compared to midazolam (Cohen's d = 0.7, p = 0.03). No formal adjustment for multiple testing was made as this is a pilot study and all secondary analyses are considered hypothesis-generating.Ketamine was associated with a numeric reduction in TSST-induced anxiety, equivalent to a medium-to-large effect size. However, this did not reach statistical significance . In a subset of subjects, ketamine appeared to blunt SAM reactivity following an acute stressor. Future studies with larger sample size are required to further investigate the pro-resilient effect of ketamine.
View details for DOI 10.1016/j.ynstr.2022.100505
View details for Web of Science ID 000920570500001
View details for PubMedID 36620306
View details for PubMedCentralID PMC9813787
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Ketamine as a prophylactic resilience-enhancing agent
FRONTIERS IN PSYCHIATRY
2022; 13: 833259
Abstract
Stress exposure is one of the greatest risk factors for psychiatric illnesses, including major depressive disorder (MDD) and posttraumatic stress disorder (PTSD). Enhancing stress resilience could potentially protect against the development of stress-induced psychiatric disorders, yet no resilience-enhancing pharmaceuticals have been developed to date. This review serves to consider the existing evidence for a potential pro-resilience effect of ketamine in rodents as well as the preliminary evidence of ketamine as a prophylactic treatment for postpartum depression (PPD) in humans. Several animal studies have demonstrated that ketamine administered 1 week prior to a stressor (e.g., chronic social defeat and learned helplessness) may protect against depressive-like behavior. A similar protective effect has been demonstrated against PTSD-like behavior following Contextual Fear Conditioning (CFC). Recent work has sought to explore if the administration of ketamine prevented the development of postpartum depression (PPD) in humans. Researchers administered ketamine immediately following caesarian-section and found a significantly reduced prevalence of PPD in the ketamine-treated groups compared to the control groups. Utilizing ketamine as a resilience-enhancing treatment may have unique applications, including leading to a deeper understanding of the neurobiological mechanism underlying resilience. Future trials aiming to translate and replicate these findings with humans are warranted.
View details for DOI 10.3389/fpsyt.2022.833259
View details for Web of Science ID 000838967800001
View details for PubMedID 35966469
View details for PubMedCentralID PMC9365980
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Antidepressant effect of prolonged twice-weekly intranasal esketamine treatments after nonresponse to electroconvulsive therapy in a patient with treatment-resistant depression
ANNALS OF CLINICAL PSYCHIATRY
2022; 34 (1): 61-64
View details for DOI 10.12788/acp.0055
View details for Web of Science ID 000834882100012
View details for PubMedID 35166666
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The Adaptation and Evaluation of a Pilot Mindfulness Intervention Promoting Mental Health in Student Athletes
JOURNAL OF CLINICAL SPORT PSYCHOLOGY
2021; 15 (3): 206-226
View details for DOI 10.1123/jcsp.2019-0083
View details for Web of Science ID 000719457400003
https://orcid.org/0009-0001-6765-7686