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Omar Ahmed

· Associate Professor of Psychology, Neuroscience & Biomedical EngineeringVerified

University of Michigan · Psychology

Active 2006–2026

h-index24
Citations2.1k
Papers6320 last 5y
Funding$24.0M1 active
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About

Omar Ahmed is an Associate Professor of Psychology, Neuroscience, and Biomedical Engineering at the University of Michigan. He holds a B.Sc. in Neuroscience and a Ph.D. in Neuroscience from Brown University, and completed a postdoctoral fellowship in Neurology at Harvard Medical School. His research focuses on behavioral neural circuits, specifically how space, time, and speed are encoded by the brain's spatial navigation and memory circuits, and how this information is consolidated during sleep. His lab studies how these neural circuits go awry in disorders such as Alzheimer's disease, Parkinson's disease, and epilepsy, with the aim of identifying novel therapeutic targets. His work involves working with both patients and transgenic rodent models to understand neural mechanisms underlying these conditions.

Research topics

  • Computer Science
  • Neuroscience
  • Biology
  • Medicine
  • Psychology
  • Anesthesia

Selected publications

  • A Single Dose of a Psychedelic Drug Repairs Prefrontal Cortex Synaptic Physiology in a Mouse Model of Prenatal Alcohol Exposure

    Brain and Behavior · 2026-04-01

    articleOpen accessSenior authorCorresponding

    BACKGROUND: Prenatal alcohol exposure (PAE) can cause fetal alcohol spectrum disorders (FASDs), which are characterized by neural circuit and behavioral dysfunction due to impaired brain development. At the neural and behavioral levels, PAE is associated with disrupted cortical synaptic transmission and lifelong impairments in learning and cognitive control. Despite the prevalence of FASDs (affecting up to one in 20 school-aged children in the United States) and the associated personal, familial, and societal costs, there are currently no treatments to reverse neural circuit dysfunction. METHODS: Using whole-cell patch-clamp electrophysiology, we investigated intrinsic excitability and synaptic activity in prefrontal cortex (PFC) pyramidal neurons from adolescent mice prenatally exposed to ethanol (6.6%) and later given a single injection of either saline or 25CN-NBOH, a psychedelic neuroplastogen. RESULTS: We found that PAE reduced intrinsic excitability and synaptic drive in PFC pyramidal neurons. 25CN-NBOH treatment partially rescued intrinsic excitability deficits and restored synaptic drive. CONCLUSIONS: Psychedelic neuroplastogens may show promise as potential therapeutics for synaptic deficits associated with PAE and should be further explored in preclinical models.

  • Single-dose psychedelic enhances cognitive flexibility and reversal learning in mice weeks after administration

    Psychedelics. · 2025-04-22 · 9 citations

    articleOpen accessSenior author

    Psychedelic compounds have demonstrated remarkable therapeutic potential for treating neuropsychiatric disorders by promoting sustained neuroplasticity in the prefrontal cortex (PFC). Cognitive flexibility-the ability to adapt previously learned rules to novel situations-represents a critical PFC function that is frequently impaired in depression, PTSD, and neurodegenerative conditions. In this study, we demonstrate that a single administration of the selective serotonin 2A receptor agonist 25CN-NBOH produces significant, long-lasting improvements in cognitive flexibility in both male and female mice when measured 2-3 weeks posttreatment. Using a novel automated sequential learning paradigm, psychedelic-treated mice showed superior adaptability in rule reversal tasks compared to saline controls, as evidenced by enhanced poke efficiency, higher percentages of correct trials, and increased reward acquisition. These behavioral findings complement existing cellular research showing psychedelic-induced structural remodeling in the PFC and uniquely demonstrate sustained cognitive benefits persisting weeks after a single psychedelic dose. Our automated behavioral task provides a high-throughput method for evaluating cognitive flexibility effects of various psychedelic compounds, offering important implications for therapeutic applications in conditions characterized by cognitive rigidity, including depression, PTSD, and potentially Alzheimer's disease.

  • Comparison Between GIP/GLP-1 Co-agonists and GLP-1 Agonists on Pulmonary Outcomes in COPD Patients

    American Journal of Respiratory and Critical Care Medicine · 2025-05-01

    article

    Abstract RATIONALE: Recent studies indicated that glucagon-like peptide-1 agonists (GLP-1a) are associated with a decreased rate of chronic obstructive pulmonary disease (COPD) exacerbations in patients with COPD and type 2 diabetes (T2DM). Tirzepatide, a glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 co-agonist that shares a similar glucose-lowering pathway with GLP-1a, has been approved for T2DM treatment. However, it remains uncertain whether tirzepatide offers superior pulmonary benefits than GLP-1a. We aimed to investigate the impact of GIP/GLP-1 co-agonist versus GLP-1a in COPD patients with T2DM. METHODS: We performed a retrospective cohort study utilizing the TriNetX Analytics Network Database and included adults (≥18 years) with COPD and T2DM from January 2022 to September 2023. We compared patients receiving GIP/GLP-1 co-agonist with those on GLP-1a, who had at least two prescriptions for these medications within one year before the index COPD diagnosis. The primary outcome was the incidence of COPD exacerbation. Secondary outcomes included acute respiratory failure, acute respiratory distress syndrome (ARDS), mechanical ventilation, and all-cause mortality. Adverse outcomes included gastroparesis, pancreatitis, and biliary diseases. We used propensity score matching and included covariates such as age, race, smoking status, oxygen dependence, sleep apnea, heart failure, body mass index (BMI), hemoglobin A1c (HbA1c), and predicted forced expiratory volume in the first second (predicted FEV1). Patients were matched in a 1:1 ratio, with a standardized mean difference of <0.1 indicating balanced covariates. Survival analysis was conducted using the Cox proportional hazards model to estimate hazard ratios (HRs) for the risk of outcomes over a 1-year follow-up period. Log-rank tests were performed to compare the survival distributions between the two groups. A p-value <0.05 was considered statistically significant. All analyses were performed using the TriNetX platform. RESULTS: The study comprised 32,812 COPD patients with T2DM. Post-matching, each cohort included 1,927 patients, with all covariates balanced between groups. GIP/GLP-1 co-agonists users had a 26% reduced risk of acute respiratory failure (HR 0.74 [95% CI: 0.59-0.94]), a 65% lower risk of ARDS (HR 0.35 [95% CI: 0.13-0.98]), and a 44% reduction in all-cause mortality (HR 0.56 [95% CI 0.38-0.83]) compared to GLP-1a users. There were no significant differences in COPD exacerbation (HR 1.03 [95% CI: 0.88-1.21]) or mechanical ventilation (HR 0.65 [95% CI: 0.38-1.10]). Additionally, no differences were observed in gastroparesis, pancreatitis, or biliary disease. CONCLUSION: GIP/GLP-1 co-agonists were associated with further reduced risks of acute respiratory failure, ARDS, and all-cause mortality compared to GLP-1a in COPD patients with T2DM.

  • Sa1528: TRANSFORMING MASLD OUTCOMES: A PROSPECTIVE STUDY ON THE IMPACT OF GLP-1 RECEPTOR AGONISTS ON LIVER HEALTH AND METABOLIC PARAMETERS

    Gastroenterology · 2025-05-01

    article
  • Psychedelic neuroplasticity of cortical neurons lacking 5-HT2A receptors

    Molecular Psychiatry · 2025-09-16 · 6 citations

    articleOpen accessSenior authorCorresponding

    Abstract Classical psychedelic drugs show promise as a treatment for major depressive disorder and related psychiatric disorders. This therapeutic efficacy stems from long-lasting psychedelic-induced neuroplasticity onto prefrontal cortical neurons and is thought to require the postsynaptic expression of serotonin 2A receptors (5-HT 2A R). However, other cortical regions such as the granular retrosplenial cortex (RSG) – important for memory, spatial orientation, fear extinction, and imagining oneself in the future, but impaired in Alzheimer’s disease – lack 5-HT 2A R and are thus considered unlikely to benefit from psychedelic therapy. Here, we show that RSG pyramidal cells lacking postsynaptic 5-HT 2A receptors still undergo long-lasting psychedelic-induced synaptic enhancement. A newly engineered CRISPR-Cas-based conditional knockout mouse line reveals that this form of psychedelic-induced retrosplenial plasticity requires presynaptic 5-HT 2A receptors expressed on anterior thalamic axonal inputs to RSG. These results highlight a broader psychedelic therapeutic utility than currently appreciated, suggesting potential for augmenting RSG circuit function in Alzheimer’s disease, post-traumatic stress disorder, and other neuropsychiatric conditions, despite the lack of postsynaptic 5-HT 2A receptors.

  • Neotenic expansion of adult-born dentate granule cells reconfigures GABAergic inhibition to enhance social memory consolidation

    Research Square · 2025-03-21

    preprintOpen accessSenior author
  • The Impact of GLP-1 Analogs on Thromboembolic Outcomes in Patients With Sarcoidosis

    American Journal of Respiratory and Critical Care Medicine · 2025-05-01 · 1 citations

    article

    Abstract Rationale Patients with sarcoidosis exhibit heightened risk for thromboembolic events from chronic inflammation, comorbidities, and treatment-related toxicity, which is further elevated in those with co-existing type 2 diabetes mellitus (T2DM). Preclinical studies suggest glucagon-like peptide-1 (GLP-1) analogs, including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 co-agonists, possess antithrombotic properties. However, their thromboembolic effects in sarcoidosis patients remains unclear. We aim to evaluate the impact of GLP-1 analogs on thromboembolic risks in patients with co-morbid sarcoidosis and T2DM. Methods We conducted a retrospective cohort using the TriNetX Analytics Network international database. Adults (≥18 years) diagnosed with both sarcoidosis and T2DM between April 2005 and September 2023 were included. Patients receiving GLP-1 analogs were compared to those on dipeptidyl peptidase-4 inhibitors (DPP-4i). Eligible patients had at least one prescription for the study medications within a year before their sarcoidosis diagnosis. The primary outcomes were arterial thromboembolic events (ATE), including myocardial infarction (MI) and ischemic stroke, and venous thromboembolic events (VTE), comprising pulmonary embolism (PE) and deep vein thrombosis (DVT). Secondary outcomes evaluated individual components of ATE and VTE. Safety outcomes included serious gastrointestinal adverse events, including gastroparesis, biliary disease, pancreatitis, and bowel obstruction. We performed propensity score matching, adjusting for demographics, body mass index (BMI), hemoglobin A1c (HbA1c), comorbidities, long term steroid use, and medication use for diabetes, sarcoidosis, and thromboembolic conditions. Patients were matched 1:1 using the TriNetX platform, with standardized mean differences <0.1 indicating balance. A Cox proportional hazards model was used to assess outcomes, with p-values <0.05 considered statistically significant. Results The study included 2,451 patients with both sarcoidosis and T2DM, with 821 patients in each matched group. Patients in the GLP-1 cohort were younger (57.2±10.9 vs. 61.7±12.0 years) with higher BMI (36.2±8.4 vs. 32.4±8.0 kg/m2) and HbA1c (7.9±1.9 vs. 7.7±1.7 %). After matching, covariates were balanced, including age (59.1±10.7 vs. 58.9±12.1 years) and hemoglobin A1c (7.7±1.7 vs. 7.8±1.8 %). The GLP-1 group maintained a slightly higher mean BMI (34.7±8.1 vs. 33.9±8.2 kg/m2), but the subgroups were otherwise well-matched. GLP-1 users had a lower risk of VTE (Hazard ratio (HR), 0.50 [95% CI: 0.26-0.97]; p=0.035), DVT (HR, 0.25 [95% CI: 0.09-0.66]; p=0.003), and MI (HR, 0.43 [95% CI: 0.20-0.93]; p=0.028) compared to DPP-4i users. No significant differences were observed in ATE, ischemic stroke, PE, or gastrointestinal adverse event risk. Conclusion GLP-1 analogs may reduce VTE and MI risks in patients with co-existing sarcoidosis and T2DM.

  • From controversy to confidence: Strengthening dengue vaccines safety reporting

    Vaccine · 2025-07-15 · 4 citations

    article
  • Neotenic expansion of adult-born dentate granule cells reconfigures GABAergic inhibition to enhance social memory consolidation

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-17 · 1 citations

    preprintOpen access

    Abstract Adult-born dentate granule cells (abDGCs) contribute to hippocampal dentate gyrus (DG)-CA3/CA2 circuit functions in memory encoding, retrieval and consolidation. Heightened synaptic and structural plasticity of immature abDGCs is thought to govern their distinct contributions to circuit and network mechanisms of hippocampal-dependent memory operations. Protracted maturation or neoteny of abDGCs in higher mammals is hypothesized to offset decline in adult hippocampal neurogenesis by expanding the capacity for circuit and network plasticity underlying different memory operations. Here, we provide evidence for this hypothesis by genetically modelling the effective impact of neoteny of abDGCs on circuitry, network properties and social cognition in mice. We show that selective synchronous expansion of a single cohort of 4 weeks old immature, but not 8 weeks old mature abDGCs, increases functional recruitment of fast spiking parvalbumin expressing inhibitory interneurons (PV INs) in CA3/CA2, number of PV IN-CA3/CA2 synapses, and GABAergic inhibition of CA3/CA2. This transient increase in feed-forward inhibition in DG-CA2 decreased social memory interference and enhanced social memory consolidation. In vivo local field potential recordings revealed that the expansion of a single cohort of 4-week-old abDGCs increased baseline power, amplitude, and duration, as well as sensitivity to social investigation-dependent rate changes of sharp-wave ripples (SWRs) in CA1 and CA2, a neural substrate for memory consolidation. Inhibitory neuron-targeted chemogenetic manipulations implicate CA3/CA2 INs, including PV INs, as necessary and sufficient for social memory consolidation following neotenic expansion of the abDGC population and in wild-type mice, respectively. These studies suggest that neoteny of abDGCs may represent an evolutionary adaptation to support cognition by reconfiguring PV IN-CA3/CA2 circuitry and emergent network properties underlying memory consolidation.

  • Pulmonary Impact of Sodium-glucose Cotransporter-2 Inhibitors in Patients With Chronic Obstructive Pulmonary Disease Receiving Single-inhaler Triple Therapy

    American Journal of Respiratory and Critical Care Medicine · 2025-05-01

    article

    Abstract Introduction Patients with chronic obstructive pulmonary disease (COPD) requiring single-inhaler triple therapy (SITT) are prone to various respiratory risk, including frequent exacerbations, pneumonia, and intubation. Emerging evidence suggests that sodium-glucose cotransporter-2 inhibitors (SGLT-2i) may reduce COPD exacerbations by lowering inflammation. This study examines the pulmonary impact of SGLT-2i in patients with COPD using SITT and type 2 diabetes mellitus (T2DM). Methods This retrospective cohort study utilized the TriNetX Analytics Network international database. Adults (aged ≥18 years) diagnosed with both COPD receiving SITT and T2DM between March 2013 and October 2023 were included. Patients treated with SGLT-2i were compared to those receiving dipeptidyl peptidase-4 inhibitors (DPP-4i). The index date was set as the initiation of SITT. Efficacy outcomes were defined as COPD exacerbations, pneumonia, acute respiratory distress syndrome (ARDS), and intubation. Safety outcomes included urinary tract infection (UTI), lower limb amputation, and ketoacidosis. All outcomes were defined as incident events occurring one year following the index date. Propensity score matching (1:1) was conducted to adjust for baseline characteristics such as age, body mass index (BMI), hemoglobin A1c (HbA1c), predicted forced expiratory volume in 1 second (FEV1), blood eosinophil counts, comorbidities, and concurrent medications, with standardized mean difference <0.1 indicating adequately balanced covariates between two groups. We used Cox proportional hazards model to estimate the association between SGLT2i use and each outcome, with p-values <0.05 indicating statistical significance. Results The study included 8,824 patients with COPD using SITT and T2DM. After matching, 2,404 patients remained in each group with balanced characteristics, including age (69.9 ± 10.1 vs. 69.9 ± 10.9 years), BMI (32.0 ± 8.1 vs. 31.9 ± 8.0 kg/m²), HbA1c (7.5 ± 1.8 vs. 7.4 ± 1.7%), predicted FEV1 (58.7 ± 17.1 vs. 60.4 ± 19.8%), blood eosinophil counts (0.8 ± 6.7 vs 0.8 ±6.2) and other relevant factors. Compared to the DPP-4i group, the SGLT-2i group showed reduced pneumonia (HR: 0.68, 95% CI: 0.53-0.86, p=0.001) and intubation (HR: 0.62, 95% CI: 0.42-0.94, p=0.021) risk. There were no differences in COPD exacerbations and ARDS between the two groups. The risk of safety outcomes was not increased. Conclusion SGLT-2i may offer protective pulmonary benefits in patients with COPD receiving SITT and T2DM. Further prospective studies are needed to confirm the efficacy and safety of SGLT-2i in this population.

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