About

Thomas Rogers is an Assistant Adjunct Professor in the Department of Medicine at UC San Diego. His research focuses on the development and characterization of broadly neutralizing antibodies against coronaviruses, including SARS-CoV-2 and related viruses. His work involves targeted isolation of diverse human protective antibodies, understanding their mechanisms of protection, and exploring their potential as therapeutic agents. Rogers has contributed to the discovery of conserved sites on beta-coronavirus spike proteins, which confer protection against multiple strains, and has been involved in the development of antibody-based strategies to prevent and treat viral infections. His research also includes the use of advanced techniques such as microfluidics combined with electron microscopy to rapidly map antibody-viral glycoprotein complexes, and the design of vaccines and inhibitors targeting viral proteases.

Research topics

• Medicine
• Psychology
• Neuroscience
• Internal medicine
• Pathology
• Psychiatry
• Machine Learning
• Biology
• Political Science
• Computer Science
• Artificial Intelligence
• Theoretical computer science
• Gastroenterology
• Oncology
• Mathematics
• Physical therapy
• Econometrics
• Data science

Selected publications

• Insula Network Microstructural Injury Links Low-Level Blast Exposure to Clinical Depression in Military Special Operations Forces Soldiers

  medRxiv · 2026-05-15

  articleOpen access

  Special Operations Forces (SOF) sustain repeated low-level blast (LLB) exposures; while most remain resilient, a subset develop depression, sleep disruption and reduced wellbeing that threaten readiness. We asked whether sub-concussive LLB chronically injures an insula-centered cortico-striato-thalamic network and whether network architecture explains divergent outcomes. In a mouse model parameterized to SOF blast exposure monitoring data, ninety 3-psi blasts over three weeks produced persistent diffusion and connectivity deficits across insular, striatal, pallidal and thalamic nodes, accompanied by tauopathy, neuroinflammation, vascular amyloid, and durable sleep and metabolic abnormalities. In SOF Soldiers, measures of cumulative LLB exposure predicted right insula-striatal diffusion/neurite disruption and increased depression risk. Interventional multi-mediator modeling showed that right insula-striatal microstructural injury mediated the effect of LLB to increase depression risk, while moderator screening identified features that amplify or buffer this mediation, defining risk and resilience zones. These findings enable precision blast-medicine integrating exposure dose, circuit biomarkers and moderator profiles.

  PublisherDOI

• Neuroprotection trial design in progressive supranuclear palsy: challenges and solutions

  Alzheimer s & Dementia Translational Research & Clinical Interventions · 2026-04-01

  articleOpen accessSenior author

  INTRODUCTION: We review the specific challenges posed to neuroprotective trial design by progressive supranuclear palsy (PSP), a rare disorder difficult to diagnose and to assess quantitatively. METHODS: Focusing on reducing the size and cost of trials, we review elements of PSP neuroprotection trial methodology and formulate a new minimum clinically important difference (MCID) for PSP to be used as a potential outcome milestone. RESULTS: While the original, 28-item version of the PSP Rating Scale (PSPRS) remains the best-validated and most widely published clinical outcome measure, promising improvements include the PSPRS-15 and -10; magnetic resonance imaging (MRI) volumetry; wearable movement-sensitive devices; platform, futility, basket, factorial, adaptive, and multistage designs; customized endpoints; baseline predictor stratification; and the replacement of a continuous disability scale with attainment of milestones, possibly including our newly calculated MCID. DISCUSSION: The specific assessment tools we deem most valuable could be used individually or in combination to reduce the required N and cost of PSP neuroprotection trials.

  PublisherDOI

• Safety and efficacy of crenezumab in cognitively unimpaired carriers of the PSEN1 mutation at risk for autosomal-dominant Alzheimer's disease in Colombia (API ADAD Colombia Trial): a phase 2, randomised, double-blind, placebo-controlled trial

  The Lancet Neurology · 2026-01-22

  articleOpen access

  BACKGROUND: mutation at high imminent risk of developing symptoms due to Alzheimer's disease. METHODS: autosomal-dominant mutation were randomly assigned 1:1 to receive placebo or subcutaneous crenezumab (investigators and participants were masked to treatment allocation), with an initial 300 mg dose every 2 weeks that increased to 720 mg every 2 weeks, and a later optional increase to 60 mg/kg intravenously every 4 weeks. Randomisation was stratified by age, education, APOE ɛ4 carrier status, and baseline Clinical Dementia Rating. Mutation non-carriers received placebo and were included in a 1:2 ratio of non-carriers to carriers to maintain genotype masking and include a genetic kindred control. Dual primary outcomes were the annualised rates of change in the Alzheimer's Prevention Initiative (API) preclinical autosomal-dominant Alzheimer's disease (ADAD) composite test total score and Free and Cued Selective Reminding Test-Cueing Index (FCSRT-CI) assessed in randomised participants who received at least one dose of the study drug, according to treatment assignment. Primary endpoints were assessed with a random coefficient regression model with a missing-at-random assumption adjusting for randomisation factors. Safety endpoints for mutation carriers were assessed in randomised participants who received at least one dose of the study drug. This trial is registered with ClinicalTrials.gov (NCT01998841) and is completed. FINDINGS: 619 Colombian API registrants were prescreened, 315 were assessed for eligibility, and 252 were enrolled (crenezumab-carrier, n=85; placebo-carrier, n=84; placebo-non-carrier, n=83; 160 [63%] women and 92 [37%] men) between Dec 20, 2013, and Feb 27, 2017. 237 (94%) completed the trial, with final data collection on March 22, 2022. The annualised rate of change in the API ADAD composite was -1·10 (SE 0·29) in the crenezumab group and -1·43 (0·29) in the placebo group (between-group difference 0·33 [95% CI -0·48 to 1·13]; p=0·43). The annualised rate of change in FCSRT-CI was -0·03 (0·00) in the crenezumab group and -0·04 (0·00) in the placebo group (between-group difference 0·01 [0·00 to 0·02]; p=0·16). All participants had at least one adverse event; serious adverse events occurred in 23 (27%) of 84 in the crenezumab group and 21 (25%) of 84 in the placebo group. No fatalities occurred. INTERPRETATION: Crenezumab therapy administered for 5-8 years did not result in significant benefits on our primary clinical outcomes in cognitively unimpaired participants predisposed to developing ADAD dementia; secondary and exploratory outcomes also showed no significant effect on removal of amyloid plaques or other clinical or biomarker outcomes. Together with the results of other anti-amyloid β trials, robust fibrillar amyloid removal appears necessary for clinical efficacy in people with elevated brain amyloid. This study will further inform the biomarker, cognitive, and clinical trajectory of preclinical ADAD, the risk of clinical progression in amyloid-positive and amyloid-negative mutation carriers, and the size and design of future secondary and primary prevention trials. FUNDING: US National Institute on Aging (NIA), Banner Alzheimer's Institute, Genentech, F Hoffmann-La Roche.

  PublisherDOI

• A Randomized Controlled Trial of Prazosin for Disruptive Agitation in Alzheimer’s Disease: PEACE-AD

  The American Journal of Geriatric Psychiatry Open Science Education and Practice · 2026-05-01

  articleOpen access

  <h2>Abstract</h2> PEACE-AD was a 12-week placebo-controlled multisite randomized clinical trial testing the efficacy and safety of prazosin, an alpha-1 adrenoreceptor antagonist, in treating disruptive agitation in Alzheimer's disease (AD). It was initially designed to enroll only long-term care residents, however due to the COVID-19 pandemic, it was redesigned to be fully remote with home-dwelling participants. Randomization was 2:1 prazosin:placebo with 4-week flexible dose titration to a maximum of 4 mg a.m. and 6 mg bedtime, with 8 weeks maintenance. The primary outcome was the ADCS Clinical Global Impression of Change-Agitation (CGIC-A) with secondary outcomes including the Neuropsychiatric Inventory and the ADCS Activities of Daily Living-Severe Dementia Version, with Cohen-Mansfield Agitation Inventory (CMAI) as exploratory. There were 35 participants aged 80 ± 10 years (mean ± SD), 27 randomized to prazosin and eight to placebo. Prazosin completion rate was 59.2% (16/27); placebo was 37.5% (3/7). There were no significant treatment differences on the primary or secondary outcomes. Prazosin showed higher odds of response of moderate or marked improvement on CGIC-A (OR = 2.89 [0.37,22.9], p=0.314). CMAI scores significantly favored prazosin at week 12 (p=0.034). There were no significant differences in treatment-emergent adverse events; however, 7 serious adverse events occurred in 5 women on prazosin, none on placebo (p=0.309). This small RCT supports the possible efficacy of prazosin in treating disruptive agitation in AD, with important safety considerations with its use. This trial provides some feasibility data on conducting a fully remote trial in home dwellers with disruptive agitation.

  PublisherOA PDFDOI

• Estimation of reference curves for brain atrophy and analysis of robustness to machine effects

  Scientific Reports · 2025-10-03 · 1 citations

  articleOpen access

  Neurodegenerative diseases like Alzheimer's are difficult to diagnose due to brain complexity and imaging variability. However, volumetric analysis tools, using reference curves, help detect abnormal brain atrophy and support diagnosis and monitoring. This study evaluates the robustness of three segmentation algorithms, AssemblyNet, FastSurfer and FreeSurfer, in constructing brain volume reference curves and detecting hippocampal atrophy. Using data from 3,730 cognitively normal subjects, we built reference curves and assessed robustness to magnetic field strength (1.5T vs. 3T) using four error metrics (sMAPE, sMSPE, wMAPE, sMdAPE) with bootstrap validation. We evaluated classification performance using hippocampal atrophy rates and HAVAs scores (Hippocampal-Amygdalo-Ventricular Atrophy scores). AssemblyNet shows the lowest errors across all robustness metrics. In contrast, FastSurfer and FreeSurfer exhibit greater deviations, indicating higher sensitivity to field strength variability. AssemblyNet provides consistent hippocampal atrophy rates across all reference models, despite slightly lower sensitivity, while FastSurfer and FreeSurfer display greater variability. Specificity ranges from 0.87 to 0.91 for AssemblyNet, compared to 0.76-0.93 for FastSurfer and 0.86-0.93 for FreeSurfer. Using the HAVAs score, all methods detect high atrophy rates in Alzheimer's patients. FastSurfer achieves the highest sensitivity (0.98), while AssemblyNet reaches the best specificity (0.95) and the highest balanced accuracy (0.91). This study underscores the importance of algorithm choice for reliable brain volumetric analysis in heterogeneous imaging environments. Among the methods tested, AssemblyNet stands out as both sensitive to Alzheimer's-related atrophy and robust to acquisition variability, making it a strong candidate when analyzing hippocampal volumes in large, multi-site datasets.

  PublisherOA PDFDOI

• Uncovering atrophy progression pattern and mechanisms in individuals at risk of Alzheimer's disease

  Brain Communications · 2025-01-01 · 3 citations

  articleOpen access

  Alzheimer's disease is associated with pre-symptomatic changes in brain morphometry and accumulation of abnormal tau and amyloid-beta pathology. Studying the development of brain changes prior to symptoms onset may lead to early diagnostic biomarkers and a better understanding of Alzheimer's disease pathophysiology. Alzheimer's disease pathology is thought to arise from a combination of protein accumulation and spreading via neural connections, but how these processes influence brain atrophy progression in the pre-symptomatic phases remains unclear. Individuals with a family history of Alzheimer's disease (FHAD) have an elevated risk of Alzheimer's disease, providing an opportunity to study the pre-symptomatic phase. Here, we used structural MRI from three databases (Alzheimer's Disease Neuroimaging Initiative, Pre-symptomatic Evaluation of Experimental or Novel Treatments for Alzheimer Disease and Montreal Adult Lifespan Study) to map atrophy progression in FHAD and Alzheimer's disease and assess the constraining effects of structural connectivity on atrophy progression. Cross-sectional and longitudinal data up to 4 years were used to perform atrophy progression analysis in FHAD and Alzheimer's disease compared with controls. PET radiotracers were also used to quantify the distribution of abnormal tau and amyloid-beta protein isoforms at baseline. We first derived cortical atrophy progression maps using deformation-based morphometry from 153 FHAD, 156 Alzheimer's disease and 116 controls with similar age, education and sex at baseline. We next examined the spatial relationship between atrophy progression and spatial patterns of tau aggregates and amyloid-beta plaques deposition, structural connectivity and neurotransmitter receptor and transporter distributions. Our results show that there were similar patterns of atrophy progression in FHAD and Alzheimer's disease, notably in the cingulate, temporal and parietal cortices, with more widespread and severe atrophy in Alzheimer's disease. Both tau and amyloid-beta pathology tended to accumulate in regions that were structurally connected in FHAD and Alzheimer's disease. The pattern of atrophy and its progression also aligned with existing structural connectivity in FHAD. In Alzheimer's disease, our findings suggest that atrophy progression results from pathology propagation that occurred earlier, on a previously intact connectome. Moreover, a relationship was found between serotonin receptor spatial distribution and atrophy progression in Alzheimer's disease. The current study demonstrates that regions showing atrophy progression in FHAD and Alzheimer's disease present with specific connectivity and cellular characteristics, uncovering some of the mechanisms involved in pre-clinical and clinical neurodegeneration.

  PublisherOA PDFDOI

• Effects of exercise versus usual care on older adults with amnestic mild cognitive impairment: EXERT versus ADNI

  Alzheimer s & Dementia · 2025-04-01 · 5 citations

  articleOpen access

  INTRODUCTION: EXERT was a multisite randomized controlled trial (RCT) examining the effects of moderate-high intensity aerobic training (AX) versus lower-intensity stretching/balance/range of motion (SBR) on cognitive trajectories in older adults with amnestic mild cognitive impairment (aMCI). METHODS: Preplanned post-hoc analyses were conducted to compare each arm to a propensity-matched usual care (no intervention) group from Alzheimer's Disease Neuroimaging Initiative 1 (ADNI-1) selected for similarity across key characteristics. Differences in 12-month trajectories in the primary endpoint (ADAS-Cog-Exec) and magnetic resonance imaging (MRI) volumes in prespecified brain regions were compared. RESULTS: AX and SBR showed significantly less 12-month cognitive decline than ADNI-1 (AX:n = 109, β = 0.169, 95% confidence interval [CI] 0.011-0.328; SBR:n = 105, β = 0.181, 95% CI 0.007-0.354). There were trends of less prefrontal cortex volume loss for both EXERT groups and less AD signature region volume loss for SBR relative to ADNI-1 over 12 months. DISCUSSION: Moderate-high intensity aerobic or low-intensity flexibility exercise for 12 months in participants with aMCI may provide protection against decline relative to usual care. CLINICAL TRIAL REGISTRATION: The EXERT clinical trial is registered at clinicaltrials.gov (NCT02814526). HIGHLIGHTS: EXERT was a randomized controlled trial in sedentary older adults with aMCI. EXERT arms were propensity-matched to a usual care (no intervention) group (Alzheimer's Disease Neuroimaging Initiative 1 [ADNI-1]). High and low-intensity exercise arms had less 12-mo cognitive decline than ADNI-1. There were trends of less prefrontal cortex volume loss for each arm versus ADNI-1.

  PublisherOA PDFDOI

• Bidirectional associations between PTSD severity and glycemic control in trauma-exposed women with type 2 diabetes

  medRxiv · 2025-12-01

  preprintOpen access

  Abstract Objective Posttraumatic stress disorder (PTSD) is linked with metabolic disturbance and increased risk of Type 2 diabetes (DM2), yet mechanisms explaining this connection have yet to be defined. Here we examine commonly hypothesized risk factors influencing the strength and directionality of the relationship between PTSD and DM2 severity in trauma-exposed black women with DM2. Methods We examined the relationships among PTSD severity (Clinician-Administered PTSD Scale, CAPS), glycemic control (A1c), age, smoking, body mass index (BMI), depression (Beck Depression Inventory, BDI) and medications in trauma-exposed Black women with DM2 recruited from an urban hospital between 2013-2015 (n=95) as a part of the Grady Trauma Project. Missing data were handled with multiple imputation. Relationships were assessed using lasso regression performed on each imputed dataset. Mediation analysis tested whether BMI or depression mediated associations between PTSD severity and glycemic control. Results Lasso regression identified BDI, ACE inhibitor/ARB/beta blocker use, and CAPS severity as predictors in the final model predicting A1c. In pooled linear regression analyses across imputed datasets, overall model fit was modest, and none of these predictors were statistically significant. Lasso regression in the reverse direction yielded BMI, BDI, ACE inhibitor/ARB use, and A1c for the final model predicting CAPS severity. In pooled analyses, model fit was substantially stronger and BDI emerged as the only statistically significant predictor (p&lt;0.05). Mediation analyses indicated that BDI, but not BMI, significantly mediated the effect of A1c on CAPS severity, as well as to a lesser extent the reverse relationship, the effect of CAPS severity on A1c. Conclusion In this examination of the relationships between PTSD and DM2 severity, CAPS severity and A1c were found to be bidirectionally correlated in lasso regression models, with BDI emerging as a significant predictor and mediator of these relationships. BMI was not found to be a mediator in either direction. These results suggest the possibility of a reciprocal relationship between PTSD and DM2, where worsening of either condition may influence worsening of the other, where treating one condition in isolation may not be sufficient to prevent increased overall morbidity and mortality. Further research should include physiological interventions to ascertain causality in these relationships.

  PublisherOA PDFDOI

• Effects of exercise on cognition and Alzheimer's biomarkers in a randomized controlled trial of adults with mild cognitive impairment: The EXERT study

  Alzheimer s & Dementia · 2025-04-01 · 16 citations

  articleOpen access

  INTRODUCTION: The EXERT study (Exercise in Adults with Mild Memory Problems) was a Phase 3, multicenter, randomized controlled trial that examined effects of exercise on cognition and other measures of brain health in sedentary older adults with amnestic mild cognitive impairment (MCI). METHODS: Participants were randomized to moderate-high intensity aerobic training (AX) or low-intensity stretching/balance/range of motion (SBR) for 18 months. Exercise was supervised for the first 12 months. Assessments were administered at baseline and every 6 months. The primary outcome was a global cognitive composite. RESULTS: A total of 296 participants were enrolled, and intervention adherence was high (supervised session attendance: AX = 81%, SBR = 87%). Intervention effects on cognition did not differ for AX and SBR (regression = -0.078, standard error [SE] = 0.074; p = 0.3). Notably, there was no 12 month cognition decline for either group, and mean 12 month hippocampal volume loss for both groups was low at 0.51%. DISCUSSION: Exercise intensity did not differentially affect cognitive trajectory. Intervention delivery was successful (high adherence) and cognition remained stable over 12 months for both MCI groups, an association that warrants further study. HIGHLIGHTS: Exercise in Adults with Mild Memory Problems (EXERT) was a large multisite randomized controlled trial of moderate-high intensity aerobic training versus lower-intensity flexibility and balance exercise in sedentary older adults with amnestic mild cognitive impairment (MCI). A sensitive and validated measure of global cognitive function, the Alzheimer's Disease Assessment Scale-Cognition supplemented with tests of executive function (ADAS-Cog-Exec), was used to assess intervention efficacy with 12 months of supervised exercise. There was no intervention group difference on the 12-month cognitive trajectory of the ADAS-Cog-Exec. Intervention delivery was successful (high adherence), and cognition remained stable over 12 months for both exercise groups. Regular supported moderate-high or lower-intensity exercise may stall decline in adults with amnestic MCI, but further investigation is needed.

  PublisherOA PDFDOI

• Surface-based morphometry reveals divergent aging trajectories in veterans with and without traumatic brain injury

  GeroScience · 2025-09-29

  articleOpen access

  Abstract This study investigates how traumatic brain injury (TBI) alters cortical aging by comparing cortical thickness (CT) and surface area (SA) in 34 brain regions between TBI survivors and age-matched controls. Using a cross-sectional retrospective design, 105 Vietnam Veterans (32 with moderate-to-severe TBI, 73 controls) were analyzed via surface-based morphometry. Principal Component Analysis (PCA) reduced dimensionality, and Multivariate Analysis of Covariance tested group differences while controlling for age, education, depression, Post-Traumatic Stress Disorder, and intracranial volume. Findings revealed divergent morphometric signatures of aging: the proportion of SA variance explained by the first principal component (PC1) was lower in the TBI cohort compared to controls, particularly in parietal and limbic regions. Conversely, CT variance explained by PC1 was higher in TBI compared to controls, with fewer factor loadings in frontal and occipital regions, suggesting differential structural aging patterns due to TBI. Regression analysis demonstrated a stronger association of SA with age in TBI (R 2 = 0.619, p = 0.01), while CT exhibited significant negative age-related thinning in TBI-specific regions (R 2 = 0.450, p &lt; 0.001). Together, these results suggest that TBI survivors exhibit structured, yet distinct, cortical remodeling, contrasting with the more diffuse patterns seen in normal aging. The differentiated organization of brain areas based on CT and SA points to brain morphology-based biomarkers capable of distinguishing pathological from normative aging trajectories. These biomarkers hold translational potential for refining diagnostic models of brain age and informing targeted neuromodulation or rehabilitation strategies to support cognitive and functional resilience in older adults with TBI. Graphical Abstract

  PublisherOA PDFDOI

Recent grants

• NIH Grant U01AG010483

  NIH · $218.6M · 2012

• NIH Grant P01NS044233

  NIH · $25.6M · 2018

Frequent coauthors

• Mary Sano

  Icahn School of Medicine at Mount Sinai

  304 shared

• Paul Aisen

  University of Southern California

  244 shared

• Clifford R. Jack

  WinnMed

  228 shared

• Paul Aisen

  University of Southern California

  228 shared

• Christopher H. van Dyck

  Yale University

  226 shared

• Pierre N. Tariot

  Banner Alzheimer’s Institute

  201 shared

• David S. Knopman

  Mayo Clinic

  197 shared

• Michael Grundman

  University of California, San Diego

  195 shared

Education

• Ph.D. (biostatistics), Biostatistics

  University of Washington

  1983

• Bachelor of Arts (mathematics), Mathematics

  Pomona College

  1977

• High School Diploma

  Claremont High School

  1973