Bio


Dr. Cellas Hayes is a first-generation college graduate, neuroscientist, and postdoctoral fellow at Stanford University. He holds a bachelor’s degree in Biology and minors in Classics, and Latin from the University of Mississippi (2019) and earned his Ph.D. in Pharmaceutical Sciences with an emphasis in Pharmacology (2022), where he received advanced neuroscience research training under Dr. Nicole Ashpole’s guidance.
At Stanford, Dr. Hayes employs cutting-edge epidemiological and biostatistical methods with high-dimensional biological data to investigate the impact of cerebrovascular and Alzheimer’s disease pathologies on age-related outcomes such as cognitive decline and dementia. He has established national collaborations including the Strong Heart Study, Cardiovascular Health Study, Healthy Aging Brain Study - Health Disparities, and the National Alzheimer’s Coordinating Center.
Dr. Hayes is becoming a recognized leader in his field and beyond, serving as a Stanford Propel Postdoctoral Fellowship Alumni, a Burroughs Wellcome Fund PDEP Fellow, and a HABS-HD Health Enhancement Scientifist Program Fellow, and diversity supplement recipient. He is the founder and chair of the National Black Postdocs Emergency Support Program and a former co-president of the Stanford Black Postdocs Association. As a postdoc, Dr. Hayes has accrued over 500K in fellowship funds while participating in notable professional development programs like the NIH NIMHD HDRI and NIA Butler Williams Scholars Program. At UM, Dr. Hayes was the first recipient to receive a NIH NRSA F31 in 37 years while also being a Southern Regional Education Board Scholar and UMMC-GTEC Smith Scholars Program.
Passionate about mentorship and education, Dr. Hayes develops innovative resources and curricula through the Stanford Grant Writing Academy, where he has trained postbaccalaureate, Ph.D., and postdoctoral scholars in grant writing and career development.

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All Publications


  • STROKE INCIDENCE AND HIGH-SENSITIVITY C-REACTIVE PROTEIN AMONG AFRICAN AMERICANS: THE JACKSON HEART STUDY ETHNICITY & DISEASE Hayes, C. A., Thorpe, R. J., Dhamoon, M., Heitman, E., Norris, K. C., Beech, B. M., Bruce, M., Walker, B., Reneker, J. C. 2025; 35 (1): 1-7
  • Population intervention models of racial ethnic disparities in cognitive outcomes from cardiometabolic risk factors - HABS-HD. Alzheimer's research & therapy Hayes, C. A., Abdullah, L., Gills, J., Odden, M. C., Health and Aging Brain Study (HABS-HD) Study Team 2025; 17 (1): 217

    Abstract

    BACKGROUND: Alzheimer's disease and related dementias are major public health challenges, with the apolipoprotein (APOE) epsilon4 allele being a significant genetic risk factor. Cardiometabolic risk factors such as diabetes, hypertension, dyslipidemia, obesity, and tobacco use are also linked to cognitive impairment. The objective of this study was to (1) characterize both independent and interactive associations of racial/ethnic group (Non-Hispanic White (NHW), Non-Hispanic Black (NHB) and Hispanic), APOE epsilon4 genotype, and multiple cardiometabolic risk factors with performance across four cognitive domains. Secondarily, we aimed to quantify the hypothetical population-level cognitive gains that could result from eliminating each modifiable risk factor within each racial/ethnic group.METHODS: We analyzed baseline data from 3,833 HABS-HD participants (1,348 NHW; 1,065 NHB; 1,420 Hispanic; mean age 65.3±8.6years; 62.0% female). APOE genotype, consensus-determined cardiometabolic status, and harmonized cognitive domain scores (episodic memory, executive function, processing speed, language) were obtained. Multivariable linear regressions assessed independent effects of race/ethnicity, APOE epsilon4 carriage, and each cardiometabolic factor on domain-specificz-scores, adjusting for age, sex, and education (Bonferroni-corrected). Interaction terms tested effect modification by race/ethnicity. Counterfactual population intervention models estimated the mean cognitive gain from hypothetically eliminating each modifiable risk factor within each racial/ethnic group.RESULTS: NHB Hispanic, and NHW participants prevalences wereAPOE epsilon4 (32.2%, 27.4%, 17.6%), diabetes (26.1%, 35.0%, 13.9%), hypertension (79.0%, 63.6%,58.2%), obesity (56.8%, 50.3%,38.5%), and tobacco dependence (12.9%, 7.5%, 3.9%). In adjusted models, NHB and Hispanic ethnicity, APOE epsilon4, diabetes, hypertension, and tobacco dependence each independently predicted lower performance across all four cognitive domains (adjusted p<.001), whereas obesity showed domain-specific positive associations. No race*risk-factor interactions remained significant after correction. In intervention models, hypothetically eliminating diabetes and hypertension yielded the largest predicted improvements, especially in executive function and language, with the greatest gains projected among NHB and Hispanic racial ethnic group.CONCLUSIONS: Cardiometabolic health markedly contributes to racial ethnic differences in cognitive aging beyond APOE epsilon4 effects. Population-level interventions targeting diabetes and hypertension could narrow NHB and Hispanic cognitive deficits, informing precision public-health strategies for dementia prevention.

    View details for DOI 10.1186/s13195-025-01866-9

    View details for PubMedID 41035086

  • Micro infarcts are associated with cognitive impairment in neurofibrillary tangle predominant decedents: evidence from the NACC autopsy cohort. Alzheimer's research & therapy Martinez, N., Bharani, K. L., Hasan, S., Hayes, C. A. 2025; 17 (1): 216

    Abstract

    BACKGROUND: A subset of older adults develops high neurofibrillary tangle burden with minimal amyloid, a biomarker profile consistent with suspected non-Alzheimer's pathophysiology or primary age-related tauopathy. Yet its cognitive correlates are unclear, particularly when vascular neuropathologies coexist. We examined whether vascular neuropathologies are linked to cognitive impairment proximate to death and pre-mortem cognitive decline among decedents with intermediate-to-high Braak stage (III-VI) and absent/low neuritic plaques.METHODS: In 579 autopsied participants from the National Alzheimer's Coordinating Center cohort (Braak III-VI; CERAD C0-C1), we evaluated arteriolosclerosis, atherosclerosis of the circle of Willis, cerebral amyloid angiopathy, gross infarcts/lacunes, and microinfarcts effect on harmonized memory, executive function, and language z-scores proximate to death using multivariable linear regression (adjusted for age, sex, education, APOE epsilon4 status). Linear mixed-effects models assessed interactions between each vascular neuropathology and years-to-death on pre-mortem longitudinal decline.RESULTS: At the last assessment, microinfarcts were associated with lower memory (beta=-0.28, 95% CI -0.51 - -0.05; p=0.02), executive function (beta=-0.24, 95% CI -0.44 - -0.04; p=0.02), and language (beta=-0.21, 95% CI -0.38 - -0.04; p=0.02). These associations remained after controlling for cardiovascular risk, neuritic plaques and Braak stage, last assessment and death interval, and co-existing vascular neuropathologies. Microinfarcts were not associated with the rates of pre-mortem cognitive decline.CONCLUSIONS: Microinfarcts are contributors to domain-specific cognitive deficits in tangle-predominant, low-amyloid older adults. These findings underscore a vascular-neurodegenerative pathway distinct from classic Alzheimer's disease. Thus, targeting microvascular injury may mitigate impairment in this underrecognized phenotype.

    View details for DOI 10.1186/s13195-025-01863-y

    View details for PubMedID 41035071

  • Application of modified Poisson regression for risk estimation of major neuropathology outcomes: National Alzheimer's coordinating center. Journal of Alzheimer's disease : JAD Hayes, C. A., Odden, M. C., Thorpe, R. J. 2025: 13872877251375099

    Abstract

    Odds ratios (OR) can overestimate risk when the prevalence of outcomes is more than 10%. We compared logistic and modified Poisson models in 5843 National Alzheimer's Coordinating Center decedents to examine associations of apolipoprotein (APOE) ε4, age at death, sex, and education with 7 neuropathologies. OR for neuritic plaques (6.28) and Braak stage (4.90) attenuated to prevalence rate ratios of 1.38 and 1.08; similar attenuation occurred for Lewy body disease, arteriolosclerosis, cerebral amyloid angiopathy, and infarcts. Modified Poisson regression is critical for valid risk estimation, reliable interpretations, and accurate risk stratification in non-rare outcome studies.

    View details for DOI 10.1177/13872877251375099

    View details for PubMedID 40924589

  • Targeting the cardiometabolic bottleneck to slow polypathology and cognitive decline. Alzheimer's & dementia : the journal of the Alzheimer's Association Hayes, C. A., Younes, K. 2025; 21 (9): e70684

    View details for DOI 10.1002/alz.70684

    View details for PubMedID 40916741

    View details for PubMedCentralID PMC12415439

  • Sex differences in the association of cardiometabolic risk scores and blood pressure measurements with white matter hyperintensities in diverse older adults-HABS-HD. Frontiers in aging neuroscience Hayes, C. A., Vintimilla, R., Chaudhuri, S., Odden, M. C. 2025; 17: 1607646

    Abstract

    We aimed to determine whether cardiometabolic risk factors and blood-pressure (BP) metrics were differentially associated with white matter hyperintensities volume (WMHV) in males versus females in the Health and Aging Brain Study-Health Disparities.We analyzed 3,585 community-dwelling adults (2,207 females) from non-Hispanic White, non-Hispanic Black, and Hispanic groups who underwent BP measurement and WMHV quantification. Linear regression models assessed (i) individual risk factors (diabetes, hypertension, dyslipidemia, obesity, tobacco dependence), (ii) a composite risk score, and (iii) four BP metrics (systolic, diastolic, pulse pressure, mean arterial pressure), each including a sex-interaction term and adjusting for age, education, race/ethnicity, and scanner. A second BP model also controlled for all five risk factors.Diabetes (β = 0.46, 95% CI 0.28-0.64), hypertension (β = 0.47, 0.30-0.64), and higher composite risk (β = 0.19, 0.12-0.26) were associated with greater WMHV. Diastolic BP (β = 0.18, 0.11-0.26) and mean arterial pressure (β = 0.14, 0.07-0.21) related to larger WMHV, with diastolic BP remaining significant after full adjustment (β = 0.14, 0.07-0.22). No sex interactions survived correction.These findings underscore the importance of aggressive cardiometabolic and BP control, particularly diastolic BP, to mitigate WMHV in both sexes.

    View details for DOI 10.3389/fnagi.2025.1607646

    View details for PubMedID 40831584

    View details for PubMedCentralID PMC12358495

  • Racial and ethnic differences in cardiometabolic predictors of white matter hyperintensities burden among males: The HABS-HD study. Journal of Alzheimer's disease : JAD Hayes, C. A., Jones, R., Thorpe, R. J. 2025: 13872877251365128

    Abstract

    Background: Cardiometabolic conditions accelerate white-matter hyperintensity (WMH) accumulation-a vascular injury marker linked to increased Alzheimer's disease risk-yet how these relationships vary by race and ethnicity in males is poorly understood. Objective: To quantify racial ethnic-specific associations between cardiometabolic risk factors, blood-pressure indices, and WMH volume in Non-Hispanic White (NHW), Non-Hispanic Black (NHB), and Hispanic males. Methods: We analyzed 1378 males (558 NHW, 375 NHB, 445 Hispanic) from the Healthy Aging Brain Study-Health Disparities. Five binary exposures (hypertension, diabetes, dyslipidemia, obesity, tobacco dependence), four continuous blood-pressure metrics (systolic, diastolic, pulse, mean arterial pressure), and a principal-component cardiometabolic score were regressed on log-transformed, intracranial volume-adjusted WMH volume in race-stratified models. Results: Hispanic males exhibited the broadest vulnerability: hypertension, diabetes, and tobacco dependence each predicted higher WMH (β range 0.60-0.77, p ≤ 0.002), and the composite score had the strongest association (β = 0.26, 0.13-0.39, p < 0.001). Additionally, every 10-mm Hg rise in systolic, diastolic, pulse, or mean arterial pressure further increased WMH in Hispanic males (e.g., systolic β = 0.18, 0.11-0.26), an effect absent in NHW and NHB males. Conclusions: Cardiometabolic and hemodynamic drivers of WMH differ markedly across racial and ethnic groups of males, with Hispanic males showing the most pervasive risk profile, NHB males selective associations, and NHW males limited links. Tailored vascular-risk interventions may be essential to curb WMH-related pathways to Alzheimer's disease in racially and ethnically diverse male populations.

    View details for DOI 10.1177/13872877251365128

    View details for PubMedID 40760862

  • Microinfarcts are Associated with Cognitive Impairment in Neurofibrillary Tangle Predominant Decedents: Evidence from the NACC Autopsy Cohort. Research square Martinez, N. C., Bharani, K. L., Hasan, S., Hayes, C. A. 2025

    Abstract

    Background: A growing number of older adults exhibit neurofibrillary tangle pathology without significant amyloid deposition, a biomarker profile consistent with suspected non-Alzheimer's pathophysiology or primary age-related tauopathy. The cognitive consequences within this subgroup remain poorly characterized, particularly with respect to vascular comorbidity. This study investigates whether vascular neuropathologies are associated with pre-mortem cognitive decline among individuals with predominately neurofibrillary tangles and low to none neuritic plaque pathology detected post-mortem.Methods: The sample included autopsy-confirmed data from 579 participants in the National Alzheimer's Coordinating Center (NACC) cohort with intermediate-to-high Braak stage (B2-B3) and absent or minimal neuritic plaques (C0-C1). Vascular neuropathologies included arteriolosclerosis, atherosclerosis of the circle of Willis, gross infarcts/ lacunes, and microinfarcts were assessed for associations with global cognition (Clinical Dementia Rating Sum of Boxes, CDR-SOB) and harmonized cognitive domain specific performance (memory, executive function, and language) using multivariable regression adjusted for age, sex, education, and apolipoprotein epsilon4 status. Sensitivity analyses further controlled for cardiovascular risk, excluded individuals with any neuritic plaques, and controlling for individual neuritic plaque and Braak staging.Results: Cross-sectionally, microinfarcts were consistently associated with poorer memory (beta = - 0.28, p = 0.02), executive function (beta = - 0.24, p = 0.02), and language (beta = - 0.21, p = 0.02) approximate to death. Gross infarcts were associated with language impairment and higher CDR scores. These associations remained significant after adjusting for cardiovascular risk and were even stronger when restricted to strictly neuritic amyloid negative individuals.Conclusions: Microinfarcts may represent a key driver of cognitive impairment in neurofibrillary tangle predominant individuals. These findings highlight a vascular-neurodegenerative pathway that warrants consideration in non-neuritic plaque models of cognitive decline and may inform targeted prevention strategies.

    View details for DOI 10.21203/rs.3.rs-7036276/v1

    View details for PubMedID 40709257

  • Age-dependent interactions of APOE isoform 4 and Alzheimer's disease neuropathology: findings from the NACC. Acta neuropathologica communications Hayes, C. A., Thorpe, R. J., Odden, M. C. 2025; 13 (1): 102

    Abstract

    Alzheimer's disease related pathologies, neurodegenerative pathologies, and vascular neuropathologies are common in older adults at death. Previous studies using the National Alzheimer's Coordinating Center (NACC) have not investigated the association between age at death and apolipoprotein E (APOE) epsilon4 and the prevalence of neuropathologies found at autopsy. We used autopsy confirmed neuropathology data from the NACC to examine the interactive effects of age and APOE epsilon4 on various neuropathologies (N=5,843) using modified Poisson regression to estimate the prevalence ratios. Significant interactions between APOE epsilon4 and age at death were observed for neuritic plaques, Braak staging, diffuse neuritic plaques, and Lewy body disease pathology, with the effect of APOE epsilon4 decreasing at older ages. In contrast, a significant positive interaction was found for hemorrhages/microbleeds, indicating that the association between APOE epsilon4 and microbleeds strengthens with increasing age. These findings suggest that future therapeutic strategies should consider both genetic risk and age to effectively target AD progression.

    View details for DOI 10.1186/s40478-025-02012-0

    View details for PubMedID 40382659

  • Racial ethnic variations in the cardiometabolic determinants and blood pressure of white matter hyperintensities among females-The HABS-HD Study. Alzheimer's & dementia : the journal of the Alzheimer's Association Hayes, C. A., Odden, M. C., Vintimilla, R., Thorpe, R. J. 2025; 21 (5): e70327

    Abstract

    White matter hyperintensity volume (WMH), markers of cerebral small vessel disease, are disproportionately prevalent among Black/African American and Hispanic individuals. While cardiometabolic risk factors contribute to WMHs, their association across racial ethnic groups among females remains unclear. This study examines associations among cardiometabolic risk factors, blood pressure, and WMH volume in non-Hispanic White (NHW), non-Hispanic Black (NHB), and Hispanic females.Using the Health and Aging Brain Study Health Disparities (HABS-HD) cross-sectional visit 1 data (N = 2209), we assessed cardiometabolic risk factors and blood pressure measures in relation to WMH volume via multivariable linear regression models stratified by race/ethnicity.Hypertension was associated with increased WMH volume in NHW females. Diabetes was a significant predictor in Hispanics. Systolic blood pressure and mean arterial pressure were associated with WMH volume in NHB.Findings highlight racial differences in cardiometabolic contributions to WMH burden, emphasizing the need for tailored prevention strategies in racially and ethnically diverse female populations.Overall, there was a main effect of hypertension; however, in stratified analyses hypertension was significantly was associated with greater white matter hyperintensity (WMH) burden in non-Hispanic White females. Non-Hispanic Black females presented with a worse cardiometabolic profile, but this composite was not associated with WMH burden. There was a positive association with the risk composite in non-Hispanic White and Hispanic females. Systolic blood pressure and mean arterial pressure were associated with greater WMH in non-Hispanic Black females, highlighting differential blood pressure contributions to WMH burden.

    View details for DOI 10.1002/alz.70327

    View details for PubMedID 40420353

    View details for PubMedCentralID PMC12106056

  • The impact of arteriolosclerosis on cognitive impairment in decedents without severe dementia from the National Alzheimer's Coordinating Center. Alzheimer's & dementia : the journal of the Alzheimer's Association Hayes, C. A., Young, C. B., Abdelnour, C., Reeves, A., Odden, M. C., Nirschl, J., Crane, P. K., Poston, K. L., Mormino, E. C., Younes, K. 2025; 21 (3): e70059

    Abstract

    Alzheimer's disease neuropathologic change (ADNC), Lewy body disease (LBD), and vascular neuropathologies occur together. Previous studies have been limited by a large majority of participants with severe dementia or advanced stages of pathologies, which limits the detectability of cognitive effects from vascular neuropathologies.Using neuropathology data from the National Alzheimer's Coordinating Center, we examined the association of vascular neuropathologies with cognitive scores in participants without severe dementia (N = 1526) using multivariable linear regression.Controlling for age, sex, education, LBD, and ADNC, arteriolosclerosis was associated with lower memory (β = -0.16 ± 0.06, p < 0.001), executive function (β = -0.25 ± 0.05, p < 0.001), and language scores (β = -0.20 ± 0.05, p < 0.001). The effects of arteriolosclerosis remained when controlling for vascular risk factors.Vascular neuropathologies exhibit distinct relationships with cognition. Arteriolosclerosis is an independent contributor to cognition. Further research should be conducted on whether arteriolosclerosis can serve as a surrogate marker for cognitive decline in early disease stages.In individuals who do not have severe dementia, vascular neuropathologies are common, and the combination of pathologies is heterogeneous in a convenience sample from the Alzheimer's Disease Research Center that reported all the neuropathology data elements for this investigation. Arteriolosclerosis is associated with several cognitive domain scores, including memory, executive function, and language when controlling for the effects of Alzheimer's disease neuropathologic change and Lewy body disease. These results reinforce the importance of vascular pathology for cognition among people along the Alzheimer's disease spectrum.

    View details for DOI 10.1002/alz.70059

    View details for PubMedID 40110658

  • Stroke Incidence and High-Sensitivity C-Reactive Protein Among African Americans: The Jackson Heart Study. Ethnicity & disease Hayes, C. A., Thorpe, R. J., Dhamoon, M., Heitman, E., Norris, K. C., Beech, B. M., Bruce, M., Walker, B., Reneker, J. C. 2025; 35 (1): 1-7

    Abstract

    Strokes are a leading cause of death and disability among African Americans in the United States. Biological markers to predict stroke remain elusive; thus, our objective was to investigate whether inflammation, as measured by high-sensitivity C-reactive protein (hs-CRP), was associated with stroke incidence among African Americans enrolled in the Jackson Heart Study (JHS).Baseline hs-CRP levels were categorized in quintiles: quintile 1 (0.0084 mg/L); quintile 2 (0.0085-0.0189 mg/L); quintile 3 (0.0190-0.036 mg/L); quintile 4 (0.037-0.0675 mg/L); quintile 5 (≥0.0676 mg/L). Nonfatal stroke incidence was ascertained from passive community surveillance through annual phone calls and adjudicated via hospital records. At baseline, stroke risk factors/covariates were compared across quintiles using a one-way analysis of variance and a chi-square test. The association between baseline hs-CRP levels and stroke incidence was determined using a Cox regression analysis to estimate hazard ratios (HRs) and 95% confidence intervals (CI).In the unadjusted model, hs-CRP levels in quintile 2 (HR, 1.48; 95% CI, 0.96-2.29), quintile 3 (HR, 1.44; 95% CI, 0.93-2.24), and quintile 4 (HR, 1.09; 95% CI, 0.68-1.74) were not associated with stroke incidence when compared with quintile 1 (reference). However, individuals within quintile 5 (HR, 1.78; 95% CI, 1.17-2.72) exhibited a significantly increased risk for stroke compared with those in the reference quintile. This risk persisted after adjusting for stroke risk factors (demographics, anthropometrics, health condition covariates, health behavioral risk factors, and cardiovascular disease history) for quintile 5 (HR, 1.87; 95% CI, 1.17-2.98) compared with reference quintile 1.An increased and independent risk of nonfatal stroke appears at the highest quintile of hs-CRP values (≥0.0676 mg/L) among JHS participants.

    View details for DOI 10.18865/EthnDis-2023-78

    View details for PubMedID 40124641

    View details for PubMedCentralID PMC11928021

  • Insulin-like growth factor-1 and cognitive health: Exploring cellular, preclinical, and clinical dimensions. Frontiers in neuroendocrinology Hayes, C. A., Wilson, D., De Leon, M. A., Mustapha, M. J., Morales, S., Odden, M. C., Ashpole, N. 2024: 101161

    Abstract

    Age and insulin-like growth factor-1 (IGF-1) have an inverse association with cognitive decline and dementia. IGF-1 is known to have important pleiotropic functions beginning in neurodevelopment and extending into adulthood such as neurogenesis. At the cellular level, IGF-1 has pleiotropic signaling mechanisms through the IGF-1 receptor on neurons and neuroglia to attenuate inflammation, promote myelination, maintain astrocytic functions for homeostatic balances, and neuronal synaptogenesis. In preclinical rodent models of aging and transgenic models of IGF-1, increased IGF-1 improves cognition in a variety of behavioral paradigms along with reducing IGF-1 via knockout models being able to induce cognitive impairment. At the clinical levels, most studies highlight that increased levels of IGF-1 are associated with better cognition. This review provides a comprehensive and up-to-date evaluation of the association between IGF-1 and cognition at the cellular signaling levels, preclinical, and clinical levels.

    View details for DOI 10.1016/j.yfrne.2024.101161

    View details for PubMedID 39536910

  • Empowering Early Career Researchers: The Jackson Heart Study Smith Scholars Program. Journal of racial and ethnic health disparities Hayes, C. A., Jones, R. 2024

    Abstract

    The University of Mississippi Medical Center Graduate Training and Education Center houses the Robert E. Smith, MD, Scholars Program, a two-year certificate program that equips predoctoral trainees from five Mississippi universities with advanced research skills in cardiovascular epidemiology. Funded by the National Heart, Lung, and Blood Institute (NHLBI), the program focuses on addressing health disparities, minority health, and health inequities in underserved communities. Trainees receive mentorship, career coaching, and a $7,500 annual stipend, building a foundation for postdoctoral opportunities and expanding professional networks. The Smith Scholars Program emphasizes population health and provides interdisciplinary training in areas such as biostatistics, scientific communication, and cardiovascular health. It is uniquely positioned to address systemic challenges, particularly in Mississippi, a state with high cardiovascular disease prevalence and limited research funding. The program's regional advantage and its partnership with the Jackson Heart Study offer scholars exposure to health disparities in Black/African American communities, preparing them to contribute to innovative, community-based research. Additionally, it fosters collaborative science, enabling participants to overcome academic barriers and engage with large-scale health equity research efforts. The Smith Scholars Program has been instrumental in shaping the career trajectories of its participants, facilitating their transition to postdoctoral positions and independent research roles.

    View details for DOI 10.1007/s40615-024-02226-3

    View details for PubMedID 39455520

  • Revolutionizing Postdoctoral Training Using the Social Ecological Model: Insights and Experiences from the Propel Scholars GEN BIOTECHNOLOGY Hayes, C. A., Headley, C. A., Nava, A. R., Vizcarra, E. A., Garcia, K. C., Mullen, M. S., Morales, J., Venida, A. C., Follis, S. 2024
  • Revolutionizing Postdoctoral Training Using the Social Ecological Model: Insights and Experiences from the Propel Scholars. GEN biotechnology Hayes, C. A., Headley, C. A., Nava, A. R., Vizcarra, E. A., Garcia, K. C., Mullen, M. M., Morales, J. F., Venida, A. C., Follis, S. 2024; 3 (4): 196-206

    Abstract

    The dissatisfaction within the postdoctoral training phase has led to the drastic reduction in the number of U.S. citizens pursuing postdoctoral positions within the biological and biomedical sciences fields. Even more so, there is an obvious disparity in not only the recruitment but the retention among underrepresented groups to pursue careers as academic scientists. The proposed social-ecological model and National Institute of Health advisory committee suggests reforming the postdoctoral training phase to overcome these downward trends and disparities. Importantly, some programs like the Stanford Propel Postdoctoral Program were integrating this framework and recommendations without knowledge that they would be released 2 years later. The goal of the Propel Program is to provide social, cohort, financial, and institutional support to diverse cohorts of postdoctoral trainee to diversify the professoriate. Within this piece, several of the Propel scholars come together to provide their perspectives on how the Propel Program has benefited their postdoctoral training experience.

    View details for DOI 10.1089/genbio.2024.0014

    View details for PubMedID 40709103

    View details for PubMedCentralID PMC12288851

  • Unlocking the power of virtual networking for early-career researchers. eLife Hayes, C. A., Moore, J. T., Headley, C. A., Berrios-Negron, A. L., Lambert, W. M. 2024; 13

    Abstract

    Many successful researchers in the biomedical sciences have benefitted from mentors and networks earlier in their career. However, early-career researchers from minoritized and underrepresented groups do not have the same access to potential mentors and networks as many of their peers. In this article we describe how 'cold emails' and social media platforms - notably Twitter/X and LinkedIn - can be used to build virtual networks, and stress the need to invest in maintaining networks once they have been established.

    View details for DOI 10.7554/eLife.96381

    View details for PubMedID 38501601

  • Academic ethics of mental health: the national black postdocs framework for the addressment of support for undergraduate and graduate trainees. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology Hayes, C. A., Berrios-Negron, A. L., Tamir, T., Hardeman, K. N., Heyward, F. D. 2024

    View details for DOI 10.1038/s41386-023-01787-x

    View details for PubMedID 38191654

    View details for PubMedCentralID 7199285

  • Neuronal and Astrocyte Insulin-like Growth Factor-1 Signaling Differentially Modulates Ischemic Stroke Damage. bioRxiv : the preprint server for biology Hayes, C. A., Morgan, N. I., Thomas, K. C., Pushie, M. J., Vijayasankar, A., Ashmore, B. G., Wontor, K., De Leon, M. A., Ashpole, N. M. 2023

    Abstract

    Ischemic stroke is a leading cause of death and disability, as therapeutic options for mitigating the long-term deficits precipitated by the event remain limited. Acute administration of the neuroendocrine modulator insulin-like growth factor-1 (IGF-1) attenuates ischemic stroke damage in preclinical models, and clinical studies suggest IGF-1 can reduce the risk of stroke and improve overall outcomes. The cellular mechanism by which IGF-1 exerts this protection is poorly defined, as all cells within the neurovascular unit express the IGF-1 receptor. We hypothesize that the functional regulation of both neurons and astrocytes by IGF-1 is critical in minimizing damage in ischemic stroke. To test this, we utilized inducible astrocyte-specific or neuron-specific transgenic mouse models to selectively reduce IGF-1R in the adult mouse brain prior to photothrombotic stroke. Acute changes in blood brain barrier permeability, microglial activation, systemic inflammation, and biochemical composition of the brain were assessed 3 hours following photothrombosis, and significant protection was observed in mice deficient in neuronal and astrocytic IGF-1R. When the extent of tissue damage and sensorimotor dysfunction was assessed for 3 days following stroke, only the neurological deficit score continued to show improvements, and the extent of improvement was enhanced with additional IGF-1 supplementation. Overall, results indicate that neuronal and astrocytic IGF-1 signaling influences stroke damage but IGF-1 signaling within these individual cell types is not required for minimizing tissue damage or behavioral outcome.

    View details for DOI 10.1101/2023.04.02.535245

    View details for PubMedID 37034764