HJNO Jul/Aug 2026

CTE 28 JUL / AUG 2026 I  U.S. HEALTHCARE JOURNALS association of longer duration of football play with worse neurocognitive functioning in former NFL players 60 and higher cumu- lative head impact exposure with later-life depression, apathy, and cognitive impair- ment in former high school and college players. 22 Our study furnishes additional support for such associations. We found no associations between AFE and our outcomes. The literature on AFE is mixed, 61 and relationships between AFE and clinical symptoms have been found primarily in older symptomatic individu- als. Among former professional and ama- teur players, Alosco et al 27 identified an association between younger AFE to foot- ball and heightened odds for impairment in self-reported neuropsychiatric and execu- tive function, whereas another study 62 of 45 former NFL players failed to find an asso- ciation between years of exposure to pre– high school football and neurological and neuropsychological outcomes. Studies have failed to find associations betweenAFE and neurocognitive outcomes in younger and healthier groups. 28,63 A survey-based study also did not find an effect forAFE in middle- aged to older former adult high school foot- ball players, 29 and neither did a study among 19 former NFL players. 30 These inconsisten- cies could be partially attributable to lifes- pan effects. AFEmay serve as an individual risk factor that may decrease resilience to pathology later in life rather than a direct causal factor. Our study did not find any significant associations between AFE and our outcomes, potentially due to our sample being younger (mean age, 55 years) and cog- nitively healthy (based on ECog). Limitations This study has limitations. Selection biases limit generalizability of our findings, including requirement for an internet- connected device and digital literacy, lack of educational and ethnocultural diversity in the sample, and that individuals without mood and/or neurocognitive symptoms may be less likely to participate. This sample does not reflect the population of US football players. 64 Only 785 football players completed a Paired Associates Learning Test, and this was not representative of the larger cohort. There are limitations to self-report data, including potential recall bias and error and missingness in some measures. There are also limitations to the way the propensity score matching procedure was conducted. Causality cannot be inferred by this study because matching was performed retrospectively rather than via random assignment to football vs nonfootball conditions. Additionally, there were likely geographic differences and differences in recruitment of HITSS vs BHR participants, which could have impacted study participation and motives for joining. Furthermore, unmeasured social determinants of health could affect outcomes independent of RHI. The analysis did not distinguish between starter and reserve players; because starters likely had highest intensity head impact exposure, this omission may bias the results toward the null. Additionally, sport history is not assessed in the BHR battery. Additionally, the small sample size of youth players was a limitation for ascertaining effects of youth play on outcomes. CONCLUSIONS In this cross-sectional study of American football players from all levels of play and a well-matched control group, we observed a robust association consistent with a dose- response pattern between years and level of football play and cognitive and neuro- psychiatric outcomes. Because millions of US men have played tackle football, under- standing contributions of football expo- sure to brain health is crucial. Although the current results do not provide insights into individual risk, in combination with existing literature, consideration of years and level of football play offers a practical method to guide clinicians and researchers in determination of risk for later-life cogni- tive and neuropsychiatric symptoms. Future research should examine the role of individ- ual risk and resilience factors (eg, genetics, medical comorbidities, and social determi- nants of health) on these outcomes. n REFERENCES 1. Belanger HG, Vanderploeg RD, McAllister T. Subconcussive blows to the head: a formative review of short-termclinical outcomes. J Head Trauma Rehabil. 2016;31(3):159-166. doi:10.1097/ HTR.0000000000000138 2. Nathanson JT, Connolly JG, Yuk F, et al. Concussion incidence in professional football: position-specific analysiswith use of a novel metric. Orthop J Sports Med. 2016;4(1):2325967115622621. doi:10.1177/2325967115622621 3. McKee AC, Stein TD, Huber BR, et al. Chronic traumatic encephalopathy (CTE): criteria for neuropathologicaldiagnosis and relationship to repetitive head impacts. Acta Neuropathol. 2023;145(4):371-394. doi:10.1007/ s00401-023- 02540-w 4. McKee AC, Mez J, Abdolmohammadi B, et al. Neuropathologic and clinical findings in young contact sportathletes exposed to repetitive head impacts. JAMA Neurol. 2023;80(10):1037-1050. doi:10.1001/jamaneurol.2023.2907 5. Alosco ML, Mez J, Tripodis Y, et al. Age of first exposure to tackle football and chronic traumaticencephalopathy. Ann Neurol. 2018;83(5):886-901. doi:10.1002/ana.25245 6. Mez J, Daneshvar DH, Kiernan PT, et al. Clinicopathological evaluation of chronic traumatic encephalopathy inplayers of American football. JAMA. 2017;318(4):360-370. doi:10.1001/ jama.2017.8334 7. Adams JW, Kirsch D, Calderazzo SM, et al. Substantia nigra pathology, contact sports play, and parkinsonism inchronic traumatic encephalopathy. JAMA Neurol. 2024;81(9):916-924. doi:10.1001/ jamaneurol.2024.2166 8. Standring OJ, Friedberg J, Tripodis Y, et al. Contact sport participation and chronic traumatic encephalopathy are associated with altered severity and distribution of cerebral amyloid angiopathy. Acta Neuropathol. 2019;138 (3):401-413. doi:10.1007/ s00401-019-02031-x 9. Adams JW, Alvarez VE, Mez J, et al. Lewy body pathology and chronic traumatic encephalopathy associated with contact sports. J Neuropathol Exp Neurol. 2018;77(9):757-768. doi:10.1093/jnen/nly065 10. Stein TD, Crary JF. Chronic traumatic encephalopathy and neuropathological comorbidities. Semin Neurol.2020;40(4):384-393. doi:10.1055/s-0040-1713628 11. Daneshvar DH, Mez J, Alosco ML, et al. Incidence of and mortality from amyotrophic lateral sclerosis in NationalFootball League athletes. JAMA Netw Open. 2021;4(12):e2138801. doi:10.1001/ jamanetworkopen.2021.38801 12. Alosco ML, Stein TD, Tripodis Y, et al. Association of white matter rarefaction, arteriolosclerosis, and tau withdementia in chronic traumatic encephalopathy. JAMA Neurol. 2019;76(11):1298-1308. doi:10.1001/ jamaneurol.2019.2244 13. Arciniega H, Baucom ZH, Tuz-Zahra F, et al. Brain morphometry in former American football players: findingsfrom the DIAGNOSE CTE research project. Brain. 2024;147(10):3596-3610. doi:10.1093/brain/ awae098 14. Gardner RC, Hess CP, Brus-Ramer M, et al. Cavum septum pellucidum in retired American pro- football players. J Neurotrauma. 2016;33(1):157-161. doi:10.1089/neu.2014.3805 15. Adler CM, DelBello MP, Weber W, et al. MRI evidence of neuropathic changes in former college football players. Clin J Sport Med. 2018;28(2):100-105. doi:10.1097/JSM.0000000000000391 16. Alosco ML, Mian AZ, Buch K, et al. Structural MRI profiles and tau correlates of atrophy in autopsy- confirmed CTE. Alzheimers Res Ther. 2021;13(1):193. doi:10.1186/s13195-021-00928-y 17. Ford JH, Giovanello KS, Guskiewicz KM. Episodic memory in former professional football players with a historyof concussion: an event-related