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The article discusses the selection of members for a medical mission with consideration of their unique qualities to ensure the team's wide cultural range and competence. Topics covered include the Synergy Model that pairs a nurse and patient based on common qualities, the required criteria for medical mission trip candidates, the scoring of candidates, and the team's composition. Also noted is a culturally competent team's ability to meet the needs of specific healthcare populations.

Within the uncertainties of involved astronomical and biological parameters, the Drake Equation typically predicts that there should be many exoplanets in our galaxy hosting active, communicative civilizations (ACCs). These optimistic calculations are however not supported by evidence, which is often referred to as the Fermi Paradox. Here, we elaborate on this long-standing enigma by showing the importance of planetary tectonic style for biological evolution. We summarize growing evidence that a prolonged transition from Mesoproterozoic active single lid tectonics (1.6 to 1.0 Ga) to modern plate tectonics occurred in the Neoproterozoic Era (1.0 to 0.541 Ga), which dramatically accelerated emergence and evolution of complex species. We further suggest that both continents and oceans are required for ACCs because early evolution of simple life must happen in water but late evolution of advanced life capable of creating technology must happen on land. We resolve the Fermi Paradox (1) by adding two additional terms to the Drake Equation: foc (the fraction of habitable exoplanets with significant continents and oceans) and fpt (the fraction of habitable exoplanets with significant continents and oceans that have had plate tectonics operating for at least 0.5 Ga); and (2) by demonstrating that the product of foc and fpt is very small (< 0.00003–0.002). We propose that the lack of evidence for ACCs reflects the scarcity of long-lived plate tectonics and/or continents and oceans on exoplanets with primitive life. [ABSTRACT FROM AUTHOR]

[Display omitted] • A transition from 695 Ma I-type, convergent margin magmatism in the north to 635 Ma alkalic, within magmatism in the south is recorded. • Our results thus document a chronologic and tectonic transition from synorogenic, intra-oceanic arc to post-collision within-plate magmatism in the Ediacaran. • Our results also illustrate the viability of dikes as markers of orogénesis. The tectonic evolution of the Arabian-Nubian Shield began with formation of intra-oceanic arcs followed by collisions between these in Tonian-Cryogenian time and culminated in Ediacaran continental collision to form Gondwana. We provide new insights into the middle stage of this tectonic evolution by focusing on two Neoproterozoic dike swarms of different age in northern Arabia. The 695–700 Ma Za'am dikes were emplaced about the time of collision between the Midyan and Hijaz terranes whereas the 635 Ma Bayda dikes were emplaced ∼ 60 million years after collision. These record a shift from relatively unfractionated 695 Ma arc-type magmas in the south to fractionated 635 Ma within-plate alkaline magmas in the north. Our results document mantle source and crustal evolution beneath the Midyan terrane during and after terrane accretion, revealing a tectono-magmatic transition from SSZ-type magmas accompanying arc collision to post-terrane accretion within-plate magmatism through Cryogenian time. In addition, our results confirm the potential of dike studies for reconstructing the tectono-magmatic-metallogenic evolution of orogens. [ABSTRACT FROM AUTHOR]

The Cadomian orogeny reflects S -directed subduction on the northern margin of Greater Gondwana in Ediacaran – Cambrian time (∼600-500 Ma). It is well known from the eastern seaboard of North America, western and southern Europe, Turkey and Iran but is rarely identified in what was its backarc in N. Africa and Arabia. Here I summarize evidence for the Cadomian across ∼6500 km of Arabia and N. Africa from Oman to Morocco. The beginning of the Cadomian in Afro-Arabia cuts across and overlaps in time with earlier Neoproterozoic orogenies leading to the formation of Greater Gondwana, so emphasis is on rocks <570 Ma. Three Cadomian backarc crustal tracts or segments are identified. The eastern segment (Oman, Persian Gulf, eastern Saudi Arabia) mostly consists of buried transtensional basins with little igneous activity. The central segment was characterized by lower crust magma underplating and strong uplift along a N –S axis (Jordan) accompanied by rifting leading to deposition of thick sediments reminiscent of a passive continental margin, and strong evidence for regional metasomatism (Israel). The Zenifim passive margin is 580–610 Ma, older than our arbitrary 570 Ma limit for identifying the Cadomian but clearly post-dates terminal continental collision to form the East African Orogen and so must be related to Cadomian back-arc rifting. Along with related NE-SW trending dike swarms in NE Egypt and Jordan, the orientation of the Zenifim rifted margin, orthogonal to the Cadomian convergent margin, is another indication of strong Cadomian transtension. In contrast, the western segment (Libya, Algeria, Morocco) experienced abundant igneous activity, with evidence for this found especially far south in Libya. Recognition of the Cadomian orogeny in northern Africa provides a useful first step in breaking out distinct tectonic episodes in the ∼300 m.y. long Pan-African orogeny, at least in the north. Finally, the orthogonal relationship between older N –S orogens in the interior of Greater Gondwana and the E -W Cadomian orogen illustrates how the Neoproterozoic plate mosaic grew by subduction initiation exploiting lithospheric weaknesses along its continental margin. Ten recommendations for future research are also suggested. • The ∼550 Ma Cadomian orogeny in N. Africa and Arabia is reviewed for the first time. • N. Africa-Arabia Cadomian crosscuts older Neoproterozoic structures. • N. Afro-Arabia Cadomian is mostly transtensional basins in E, magmatic rocks in W. • Rifted continental margin offshore Israel suggests Cadomian basins lie further W. • 10 suggestions for research are provided. [ABSTRACT FROM AUTHOR]

Background: Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy more frequently found in deceased former football players. CTE has heterogeneous clinical presentations with multifactorial causes. Previous literature has shown substance use (alcohol/drug) can contribute to Alzheimer's disease and related tauopathies pathologically and clinically. Objective: To examine the association between substance use and clinical and neuropathological endpoints of CTE. Methods: Our sample included 429 deceased male football players. CTE was neuropathologically diagnosed. Informant interviews assessed features of substance use and history of treatment for substance use to define indicators: history of substance use treatment (yes vs no, primary variable), alcohol severity, and drug severity. Outcomes included scales that were completed by informants to assess cognition (Cognitive Difficulties Scale, BRIEF-A Metacognition Index), mood (Geriatric Depression Scale-15), behavioral regulation (BRIEF-A Behavioral Regulation Index, Barratt Impulsiveness Scale-11), functional ability (Functional Activities Questionnaire), as well as CTE status and cumulative p-tau burden. Regression models tested associations between substance use indicators and outcomes. Results: Of the 429 football players (mean age = 62.07), 313 (73%) had autopsy confirmed CTE and 100 (23%) had substance use treatment history. Substance use treatment and alcohol/drug severity were associated with measures of behavioral regulation (FDR-p-values<0.05, ΔR2 = 0.04–0.18) and depression (FDR-p-values<0.05, ΔR2 = 0.02–0.05). Substance use indicators had minimal associations with cognitive scales, whereas p-tau burden was associated with all cognitive scales (p-values <0.05). Substance use treatment had no associations with neuropathological endpoints (FDR-p-values>0.05). Conclusions: Among deceased football players, substance use was common and associated with clinical symptoms. [ABSTRACT FROM AUTHOR]

BackgroundMethodsResultsConclusionsFormer professional collision sport (CS) athletes, particularly American football players, are at risk of developing chronic health conditions; however, little is known about the health outcomes of amateur athletes.A 60-item health survey examined self-reported symptoms and diagnoses among former Division 1 Collegiate CS athletes and non- or limited-contact sport (non-CS) athletes. Binary logistic regressions tested the association between playing CS and health outcomes.Five hundred and two (6.2%) participants completed the survey: 160 CS athletes (mean age: 59.2, SD = 16.0) and 303 non-CS athletes (mean age: 54.0, SD = 16.9). CS athletes had increased odds of reported cognitive complaints and neuropsychiatric symptoms including memory (Padj < 0.01), attention/concentration (Padj = 0.01), problem solving/multi-tasking (Padj = 0.05), language (Padj = 0.02), anxiety (Padj = 0.04), impulsivity (Padj = 0.02), short-fuse/rage/explosivity (Padj < 0.001), and violence/aggression (Padj = 0.02). CS athletes also reported higher rates of sleep apnea (Padj = 0.02). There were no group differences in cardiovascular and physical health outcomes.Former CS athletes reported more cognitive and neuropsychiatric complaints. The low response rate is a limitation of this study; however, over 500,000 athletes play college sports each year, thus research on long-term health outcomes in this population is critical. [ABSTRACT FROM AUTHOR]

Background: Traumatic brain injury (TBI) and repetitive head impacts (RHI) have been linked to increased risk for multiple types of neurodegenerative disease, higher dementia risk, and earlier age of dementia symptom onset, suggesting transdiagnostic implications for later-life brain health. Frontotemporal dementia (FTD) and primary progressive aphasia (PPA) represent a spectrum of clinical phenotypes that are neuropathologically diverse. FTD/PPA diagnoses bring unique challenges due to complex cognitive and behavioral symptoms that disproportionately present as an early-onset dementia (before age 65). We performed a detailed characterization of lifetime head trauma exposure in individuals with FTD and PPA compared to healthy controls to examine frequency of lifetime TBI and RHI and associated clinical implications. Methods: We studied 132 FTD/PPA (age 68.9 ± 8.1, 65% male) and 132 sex-matched healthy controls (HC; age 73.4 ± 7.6). We compared rates of prior TBI and RHI (contact/collision sports) between FTD/PPA and HC (chi-square, logistic regression, analysis of variance). Within FTD/PPA, we evaluated associations with age of symptom onset (analysis of variance). Within behavioral variant FTD, we evaluated associations with cognitive function and neuropsychiatric symptoms (linear regression controlling for age, sex, and years of education). Results: Years of participation were greater in FTD/PPA than HC for any contact/collision sport (8.5 ± 6.7yrs vs. 5.3 ± 4.5yrs, p =.008) and for American football (6.2yrs ± 4.3yrs vs. 3.1 ± 2.4yrs; p =.003). Within FTD/PPA, there were dose-dependent associations with earlier age of symptom onset for TBI (0 TBI: 62.1 ± 8.1, 1 TBI: 59.9 ± 6.9, 2 + TBI: 57.3 ± 8.4; p =.03) and years of American football (0yrs: 62.2 ± 8.7, 1-4yrs: 59.7 ± 7.0, 5 + yrs: 55.9 ± 6.3; p =.009). Within bvFTD, those who played American football had worse memory (z-score: -2.4 ± 1.2 vs. -1.4 ± 1.6, p =.02, d = 1.1). Conclusions: Lifetime head trauma may represent a preventable environmental risk factor for FTD/PPA. Dose-dependent exposure to TBI or RHI influences FTD/PPA symptom onset and memory function in bvFTD. Clinico-pathological studies are needed to better understand the neuropathological correlates linking RHI or TBI to FTD/PPA onset and symptoms. [ABSTRACT FROM AUTHOR]

Background: Neuropsychiatric symptoms (NPS) can be an early manifestation of Alzheimer's disease (AD). However, the associations among NPS, cognition, and AD biomarkers across the disease spectrum are unclear. Objective: We analyzed cross-sectional mediation pathways between cerebrospinal fluid (CSF) biomarkers of AD (Aβ1-42, p-tau181), cognitive function, and NPS. Methods: Primary models included 781 participants from the National Alzheimer's Coordinating Center (NACC) data set who had CSF analyzed for AD biomarkers using Lumipulse. NPS were assessed with the Neuropsychiatric Inventory Questionnaire (NPI-Q). We assessed cognition with the harmonized MMSE/MoCA, as well as neuropsychological tests sensitive to AD pathology: story recall, naming, animal fluency, and Trails B. The Clinical Dementia Rating (CDR®) scale assessed dementia severity. Mediation models were estimated with Kemeny metric covariance in a structural equation model framework, controlling for age, education, sex, and APOEɛ4. Results: The sample was older adults (M = 73.85, SD = 6.68; 49.9% male, 390; 27.9% dementia, 218) who were predominantly white (n = 688, 88.1%). Higher p-tau181/Aβ1-42 ratio predicted higher NPI-Q, which was partially mediated by the MMSE/MoCA and, in a second model, story recall. No other pathway was statistically significant. Both the MMSE/MoCA and NPI-Q independently mediated the association between p-tau181/Aβ1-42 ratio and CDR global impairment. With dementia excluded, p-tau181/Aβ1-42 ratio was no longer associated with the NPI-Q. Conclusions: NPS may be secondary to cognitive impairment and AD pathology through direct and indirect pathways. NPS independently predict dementia severity in AD. However, AD pathology likely plays less of a role in NPS in samples without dementia. [ABSTRACT FROM AUTHOR]

Repetitive head impacts (RHIs) from football are associated with the neurodegenerative tauopathy chronic traumatic encephalopathy (CTE). It is unclear whether a history of traumatic brain injury (TBI) is sufficient to precipitate CTE neuropathology. We examined the association between TBI and CTE neuropathology in 580 deceased individuals exposed to RHIs from football. TBI history was assessed using a modified version of the Ohio State University TBI Identification Method Short Form administered to informants. There were 22 donors who had no TBI, 213 who had at least one TBI without loss of consciousness (LOC), 345 who had TBI with LOC, and, of those with a history of TBI with LOC, 36 who had at least one moderate-to-severe TBI (msTBI, LOC >30 min). CTE neuropathology was diagnosed in 405. There was no association between CTE neuropathology status or severity and TBI with LOC (odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.64–1.41; OR = 1.22, 95% CI = 0.71–2.09) or msTBI (OR = 0.70, 95% CI = 0.33–1.50; OR = 1.01, 95% CI = 0.30–3.41). There were no associations with other neurodegenerative or cerebrovascular pathologies examined. TBI with LOC and msTBI were not associated with CTE neuropathology in this sample of brain donors exposed to RHIs from American football. [ABSTRACT FROM AUTHOR]

The continental crust of Iran is dominated by abundant calc-alkaline and alkaline plutonic and volcanic rocks and by rifted basins filled with mostly terrigenous sedimentary rocks that formed at a Late Ediacaran to Cambrian extensional convergent plate margin along the northern margin of Gondwana. Here we present new zircon U–Pb age, geochemical, and isotopic data from plutonic (granite-granodiorite) and metamorphic (gneiss) rocks in the Kariznou region of NE Iran to provide insights into the nature of the Cadomian convergent margin of Iran. Geochemical data indicate calc-alkaline signatures, characterized by strong depletions in Nb, Ta, P, and Ti and arc-like trace element patterns. New zircon U–Pb ages show that calc-alkaline granitoids and granitic gneiss formed at ~564 to 537 Ma and 538 Ma, respectively. Bulk rock Sr-Nd isotopic data of calc-alkaline rocks have εNd(t) = –5.42 to −5.53 and −6.93 to −7.43 for granite and gneiss, respectively. The gneisses show stronger interaction with and/or re-melting of older continental crust than do granitic rocks. We interpret Kariznou magmatic rocks as forming in association with strong extension accompanied by crustal assimilation. Extension initiated ~570 Ma with the deposition of Late Ediacaran sediments, and magmatism began at 545–535 Ma, generating calc-alkaline magmas. The tectonomagmatic evolution of the Kariznou region encapsulates the prolonged transition of Cadomian Iran from a strongly extensional convergent margin, possibly as a result of oblique oceanic subduction and slab roll-back of the subducting Proto-Tethys oceanic lithosphere, culminating in the formation of an Early Palaeozoic passive margin on the northern side of Gondwana. [ABSTRACT FROM AUTHOR]

Background: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by hyperphosphorylated tau (p-tau) accumulation. The clinical features associated with CTE pathology are unclear. In brain donors with autopsy-confirmed CTE, we investigated the association of CTE p-tau pathology density and location with cognitive, functional, and neuropsychiatric symptoms. Methods: In 364 brain donors with autopsy confirmed CTE, semi-quantitative p-tau severity (range: 0–3) was assessed in 10 cortical and subcortical regions. We summed ratings across regions to form a p-tau severity global composite (range: 0–30). Informants completed standardized scales of cognition (Cognitive Difficulties Scale, CDS; BRIEF-A Metacognition Index, MI), activities of daily living (Functional Activities Questionnaire), neurobehavioral dysregulation (BRIEF-A Behavioral Regulation Index, BRI; Barratt Impulsiveness Scale, BIS-11), aggression (Brown-Goodwin Aggression Scale), depression (Geriatric Depression Scale-15, GDS-15), and apathy (Apathy Evaluation Scale, AES). Ordinary least squares regression models examined associations between global and regional p-tau severity (separate models for each region) with each clinical scale, adjusting for age at death, racial identity, education level, and history of hypertension, obstructive sleep apnea, and substance use treatment. Ridge regression models that incorporated p-tau severity across all regions in the same model assessed which regions showed independent effects. Results: The sample was predominantly American football players (333; 91.2%); 140 (38.5%) had low CTE and 224 (61.5%) had high CTE. Global p-tau severity was associated with higher (i.e., worse) scores on the cognitive and functional scales: MI (β standardized = 0.02, 95%CI = 0.01–0.04), CDS (β standardized = 0.02, 95%CI = 0.01–0.04), and FAQ (β standardized = 0.03, 95%CI = 0.01–0.04). After false-discovery rate correction, p-tau severity in the frontal, inferior parietal, and superior temporal cortex, and the amygdala was associated with higher CDS (β sstandardized = 0.17–0.29, ps < 0.01) and FAQ (β sstandardized = 0.21–0.26, ps < 0.01); frontal and inferior parietal cortex was associated with higher MI (β sstandardized = 0.21–0.29, ps < 0.05); frontal cortex was associated with higher BRI (β standardized = 0.21, p < 0.01). Regions with effects independent of other regions included frontal cortex (CDS, MI, FAQ, BRI), inferior parietal cortex (CDS) and amygdala (FAQ). P-tau explained 13–49% of variance in cognitive and functional scales and 6–14% of variance in neuropsychiatric scales. Conclusion: Accumulation of p-tau aggregates, especially in the frontal cortex, are associated with cognitive, functional, and certain neurobehavioral symptoms in CTE. [ABSTRACT FROM AUTHOR]

Objective: Exposure to repetitive head impacts (RHI) is associated with later‐life cognitive symptoms and neuropathologies, including chronic traumatic encephalopathy (CTE). Cognitive decline in community cohorts is often due to multiple pathologies; however, the frequency and contributions of these pathologies to cognitive impairment in people exposed to RHI are unknown. Here, we examined the relative contributions of 13 neuropathologies to cognitive symptoms and dementia in RHI‐exposed brain donors. Methods: Neuropathologists examined brain tissue from 571 RHI‐exposed donors and assessed for the presence of 13 neuropathologies, including CTE, Alzheimer disease (AD), Lewy body disease (LBD), and transactive response DNA‐binding protein 43 (TDP‐43) inclusions. Cognitive status was assessed by presence of dementia, Functional Activities Questionnaire, and Cognitive Difficulties Scale. Spearman rho was calculated to assess intercorrelation of pathologies. Additionally, frequencies of pathological co‐occurrence were compared to a simulated distribution assuming no intercorrelation. Logistic and linear regressions tested associations between neuropathologies and dementia status and cognitive scale scores. Results: The sample age range was 18–97 years (median = 65.0, interquartile range = 46.0–76.0). Of the donors, 77.2% had at least one moderate–severe neurodegenerative or cerebrovascular pathology. Stage III–IV CTE was the most common neurodegenerative disease (43.1%), followed by TDP‐43 pathology, AD, and hippocampal sclerosis. Neuropathologies were intercorrelated, and there were fewer unique combinations than expected if pathologies were independent (p < 0.001). The greatest contributors to dementia were AD, neocortical LBD, hippocampal sclerosis, cerebral amyloid angiopathy, and CTE. Interpretation: In this sample of RHI‐exposed brain donors with wide‐ranging ages, multiple neuropathologies were common and correlated. Mixed neuropathologies, including CTE, underlie cognitive impairment in contact sport athletes. ANN NEUROL 2024;95:314–324 [ABSTRACT FROM AUTHOR]

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head impacts (RHI) and pathologically defined as neuronal phosphorylated tau aggregates around small blood vessels and concentrated at sulcal depths. Cross-sectional studies suggest that tau inclusions follow a stereotyped pattern that begins in the neocortex in low stage disease, followed by involvement of the medial temporal lobe and subcortical regions with significant neocortical burden in high stage CTE. Here, we define a subset of brain donors with high stage CTE and with a low overall cortical burden of tau inclusions (mean semiquantitative value ≤1) and classify them as cortical-sparing CTE (CSCTE). Of 620 brain donors with pathologically diagnosed CTE, 66 (11%) met criteria for CSCTE. Compared to typical high stage CTE, those with CSCTE had a similar age at death and years of contact sports participation and were less likely to carry apolipoprotein ε4 (p < 0.05). CSCTE had less overall tau pathology severity, but a proportional increase of disease burden in medial temporal lobe and brainstem regions compared to the neocortex (p’s < 0.001). CSCTE also had lower prevalence of comorbid neurodegenerative disease. Clinically, CSCTE participants were less likely to have dementia (p = 0.023) and had less severe cognitive difficulties (as reported by informants using the Functional Activities Questionnaire (FAQ); p < 0.001, meta-cognitional index T score; p = 0.002 and Cognitive Difficulties Scale (CDS); p < 0.001,) but had an earlier onset age of behavioral (p = 0.006) and Parkinsonian motor (p = 0.013) symptoms when compared to typical high stage CTE. Other comorbid tauopathies likely contributed in part to these differences: when cases with concurrent Alzheimer dementia or frontal temporal lobar degeneration with tau pathology were excluded, differences were largely retained, but only remained significant for FAQ (p = 0.042), meta-cognition index T score (p = 0.014) and age of Parkinsonian motor symptom onset (p = 0.046). Overall, CSCTE appears to be a distinct subtype of high stage CTE with relatively greater involvement of subcortical and brainstem regions and less severe cognitive symptoms. [ABSTRACT FROM AUTHOR]

A combined laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS) and energy dispersive X-ray spectroscopy (EDS) study was used to map 49 elements in four Fe Mn precipitates produced from three different genetic processes (hydrogenetic, hydrothermal, and mixed-type hydrogenetic-hydrothermal) in samples obtained from the southern Mariana Arc. Results show Mn-oxide minerals are consistently found to be associated with Ba, Mo, Sb, V, Zn, and the rare earth elements and yttrium (REY), excluding Ce, whereas Fe-oxyhydroxide minerals are primarily associated with Ti, Co, Cr, Cu, Nb, and Pb. Element distributions in Fe Mn precipitates from the southern Mariana Arc differ from deposits formed in other environments; notably, there is a decoupling of As and Sb, and redox-sensitive elements are more variable than non-redox-sensitive elements. Samples previously classified as either hydrogenetic or hydrothermal in origin, based on bulk geochemical data, show characteristics of both at higher resolution. Combining high resolution in-situ data with genetic classification discrimination diagrams reveals more ambiguity in metal and metalloid origin than previously thought. Mariana Arc Fe Mn precipitates can be separated into two formation sub-types (hydrothermal or mixed hydrothermal/hydrogenetic) based on textural and compositional differences, e.g., differences in Ce/Ce and Y/Ho values and relative variations in (Zr + Y + Ce) versus (Co + Ni) versus (Mn + Fe). Improved classification and knowledge of how fast-growing hydrothermal Fe Mn precipitates form may help us identify a relatively renewable critical metal resource. [Display omitted] • High resolution laser ablation maps (∼ 1 mm2) were constructed from Mn crusts from the southern Mariana Arc. • Within each map, variation in composition is highly varied and, in some cases, different from whole rock analyses. • Results show that sources of metals to Mn crusts is highly variable in time and space. • Classification diagrams based on whole rock analyses do not reflect the true variation in metal sources to Mn crusts. [ABSTRACT FROM AUTHOR]

Former American football players are at risk for chronic traumatic encephalopathy (CTE) which may have parkinsonism as a clinical feature. Former football players were prospectively assessed for parkinsonism. 120 former professional football players, 58 former college football players, and 60 same-age asymptomatic men without repetitive head impacts, 45–74 years, were studied using the MDS-UPDRS to assess for parkinsonism, and the Timed Up and Go (TUG). Traumatic encephalopathy syndrome (TES), the clinical syndrome of CTE, was adjudicated and includes parkinsonism diagnosis. Fisher's Exact Test compared groups on parkinsonism due to small cell sizes; analysis of covariance or linear regressions controlling for age and body mass index were used otherwise. Twenty-two (12.4%) football players (13.3% professional, 10.3% college) met parkinsonism criteria compared with two (3.3%) in the unexposed group. Parkinsonism was higher in professional (p = 0.037) but not college players (p = 0.16). There were no differences on the MDS-UPDRS Part III total scores. Scores on the individual MDS-UPDRS items were low. TUG times were longer in former professional but not college players compared with unexposed men (13.09 versus 11.35 s, p < 0.01). There were no associations between years of football, age of first exposure, position or level of play on motor outcomes. TES status was not associated with motor outcomes. Parkinsonism rates in this sample of football players was low and highest in the professional football players. The association between football and parkinsonism is inconclusive and depends on factors related to sample selection, comparison groups, and exposure characteristics. • Parkinsonism/motor finding prevalence did not differ in former American football players compared to asymptomatic unexposed men. • Former players did have slowness on the Timed Up and Go (TUG) compared to the asymptomatic unexposed men. • TUG times were slower in former football players with TES-CTE probable compared to those with no TES and TES-CTE possible. [ABSTRACT FROM AUTHOR]