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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.

Introduction In primary progressive aphasia (PPA) patients with autopsy‐confirmed Alzheimer's disease (AD) or frontotemporal lobar degeneration (FLTD), we tested how the core clinical features of logopenic PPA—naming and repetition—change over time and relate to pathologic burden. Methods In PPA with AD (n = 13) or FTLD (n = 16) pathology, Boston Naming Test and Forward Digit Span measured longitudinal naming and repetition; as reference, Mini‐Mental State Examination (MMSE) measured global cognition. Pathologic burden in left peri‐Sylvian regions was related to longitudinal cognitive decline. Results PPA with AD showed greater decline in naming (P = 0.021) and repetition (P = 0.020), compared to FTLD; there was no difference in MMSE decline (P = 0.99). Across all PPA, declining naming (P = 0.0084) and repetition (P = 0.011) were associated with angular, superior‐middle temporal (naming P = 0.014; repetition P = 0.011) and middle frontal (naming P = 0.041; repetition P = 0.030) pathologic burden. Discussion Unique longitudinal profiles of naming and repetition performance in PPA with AD are related to left peri‐Sylvian pathology.

Objective:Patients with persistent post-concussion symptoms (PPCS) experience prolonged recovery (e.g., headache, fatigue, or dizziness) lasting >2 months post injury. These symptoms are thought to be maintained by several biopsychosocial factors including dysregulated stress responses, such as pain catastrophizing, that may drive behavioral avoidance and contribute to mood symptoms and cognitive difficulties. Conditions with similar symptomatology to PPCS (e.g., anxiety disorders, somatosensory disorders, chronic pain, etc.) also exhibit maladaptive thought patterns like pain catastrophizing as well as decrements in certain aspects of cognitive performance; however little is known about how pain catastrophizing might relate to neuropsychological performance in youth with PPCS. Therefore, the purpose of this study was to examine the relationship between pain catastrophizing and neuropsychological performance in youth participants with PPCS.Participants and Methods:A prospective case-control study design was used to examine 29 participants between the ages of 13 to 23. Participants were divided into two groups: 1) patients with PPCS (2-16 months post-injury; n = 15) and 2) age-matched, non-injured controls (n = 14). Participants completed the Pain Catastrophizing Scale (PCS) to determine degree of catastrophic thinking related to pain experience and the Beck Depression Inventory (BDI). Neuropsychological performance was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and a modified version of the Paced Auditory Serial Addition Test (PASAT) where performance was evaluated by total correct and error type (i.e., commission and omission) across 5 trials. ANCOVA was used to compare group differences in pain catastrophizing and neuropsychological tests scores while controlling for age and linear regressions examined the relationship between PCS total score and each neuropsychological test score while controlling for level of depression.Results:Overall, the PPCS group reported significantly higher levels of pain catastrophizing on the PCS compared to the control group (p < 0.01). For neuropsychological performance, the PPCS group scored significantly lower than the control group on List Learning (p < 0.01), Semantic Fluency (p < 0.05), and List Recall (p < 0.01) on the RBANS and made significantly higher omission errors (but not commission) on the PASAT(p <.01). Higher pain catastrophizing was also associated with poorer neuropsychological performance on the exact same tasks the PPCS group performed worse than controls. There was no significant interaction by group in the impact of PCS scores on neurocognitive performance.Conclusions:Compared to controls, youth PPCS patients reported higher levels of pain catastrophizing. Additionally, pain catastrophizing was associated with poorer neuropsychological performance. These findings suggest that increased pain catastrophizing after head injury could contribute to poorer cognitive performance in youth. As such, interventions that target maladaptive cognitive coping styles like pain catastrophizing may be especially helpful for patients with PPCS.

Objective:Approximately 10-15% of patients with mild traumatic brain injury (mTBI) report persistent, chronic symptoms more than one month later. Coping behaviors after mTBI can range from fear avoidance (FA), or a reluctance to return to activity because of the fear of symptom exaggeration, to endurance (END), or an overly aggressive return to activity. We evaluated how coping strategy relates to self-reported symptoms in patients with prolonged recovery from mTBI.Participants and Methods:Participants were 72 individuals (age 37.8 + 18.4, 65% female) who sustained a mTBI at least one month prior to assessment (median (IQR) = 5.5 (2.0-11.3) months). Participants completed the Brain Injury Recovery Disposition Scale (BIRDS) to assess FA and END behaviors, and Sport Concussion Assessment Tool (SCAT5) Symptom Inventory. A BIRDS spectrum score was calculated as the difference between FA and END scores to determine individual coping behavior on a spectrum from extreme FA (more negative) to extreme END (more positive). SCAT5 symptoms were separated into four domain scores: somatic, cognitive, sleep, and emotion. Regressions were performed for each outcome examining their potential linear and quadratic associations to coping behavior (i.e., BIRDS spectrum score). Follow-up regressions were performed covarying for age and sex to explore the potential influence of these variables on each outcome.Results:The linear and quadratic components of the BIRDS spectrum score were not significantly related to total number of persisting concussive symptoms. For overall total symptom severity, the quadratic component of the relationship was significant (B = .24, p = 0.04). Visualization of the overall trend line suggested that symptom severity was highest on the extreme FA side of the BIRDS spectrum (highly negative BIRDS spectrum score), decreased as coping behavior become more balanced (BIRDS spectrum score surrounding “0\"), plateaued, then increased abruptly on the extreme END side (highly positive BIRDS spectrum score). For cognitive symptoms, the linear component of the BIRDS spectrum score was significant (B = -.28, p = 0.02) and the quadratic component was marginally significant (B = .22, p = 0.06). The quadratic (but not linear) component was significantly related to both the severity of sleep (B = .31, p = 0.01) and emotion symptoms (B = .25, p = 0.03). Finally, neither the linear nor quadratic components were significantly related to the somatic symptom severity. After covarying for age and sex, the quadratic component remained significant for total symptom severity (p = 0.05) as well as the linear component for cognitive severity (p = 0.02).Conclusions:Both extreme “fear avoidance” and “endurance” coping styles may be related to more severe chronic mTBI symptoms, especially in domains of sleep and emotion symptoms. Patients with balance of both fear avoidance and endurance behaviors may be more likely to experience less severe symptoms even among mTBI patients with persistent complaints. Identifying coping behavior styles early after mTBI could improve prognostication and help with developing personalized treatment plans to improve patient recovery. Future research with larger sample sizes should further examine the influence of age and sex on the relationship between coping behavior and symptom severity.

Background Traumatic encephalopathy syndrome (TES) is a proposed framework for the clinical syndrome resulting from chronic traumatic encephalopathy and other neurodegenerative effects of repetitive head impacts (RHI). TES symptoms can mirror Alzheimer's disease (AD) despite absence of hallmark AD pathology. We investigated whether GFAP, NfL, and IL‐6 correlated with cognition and brain volume changes within TES relative to AD. Method We studied 96 participants from the UCSF Memory and Aging Center (N=35 RHI/TES; 24 of whom were AD biomarker‐negative, TESAD‐; N=61 biomarker‐confirmed AD phenotype, no RHI; Table 1). Plasma was analyzed for GFAP, NfL, and IL‐6 (age‐ and sex‐adjusted). Cognitive measures included composite memory and executive functioning scores (demographically‐adjusted). MRI was obtained concurrent to blood draws and several regions of interest were analyzed (demographic‐ and total intracranial volume‐adjusted): frontal, temporal, parietal, occipital, hippocampus, subcortical. Spearman’s rho assessed associations between plasma biomarkers, cognition, and brain volume. A priori alpha was p<.05, but associations with at least medium effect size (rho ≥0.3) were interpreted as potentially meaningful given small N in TES and TESAD‐ subgroups. Result In TES, higher GFAP was associated with lower hippocampal volume (rho=‐0.33, p=.09) and worse memory (rho=‐0.44, p=.02). Results were similar in TESAD‐ subgroup (GFAP‐hippocampus: rho=‐0.45, p=.07; GFAP‐memory: rho=‐0.42, p=.07). IL‐6 appeared most related to brain volume in the TESAD‐ subgroup, where higher IL‐6 correlated with lower volumes in all regions (rho’s ‐.43 ‐ ‐.63, p’s=.004 ‐ .06), but not with cognition. In AD, both higher NfL and GFAP were associated with lower brain volume in several regions and with worse cognition but, notably, neither related to hippocampal volume (NfL: rho=‐.11, p=.47; GFAP: rho=.02, p=.91). IL‐6 did not relate to brain volume or cognition in AD (Figure 1). Conclusion Plasma biomarkers reflect different regions of atrophy and cognitive change in TES vs. AD. Inflammation (IL‐6) may play a distinctive role in the pathophysiology underlying atrophy in TES. While recent work highlights astroglial activation (GFAP) is a putative AD‐related biomarker, it may uniquely relate to hippocampal changes in TES. Ongoing work is needed to unravel the clinical utility of plasma biomarkers for characterizing the neurodegenerative effects of RHI and underlying TES symptoms.

Public safety, security and risk perception is an important aspect considered in opinion mining and sentiment analysis typically carried out on social networks. This involves considering each individual’s opinion and determining a sense of what the public feels about an incident, event or place. In that sense, social networks play an important role in capturing the emotions of people. Security and safety managers can employ opinion mining and sentiment analysis as a tool to discover any unforeseen vulnerabilities in a precise manner and thereby plan and manage any associated risks. Furthermore, a continuous evaluation of risk perception can be carried out for timely and planned interventions in a seamless, effective manner to reduce or avoid any panic amongst communities. Without such advance techniques, safety and security of people, infrastructures and specific contexts can be easily compromised. Recent work in this direction has shown promising results in managing risks, especially during the COVID-19 pandemic. The purpose of the present work is to investigate the perception of risk associated with different payment systems, in Italy and the UK, during the COVID-19 pandemic, from 10 November 2020 to 13 May 2021, by means of the semantic analysis of the textual contents existing in Twitter.

Objective:Traumatic brain injury (TBI) and concussion are associated with increased dementia risk. Accurate TBI/concussion exposure estimates are relatively unknown for less common neurodegenerative conditions like frontotemporal dementia (FTD). We evaluated lifetime TBI and concussion frequency in patients diagnosed with a range of FTD spectrum conditions and related prior head trauma to cavum septum pellucidum (CSP) characteristics observable on MRI.Participants and Methods:We administered the Ohio State University TBI Identification and Boston University Head Impact Exposure Assessment to 108 patients (age 69.5 ± 8.0, 35% female, 93% white or unknown race) diagnosed at the UCSF Memory and Aging Center with one of the following FTD or related conditions: behavioral variant frontotemporal dementia (N=39), semantic variant primary progressive aphasia (N=16), nonfluent variant PPA (N=23), corticobasal syndrome (N=14), or progressive supranuclear palsy (N=16). Data were also obtained from 217 controls (“HC”; age 76.8 ± 8.0, 53% female, 91% white or unknown race). CSP characteristics were defined based on width or “grade” (0-1 vs. 2+) and length of anterior-posterior separation (millimeters). We first describe frequency of any and multiple (2+) prior TBI based on different but commonly used definitions: TBI with loss of consciousness (LOC), TBI with LOC or posttraumatic amnesia (LOC/PTA), TBI with LOC/PTA or other symptoms like dizziness, nausea, “seeing stars,” etc. (“concussion”). TBI/concussion frequency was then compared between FTD and HC using chi-square. Associations between TBI/concussion and CSP characteristics were analyzed with chi-square (CSP grade) and Mann-Whitney U tests (CSP length). We explored sex differences due to typically higher rates of TBI among males.Results:History of any TBI with LOC (FTD=20.0%, HC=19.2%), TBI with LOC/PTA (FTD:32.2%, HC=31.5%), and concussion (FTD: 50.0%, HC=44.3%) was common but not different between study groups (p’s>.4). In both FTD and HC, prior TBI/concussion was nominally more frequent in males but not significantly greater than females. Frequency of repeat TBI/concussion (2+) also did not differ significantly between FTD and HC (repeat TBI with LOC: 6.7% vs. 3.3%, TBI with LOC/PTA: 12.2% vs. 10.3%, concussion: 30.2% vs. 28.7%; p’s>.2). Prior TBI/concussion was not significantly related to CSP grade or length in the total sample or within the FTD or HC groups.Conclusions:TBI/concussion rates depend heavily on the symptom definition used for classifying prior injury. Lifetime symptomatic TBI/concussion is common but has an unclear impact on risk for FTD-related diagnoses. Larger samples are needed to appropriately evaluate sex differences, to evaluate whether TBI/concussion rates differ between specific FTD phenotypes, and to understand the rates and effects of more extensive repetitive head trauma (symptomatic and asymptomatic) in patients with FTD.

Background Repetitive head impact exposure (RHI) is the only known risk factor for chronic traumatic encephalopathy (CTE), a distinct neurodegenerative tauopathy. Most aging studies ask participants about prior traumatic brain injury (TBI), but not common sources of RHI. Understanding the public health footprint of RHI requires targeted questioning of lifetime exposure. To set the stage for our Featured Research Session on CTE, we report RHI prevalence using gold standard methods across independent aging and dementia cohorts. Method The Boston University Repetitive Head Impact Exposure Assessment (BU‐RHIEA) was administered across three cohorts: BU Alzheimer's Disease Research Center (ADRC), UCSF ADRC, and 1Florida ADRC. Participants recruited explicitly with concerns about cognitive effects of prior head trauma were excluded. The BU‐RHIEA queries participation in contact/collision sports (e.g., American football, soccer, ice hockey, boxing) and military service as well as prior TBI. We report RHI and TBI prevalence estimates from the BU‐RHIEA relative to estimates from the National Alzheimer's Coordinating Center Uniform Data Set (NACC UDS). In a subset of participants with frontotemporal dementia, we evaluated the clinical relevance of prior RHI through associations with age of symptom onset and rate of disease progression. Result Data come from 736 participants (age 70.4±9.6, 44.3% male, 43.1% cognitively impaired). Based on NACC UDS, 223 (30.2%) reported any prior TBI (Figure 1). When providing a formal TBI definition, frequency increased to 300 (40.8%). Sport and military history are not known through NACC UDS. Based on the BU‐RHIEA, 221 (30.0%) participants reported any prior contact/collision sport play. Among males, 92 (28.2%) previously played American football and 98 (30.1%) served in the military. In participants with frontotemporal dementia, prior RHI related to younger symptom onset and more rapid cognitive decline (Figure 2). Conclusion There is a high risk of underestimating the scope of RHI influence on brain aging. Among older adults, history of TBI and RHI from popular contact/collision sports is exceedingly common but unrecognized. RHI may contribute to the wide variability observed in the onset and progression of neurodegenerative conditions. Studying head trauma exposure relevant for later‐life brain health, such as sport‐ and military‐related RHI, requires dedicated questioning.

Background Plasma P‐tau217 demonstrates strong sensitivity and specificity for Alzheimer’s disease (AD) neuropathological change, but existing studies are often ethnically homogeneous. Assumptions about how well plasma P‐tau217 relates to key AD‐related cognitive outcomes like memory may not generalize. We assessed whether the association between plasma P‐tau217 and memory depended on ethnicity in a sample of Hispanic/Latino and non‐Hispanic/Latino White older adults. Method We studied 273 1Florida ADRC participants with normal cognition, mild cognitive impairment (MCI), or dementia (Table 1). All participants had plasma samples analyzed for P‐tau217 (ALZPath) and neuropsychological assessments. Using Pearson’s correlations, we first evaluated the bivariate association between P‐tau217, Craft Story verbatim recall (verbal memory), and Benson Figure recall scores (visual memory) overall and stratified by ethnicity. To determine whether ethnicity moderated the effects of P‐tau217 on memory, we used multiple linear regression to assess the interaction of P‐tau217 and ethnicity (Hispanic/Latino vs. non‐Hispanic/Latino) controlling for age, sex, education, and testing language. Post hoc sensitivity analyses separately evaluated individuals below and above internal Aβ PET‐derived P‐tau217 cutoffs for “AD positive” concentration. Result Higher P‐tau217 was significantly associated with worse verbal (r= ‐0.38, p < 0.001) and visual memory (r= ‐0.31, p < 0.001) overall and separately in Hispanic/Latino (r= ‐0.56, r= ‐0.57; p’s <.001) and non‐Hispanic/Latino White participants (r= ‐0.30, r = ‐0.34; p’s < 0.001). Ethnicity significantly moderated P‐tau217 associations with verbal (β= ‐0.38, p= 0.001) and visual memory (β = ‐0.38, p= 0.001). The negative relationship between P‐tau217 and memory was significantly stronger for Hispanic/Latino than non‐Hispanic/Latino participants. P‐tau217 and demographic covariates explained more variance in verbal (R2= 0.39) and visual memory (R2= 0.37) for Hispanic/Latino than non‐Hispanic/Latino Whites (R2= 0.16 and R2= 0.19, respectively). Post hoc analyses suggested these findings were driven by individuals on the AD continuum. Conclusion AD pathology, measured via plasma P‐tau217, may more strongly relate to memory function in Hispanic/Latino than non‐Hispanic/Latino Whites. Findings have implications for the potential roles of co‐pathology or unexplored risk factors in explaining memory loss beyond AD across demographic subgroups. Ethnically representative studies will improve translation of AD biomarkers and inform anticipated AD‐directed treatment effects.

Repetitive head impact exposure (RHI) is the only known risk factor for chronic traumatic encephalopathy (CTE), a distinct neurodegenerative tauopathy. Most aging studies ask participants about prior traumatic brain injury (TBI), but not common sources of RHI. Understanding the public health footprint of RHI requires targeted questioning of lifetime exposure. To set the stage for our Featured Research Session on CTE, we report RHI prevalence using gold standard methods across independent aging and dementia cohorts. The Boston University Repetitive Head Impact Exposure Assessment (BU-RHIEA) was administered across three cohorts: BU Alzheimer's Disease Research Center (ADRC), UCSF ADRC, and 1Florida ADRC. Participants recruited explicitly with concerns about cognitive effects of prior head trauma were excluded. The BU-RHIEA queries participation in contact/collision sports (e.g., American football, soccer, ice hockey, boxing) and military service as well as prior TBI. We report RHI and TBI prevalence estimates from the BU-RHIEA relative to estimates from the National Alzheimer's Coordinating Center Uniform Data Set (NACC UDS). In a subset of participants with frontotemporal dementia, we evaluated the clinical relevance of prior RHI through associations with age of symptom onset and rate of disease progression. Data come from 736 participants (age 70.4±9.6, 44.3% male, 43.1% cognitively impaired). Based on NACC UDS, 223 (30.2%) reported any prior TBI (Figure 1). When providing a formal TBI definition, frequency increased to 300 (40.8%). Sport and military history are not known through NACC UDS. Based on the BU-RHIEA, 221 (30.0%) participants reported any prior contact/collision sport play. Among males, 92 (28.2%) previously played American football and 98 (30.1%) served in the military. In participants with frontotemporal dementia, prior RHI related to younger symptom onset and more rapid cognitive decline (Figure 2). There is a high risk of underestimating the scope of RHI influence on brain aging. Among older adults, history of TBI and RHI from popular contact/collision sports is exceedingly common but unrecognized. RHI may contribute to the wide variability observed in the onset and progression of neurodegenerative conditions. Studying head trauma exposure relevant for later-life brain health, such as sport- and military-related RHI, requires dedicated questioning.