Associations Between Self‐reported History of Traumatic Brain Injury on Longitudinal Cognitive and Speech Changes Linked to Alzheimer's Disease Risk Factors

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发表在:Alzheimer's & Dementia vol. 21 (Dec 1, 2025)
主要作者: Goulette, Olivia
其他作者: He, Deling, Basche, Kristin E, Langhough, Rebecca E., Betthauser, Tobey J., Hermann, Bruce P, Johnson, Sterling C, Mueller, Kimberly D
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John Wiley & Sons, Inc.
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024 7 |a 10.1002/alz70857_107250  |2 doi 
035 |a 3286881234 
045 0 |b d20251201 
100 1 |a Goulette, Olivia  |u Department of Communication Sciences and Disorders, University of Wisconsin‐ Madison, Madison, WI, USA, 
245 1 |a Associations Between Self‐reported History of Traumatic Brain Injury on Longitudinal Cognitive and Speech Changes Linked to Alzheimer's Disease Risk Factors 
260 |b John Wiley & Sons, Inc.  |c Dec 1, 2025 
513 |a Journal Article 
520 3 |a Background While both traumatic brain injury (TBI) and Alzheimer's disease (AD) are known to impair cognitive, language, and speech abilities, little to no research examines how a history of TBI interacts with AD‐related predictors (e.g., amyloid and tau pathology, familial genetic factors) to influence longitudinal changes in cognitive and language outcomes. Method We included 308 cognitively unimpaired participants from the Wisconsin Registry for Alzheimer's Prevention (WRAP) with available amyloid and tau PET imaging, APOE ε4 genetic status, and self‐reported TBI history (TBI‐=0, TBI+ >=1). Within each of three AD risk groups (i.e., A+, T+, or APOE e4 carriers), we examined TBI history*age interactions in relationship with cognitive‐language outcomes using linear mixed‐effects models, adjusting for sex, and WRAT‐3 score [i.e., outcomes ∼ TBI group * age +sex+ WRAT‐3+ (1|ID)]. We examined standardized cognitive measures of executive functioning/set‐shifting (i.e., Digit Symbol Coding Test, Trail Making Test B Score), semantic‐phonological processing (i.e., animal category fluency, letter fluency [C, F, L]), and connected speech measures from picture description (i.e., Fluency Index, Words per Minute, Correct‐Information‐Units/total words). Result In the A+ subset (Ntotal=108, NTBI+=35, NTBI‐=73;, Table 1), we found that the TBI+ group exhibited greater average decline in letter fluency (p = 0.036) and the fluency index (i.e., increases in disfluent behavior; p =  0.035) compared to those without TBI (Figure 1). No significant associations were observed between TBI history and longitudinal changes outcomes in the sample of tau+ (Ntotal=73, NTBI+=25, NTBI‐=48) and APOE ε4 allele carriers (Ntotal=127, NTBI+=40, NTBI‐=87). Conclusion Our findings suggest that TBI, in combination with early AD amyloid accumulation, may accelerate communication declines, particularly manifesting as reduced letter fluency and increased speech disfluency. Presumably, these results indicate increased challenges in semantic and phonological retrieval due to the compounded impact of TBI and AD pathology in individuals who are cognitively unimpaired. Our study identifies potential early language indicators of decline; future analyses will investigate more complex TBI/biomarker relationships and additional outcomes. 
653 |a Indexes 
653 |a Alzheimer's disease 
653 |a Accumulation 
653 |a Injuries 
653 |a Fluency 
653 |a Pathology 
653 |a Age groups 
653 |a Risk factors 
653 |a Brain 
653 |a Politics 
653 |a Speech 
653 |a Retrieval 
653 |a Cognition 
653 |a Genetics 
653 |a Cognitive functioning 
653 |a Phonology 
653 |a Trauma 
653 |a Brain damage 
653 |a History 
653 |a Traumatic brain injury 
653 |a Semantic categories 
653 |a Phonological processing 
653 |a Executive function 
653 |a Lexical access 
653 |a Letters (Correspondence) 
653 |a Change agents 
653 |a Biological markers 
653 |a Language shift 
653 |a Semantic processing 
653 |a Disease 
653 |a Changes 
653 |a Semantics 
700 1 |a He, Deling  |u Department of Communication Sciences and Disorders, University of Wisconsin‐ Madison, Madison, WI, USA, 
700 1 |a Basche, Kristin E  |u Department of Communication Sciences and Disorders, University of Wisconsin‐ Madison, Madison, WI, USA, 
700 1 |a Langhough, Rebecca E.  |u Wisconsin Alzheimer's Institute, University of Wisconsin‐Madison School of Medicine and Public Health, Madison, WI, USA, 
700 1 |a Betthauser, Tobey J.  |u Wisconsin Alzheimer's Institute, University of Wisconsin‐Madison School of Medicine and Public Health, Madison, WI, USA, 
700 1 |a Hermann, Bruce P  |u Department of Neurology, University of Wisconsin‐Madison School of Medicine and Public Health, Madison, WI, USA, 
700 1 |a Johnson, Sterling C  |u Wisconsin Alzheimer's Institute, University of Wisconsin‐Madison School of Medicine and Public Health, Madison, WI, USA, 
700 1 |a Mueller, Kimberly D  |u Wisconsin Alzheimer's Institute, University of Wisconsin‐Madison School of Medicine and Public Health, Madison, WI, USA, 
773 0 |t Alzheimer's & Dementia  |g vol. 21 (Dec 1, 2025) 
786 0 |d ProQuest  |t Consumer Health Database 
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