Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
In an older-age vascular cohort, carotid stenosis is associated with processing speed and executive function cognitive deficits, which correlate with p-tau217.
СтатьяНазвание и аннотация: Перевод в очереди
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Zahra Summan, French Scott R, Arias Juan C, Ally Madeline, Wiskoski Haley, Escareno Cris, Heitkamp Emma, Vazquez Franchell, Hillis Madison, Culwell Gavin, Ainapurapu Karthik, Howell Caronae M, Johnson Kevin, Karakay Deniz, Rayasam Karthik, Taylor Lindsay, Kraemer Cody, Leon Luis, Berman Scott, Yanquez Federico, Balderman Joshua, Sabat Joseph, Hung Olivia, Lucas Layla, Bedrick Edward J, Vitali Francesca, Mushtaq Raza, Altbach Maria, Trouard Theodore P, Bilgin Ali, Reiman Eric M, Alexander Gene E, Weinkauf Craig C
Аннотация
INTRODUCTION: Asymptomatic extracranial carotid atherosclerotic disease (aECAD) has been associated with Alzheimer's disease (AD), but the earliest cognitive deficits in this hallmark vascular population are largely unknown.
METHODS: A total of 182 participants 50-85 years of age with ≥2 vascular comorbidities with/without aECAD were evaluated prospectively using a neurocognitive battery and compared to vascular comorbidities, percent stenosis, apolipoprotein E (APOE) ε4 status, and plasma phosphorylated tau (p-tau217). Dementia, stroke < 6 months, and neurological disorders were exclusionary.
RESULTS: aECAD was associated with significantly worse scores in processing speed (β = -0.19, p = 0.004) and executive function (β = -0.20, p = 0.009) domains after controlling for age, sex, education, race, and ethnicity. From these, a carotid cognitive index was created, which correlated with p-tau217 (β = -0.29, p < 0.001), accounting for demographics, vascular comorbidities, white matter lesions, and APOE ε4 status.
DISCUSSION: These data identify specific cognitive deficits associated with carotid stenosis and build further impetus to understand how vascular-related cognitive deficits contrast and complement the classic memory deficits of AD.
METHODS: A total of 182 participants 50-85 years of age with ≥2 vascular comorbidities with/without aECAD were evaluated prospectively using a neurocognitive battery and compared to vascular comorbidities, percent stenosis, apolipoprotein E (APOE) ε4 status, and plasma phosphorylated tau (p-tau217). Dementia, stroke < 6 months, and neurological disorders were exclusionary.
RESULTS: aECAD was associated with significantly worse scores in processing speed (β = -0.19, p = 0.004) and executive function (β = -0.20, p = 0.009) domains after controlling for age, sex, education, race, and ethnicity. From these, a carotid cognitive index was created, which correlated with p-tau217 (β = -0.29, p < 0.001), accounting for demographics, vascular comorbidities, white matter lesions, and APOE ε4 status.
DISCUSSION: These data identify specific cognitive deficits associated with carotid stenosis and build further impetus to understand how vascular-related cognitive deficits contrast and complement the classic memory deficits of AD.