Neurobiology of aging · 2024
Vascular risk burden is a key player in the early progression of Alzheimer's disease.
СтатьяПоддержка NIH: внешняя программаПоддержка службы здравоохранения СШАПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Ferrari-Souza João Pedro, Brum Wagner S, Hauschild Lucas A, Da Ros Lucas U, Ferreira Pâmela C L, Bellaver Bruna, Leffa Douglas T, Bieger Andrei, Tissot Cécile, Lussier Firoza Z, De Bastiani Marco Antônio, Povala Guilherme, Benedet Andréa L, Therriault Joseph, Wang Yi-Ting, Ashton Nicholas J, Zetterberg Henrik, Blennow Kaj, Martins Sheila O, Souza Diogo O, Rosa-Neto Pedro, Karikari Thomas K, Pascoal Tharick A, Zimmer Eduardo R, Alzheimer’s Disease Neuroimaging Initiative
Аннотация
Understanding whether vascular risk factors (VRFs) synergistically potentiate Alzheimer's disease (AD) progression is important in the context of emerging treatments for preclinical AD. In a group of 503 cognitively unimpaired individuals, we tested whether VRF burden interacts with AD pathophysiology to accelerate neurodegeneration and cognitive decline. Baseline VRF burden was calculated considering medical data and AD pathophysiology was assessed based on cerebrospinal fluid (CSF) amyloid-β1-42 (Aβ1-42) and tau phosphorylated at threonine 181 (p-tau181). Neurodegeneration was assessed with plasma neurofilament light (NfL) and global cognition with the modified version of the Preclinical Alzheimer's Cognitive Composite. The mean (SD) age of participants was 72.9 (6.1) years, and 220 (43.7%) were men. Linear mixed-effects models revealed that an elevated VRF burden synergistically interacted with AD pathophysiology to drive longitudinal plasma NfL increase and cognitive decline. Additionally, VRF burden was not associated with CSF Aβ1-42 or p-tau181 changes over time. Our results suggest that VRF burden and AD pathophysiology are independent processes; however, they synergistically lead to neurodegeneration and cognitive deterioration. In preclinical stages, the combination of therapies targeting VRFs and AD pathophysiology might potentiate treatment outcomes.