Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
Prediction of longitudinal synaptic loss in Alzheimer's disease using tau PET and plasma biomarkers.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Jie, Huang Qi, Chen Xing, You Zhiwen, He Kun, Mao Xiaoxie, Huang Yiyun, Franzmeier Nicolai, Schöll Michael, Guo Tengfei, Zhao Jun, Guan Yihui, Ni Ruiqing, Li Binyin, Xie Fang
Аннотация
INTRODUCTION: We investigated the associations of longitudinal synaptic loss and cognitive decline with tau burden and plasma biomarkers in Alzheimer's disease (AD).
METHODS: Twenty cognitively impaired (CI) individuals and 16 healthy controls (HC) underwent cognitive and plasma biomarker assessments, amyloid positron emission tomography (PET), tau PET, and synaptic density PET; after 1 year, tau and synaptic density PET were repeated. The relationships among tau burden, plasma biomarkers, synaptic density, and cognition were investigated.
RESULTS: The CI group had more longitudinal synapse loss and tau deposition than HCs. Longitudinal synaptic loss was positively associated with longitudinal cognitive decline, negatively with longitudinal tau deposition. Plasma glial fibrillary acidic protein (GFAP) mediates the relationship between longitudinal tau deposition and longitudinal synaptic loss. Tau burden, plasma phosphorylated tau181, and GFAP could predict longitudinal synaptic loss and cognitive decline.
CONCLUSIONS: The CI group had more longitudinal synapse loss and tau burden increases than HCs. Tau pathology and plasma GFAP could predict longitudinal synapse loss and cognitive decline.
HIGHLIGHTS: Cognitively impaired individuals had more longitudinal synapse loss in the medial temporal lobe, and increased tau burden in the widespread neocortex than healthy controls. The longitudinal change of synaptic density was negatively associated with the longitudinal change of tau burden, and positively associated with longitudinal cognitive decline. Plasma glial fibrillary acidic protein (GFAP) mediates the relationship between longitudinal tau deposition and longitudinal synaptic loss. Tau burden, plasma phosphorylated tau181, and GFAP could predict longitudinal synaptic loss and cognitive decline.
METHODS: Twenty cognitively impaired (CI) individuals and 16 healthy controls (HC) underwent cognitive and plasma biomarker assessments, amyloid positron emission tomography (PET), tau PET, and synaptic density PET; after 1 year, tau and synaptic density PET were repeated. The relationships among tau burden, plasma biomarkers, synaptic density, and cognition were investigated.
RESULTS: The CI group had more longitudinal synapse loss and tau deposition than HCs. Longitudinal synaptic loss was positively associated with longitudinal cognitive decline, negatively with longitudinal tau deposition. Plasma glial fibrillary acidic protein (GFAP) mediates the relationship between longitudinal tau deposition and longitudinal synaptic loss. Tau burden, plasma phosphorylated tau181, and GFAP could predict longitudinal synaptic loss and cognitive decline.
CONCLUSIONS: The CI group had more longitudinal synapse loss and tau burden increases than HCs. Tau pathology and plasma GFAP could predict longitudinal synapse loss and cognitive decline.
HIGHLIGHTS: Cognitively impaired individuals had more longitudinal synapse loss in the medial temporal lobe, and increased tau burden in the widespread neocortex than healthy controls. The longitudinal change of synaptic density was negatively associated with the longitudinal change of tau burden, and positively associated with longitudinal cognitive decline. Plasma glial fibrillary acidic protein (GFAP) mediates the relationship between longitudinal tau deposition and longitudinal synaptic loss. Tau burden, plasma phosphorylated tau181, and GFAP could predict longitudinal synaptic loss and cognitive decline.