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
Department of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.
Department of Nuclear Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Alzheimers Dement. 2025 May;21(5):e70333. doi: 10.1002/alz.70333.
We investigated the associations of longitudinal synaptic loss and cognitive decline with tau burden and plasma biomarkers in Alzheimer's disease (AD).
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.
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.
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.
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.
我们研究了阿尔茨海默病（AD）中纵向突触丢失和认知衰退与tau蛋白负荷及血浆生物标志物之间的关联。
20名认知受损（CI）个体和16名健康对照（HC）接受了认知和血浆生物标志物评估、淀粉样蛋白正电子发射断层扫描（PET）、tau蛋白PET以及突触密度PET；1年后，重复进行tau蛋白和突触密度PET检查。研究了tau蛋白负荷、血浆生物标志物、突触密度和认知之间的关系。
CI组比HC组有更多的纵向突触丢失和tau蛋白沉积。纵向突触丢失与纵向认知衰退呈正相关，与纵向tau蛋白沉积呈负相关。血浆胶质纤维酸性蛋白（GFAP）介导了纵向tau蛋白沉积与纵向突触丢失之间的关系。tau蛋白负荷、血浆磷酸化tau181和GFAP可预测纵向突触丢失和认知衰退。
CI组比HC组有更多的纵向突触丢失和tau蛋白负荷增加。tau蛋白病理和血浆GFAP可预测纵向突触丢失和认知衰退。
与健康对照相比，认知受损个体在内侧颞叶有更多的纵向突触丢失，在广泛的新皮层中tau蛋白负荷增加。突触密度的纵向变化与tau蛋白负荷的纵向变化呈负相关，与纵向认知衰退呈正相关。血浆胶质纤维酸性蛋白（GFAP）介导了纵向tau蛋白沉积与纵向突触丢失之间的关系。tau蛋白负荷、血浆磷酸化tau181和GFAP可预测纵向突触丢失和认知衰退。
