小胶质细胞
疾病
Tau病理学
病理
神经科学
医学
阿尔茨海默病
心理学
炎症
免疫学
作者
Samantha Rossano,Aubrey S. Johnson,Anna Smith,Galen Ziaggi,Andrew E. Roetman,Diana Guzman,Amarachukwu Okafor,Julia Klein,Zeljko Tomljanovic,Yaakov Stern,Adam M. Brickman,Seonjoo Lee,William Charles Kreisl,Patrick J. Lao
摘要
Abstract INTRODUCTION Evidence suggests microglial activation precedes regional tau and neurodegeneration in Alzheimer's disease (AD). We characterized microglia with translocator protein (TSPO) positron emission tomography (PET) within an AD progression model where global amyloid beta (Aβ) precedes local tau and neurodegeneration, resulting in cognitive impairment. METHODS Florbetaben, PBR28, and MK‐6240 PET, T1 magnetic resonance imaging, and cognitive measures were performed in 19 cognitively unimpaired older adults and 22 patients with mild cognitive impairment or mild AD to examine associations among microglia activation, Aβ, tau, and cognition, adjusting for neurodegeneration. Mediation analyses evaluated the possible role of microglial activation along the AD progression model. RESULTS Higher PBR28 uptake was associated with higher Aβ, higher tau, and lower MMSE score, independent of neurodegeneration. PBR28 mediated associations between tau in early and middle Braak stages, between tau and neurodegeneration, and between neurodegeneration and cognition. DISCUSSION Microglia are associated with AD pathology and cognition and may mediate relationships between subsequent steps in AD progression.
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