Neuroinflammation is increasingly recognized as playing a key pathogenetic role in Alzheimer's disease (AD). We examined the relationship between in vivo neuroinflammation and gray matter (GM) changes. Twenty-eight subjects with clinically probable AD (n = 14) and amyloid-positive mild cognitive impairment (n = 14) (age 71.9 ± 8.4 years, 46% female) and 24 healthy controls underwent structural 3T brain MRI. AD/mild cognitive impairment participants exhibited GM atrophy and cortical thinning in AD-related temporoparietal regions (false discovery rate–corrected p < 0.05). Patients also showed increased microglial activation in temporal cortices. Higher 11C-PK11195 binding in these regions was associated with reduced volume and cortical thickness in parietal, occipital, and cingulate areas (false discovery rate p < 0.05). Hippocampal GM atrophy and parahippocampal cortical thinning were related to worse cognition (p < 0.05), but these effects were not mediated by microglial activation. This study demonstrates an association between in vivo microglial activation and markers of GM damage in AD, positioning neuroinflammation as a potential target for immunotherapeutic strategies.

中文翻译：

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阿尔茨海默病中与小胶质细胞激活相关的灰质变化

越来越多地认识到神经炎症在阿尔茨海默病 (AD) 中起着关键的致病作用。我们检查了体内神经炎症与灰质 (GM) 变化之间的关系。28 名临床上可能患有 AD 的受试者（n = 14）和淀粉样蛋白阳性轻度认知障碍（n = 14）（年龄 71.9 ± 8.4 岁，46% 女性）和 24 名健康对照接受了结构性 3T 脑 MRI。AD/轻度认知障碍参与者在 AD 相关的颞顶区域表现出 GM 萎缩和皮质变薄（错误发现率校正 p < 0.05）。患者还显示颞叶皮质中小胶质细胞激活增加。这些区域中较高的 11C-PK11195 结合与顶叶、枕叶和扣带回区域的体积和皮质厚度减少有关（错误发现率 p < 0.05）。海马 GM 萎缩和海马旁皮质变薄与较差的认知有关（p < 0.05），但这些影响不是由小胶质细胞激活介导的。这项研究证明了体内小胶质细胞激活与 AD 中 GM 损伤标志物之间的关联，将神经炎症定位为免疫治疗策略的潜在目标。