UK Dementia Research Institute at UCL, University College London, London WC1E 6BT, UK; The Francis Crick Institute, London NW1 1AT, UK; Department of Neurosciences and Leuven Brain Institute, KU Leuven, Leuven, Belgium.
Department of Neurosciences and Leuven Brain Institute, KU Leuven, Leuven, Belgium; Laboratory for the Research of Neurodegenerative Diseases, VIB Center for Brain & Disease Research, VIB, Leuven, Belgium.
Cell Rep. 2024 Jun 25;43(6):114216. doi: 10.1016/j.celrep.2024.114216. Epub 2024 May 30.
The amyloid plaque niche is a pivotal hallmark of Alzheimer's disease (AD). Here, we employ two high-resolution spatial transcriptomics (ST) platforms, CosMx and Spatial Enhanced Resolution Omics-sequencing (Stereo-seq), to characterize the transcriptomic alterations, cellular compositions, and signaling perturbations in the amyloid plaque niche in an AD mouse model. We discover heterogeneity in the cellular composition of plaque niches, marked by an increase in microglial accumulation. We profile the transcriptomic alterations of glial cells in the vicinity of plaques and conclude that the microglial response to plaques is consistent across different brain regions, while the astrocytic response is more heterogeneous. Meanwhile, as the microglial density of plaque niches increases, astrocytes acquire a more neurotoxic phenotype and play a key role in inducing GABAergic signaling and decreasing glutamatergic signaling in hippocampal neurons. We thus show that the accumulation of microglia around hippocampal plaques disrupts astrocytic signaling, in turn inducing an imbalance in neuronal synaptic signaling.
淀粉样斑块微环境是阿尔茨海默病 (AD) 的一个关键标志。在这里,我们采用了两种高分辨率空间转录组学 (ST) 平台,CosMx 和 Spatial enhanced Resolution Omics-sequencing (Stereo-seq),来描述 AD 小鼠模型中淀粉样斑块微环境中的转录组改变、细胞组成和信号转导扰动。我们发现斑块微环境中细胞组成存在异质性,表现为小胶质细胞积累增加。我们对斑块附近神经胶质细胞的转录组改变进行了分析,得出结论:小胶质细胞对斑块的反应在不同脑区是一致的,而星形胶质细胞的反应则更为多样化。同时,随着斑块微环境中小胶质细胞密度的增加,星形胶质细胞获得了更具神经毒性的表型,并在诱导海马神经元中 GABA 能信号和减少谷氨酸能信号方面发挥关键作用。因此,我们表明海马斑块周围小胶质细胞的积累破坏了星形胶质细胞的信号转导,进而导致神经元突触信号的失衡。
Neurobiol Aging. 2014-10
Alzheimers Dement. 2024-5
J Neuroinflammation. 2010-11-16
Front Behav Neurosci. 2025-8-11
Mol Neurodegener Adv. 2025
Biomark Res. 2025-6-18