Cell | 渐冻症语言与执行功能衰退的差异细胞基础
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TL;DR - A Cell study combining spatial transcriptomics and single-nucleus RNA sequencing identifies distinct cellular mechanisms behind language and executive-function decline in ALS. The findings clarify ALS cognitive heterogeneity and suggest phenotype-specific therapeutic targets.
- Language impairment correlated with diffuse glial–vascular dysregulation in the BA44/45 language region, including altered perivascular myeloid-cell activity.
- Executive dysfunction was linked to reduced mitochondrial, oxidative-phosphorylation, and synaptic activity in deep-layer BA46 excitatory and inhibitory neurons.
- Reactive astrocytes, microglia, and stressed oligodendrocyte precursor cells increased across ALS samples, indicating a coordinated gliosis response.
- Gliosis occurred independently of TDP-43 pathology, while oligodendrocyte-lineage abundance tracked neuronal synaptic and mitochondrial dysregulation.
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Cell | 渐冻症语言与执行功能衰退的差异细胞基础
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TL;DR - A Cell study combining spatial transcriptomics and single-nucleus RNA sequencing identifies distinct cellular mechanisms behind language and executive-function decline in ALS. The findings clarify ALS cognitive heterogeneity and suggest phenotype-specific therapeutic targets.
- Language impairment correlated with diffuse glial–vascular dysregulation in the BA44/45 language region, including altered perivascular myeloid-cell activity.
- Executive dysfunction was linked to reduced mitochondrial, oxidative-phosphorylation, and synaptic activity in deep-layer BA46 excitatory and inhibitory neurons.
- Reactive astrocytes, microglia, and stressed oligodendrocyte precursor cells increased across ALS samples, indicating a coordinated gliosis response.
- Gliosis occurred independently of TDP-43 pathology, while oligodendrocyte-lineage abundance tracked neuronal synaptic and mitochondrial dysregulation.