时间：1月8日 (周四)  18:00-20:00

地点：恕园28号楼205室

主题：文献报告和工作进展

1、文献汇报：通过抑制控制实现注意与工作记忆的神经解离

主讲：吕维潇 同学

2、工作进展：大脑网络动态结构-功能耦合梯度的跨物种比较研究

主讲： 张峻瑞 同学

3、文献汇报：单核细胞能高效替换所有脑巨噬细胞，且胎肝来源的单核细胞能生成真正的SALL1阳性小胶质细胞

主讲：盛世红 同学

4、文献汇报：成熟少突胶质细胞的DOR活化调节α-酮戊二酸代谢导致老年小鼠髓鞘再生增强

主讲：陈思颍 同学

欢迎老师与同学们踊跃出席！

脑科学研究所

文献详细信息

1、题目：Neural dissociation of attention and working memory through inhibitory control

期刊信息：Nature Communications IF: 14.7 SCI: Q1 中科院：一区

摘要：Attention and working memory (WM) have traditionally been considered closely linked processes with shared neural mechanisms. In information selection, attention is often conceptualized as a gatekeeper to WM, regulating which information is encoded and stored. Here, combining tasks specifically designed to separate attention from WM encoding with a multimodal approach, we provide converging neural and causal evidence that these processes are dissociable. Functional MRI identifies the supramarginal gyrus (SMG) as the key region enabling this dissociation, while dynamic causal modeling reveals the neural circuitry through which the SMG exerts inhibitory control over attentional representations, regulating their integration into WM. Furthermore, neuromodulation via transcranial direct current stimulation (tDCS) demonstrates that enhancing SMG activity strengthens this inhibitory control. A second tDCS experiment using varied stimuli confirms the generalizability of the effect. Finally, a transcranial magnetic stimulation (TMS) experiment provides further causal evidence with greater spatial precision. These findings challenge the long-standing view that attention and WM encoding form a continuous process, demonstrating

instead that they constitute two dissociable neural processes of information selection.

2、题目：Monocytes can efficiently replace all brain macrophages and fetal liver monocytes can generate bona fide SALL1+ microglia

期刊信息：immunity IF：26.3 SCI: Q1 中科院：一区

摘要：Microglia and border-associated macrophages (BAMs) are critical for brain health, and their dysfunction is associated to disease. Replacing brain macrophages holds substantial therapeutic promise but remains challenging. Here, we demonstrate that monocytes can efficiently replace all brain macrophages. Monocytes readily replaced embryonal BAMs upon their depletion and engrafted as monocyte-derived microglia (Mo-Microglia) upon more sustained niche availability. Mo-Microglia expanded comparably to their embryonic counterparts and showed similar longevity. However, monocytes were unable to replicate the distinct identity of embryonically derived BAMs and microglia. Using xenotransplantation, we found that human monocytes exhibited similar behavior, enabling identification of putative Mo-Microglia in Alzheimer's disease individuals. In mice and humans, monocyte ontogeny shaped their identity as brain macrophages. Importantly, mouse fetal liver monocytes exhibited a distinct epigenetic landscape and could develop a bona fide microglial identity. Our results illuminate brain macrophage development and highlight monocytes as an abundant progenitor source for brain macrophage replacement therapies.

3、题目：DOR activation in mature oligodendrocytes regulates α-ketoglutarate metabolism

leading to enhanced remyelination in aged mice

期刊信息：Nature Neuroscience IF: 20.0 SCI: Q1 中科院：一区

摘要：The decreased ability of mature oligodendrocytes to produce myelin negatively affects remyelination in demyelinating diseases and aging, but the underlying mechanisms are incompletely understood. In the present study, we identify a mature oligodendrocyte-enriched transcriptional coregulator diabetes- and obesity-related gene (DOR)/tumor protein p53-inducible nuclear protein 2 (TP53INP2), downregulated in demyelinated lesions of donors with multiple sclerosis and in aged oligodendrocyte-lineage cells. Dor ablation in mice of both sexes results in defective myelinogenesis and remyelination. Genomic occupancy in oligodendrocytes and transcriptome profiling of the optic nerves of wild-type and Dor conditional knockout mice reveal that DOR and SOX10 co-occupy enhancers of critical myelinogenesis-associated genes including Prr18, encoding an oligodendrocyte-enriched, proline-rich factor. We show that DOR targets regulatory elements of genes responsible for α-ketoglutarate biosynthesis in mature oligodendrocytes and is essential for α-ketoglutarate production and lipid biosynthesis. Supplementation with α-ketoglutarate restores oligodendrocyte-maturation defects in Dor-deficient adult mice and improves remyelination after lysolecithin-induced demyelination and cognitive function in 17-month-old wild-type mice. Our data suggest that activation of α-ketoglutarate metabolism in mature oligodendrocytes can promote myelin production during demyelination and aging.