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Spatial transcriptomics analysis of adult hippocampal neurogenesis in the human brain

ABSTRACT: Adult hippocampal neurogenesis (AHN) has been extensively characterized in rodent models, but its existence in humans remains controversial. We sought to assess the phenomenon in post-mortem human hippocampal samples by combining spatial transcriptomics and fluorescent in situ hybridization. We detected very few cells expressing neural stem cell- and proliferation-specific genes in the human dentate gyrus (DG) from childhood to middle age, suggesting very low levels of hippocampal neurogenesis throughout life. However, we observed at all ages a significant number of DG cells expressing the immature neuronal marker DCX. The majority of DCX+ cells displayed an inhibitory phenotype, while the remainder were non-committed or excitatory in nature. Overall, our study investigates for the first time the extent of AHN in the human brain with spatial transcriptomic tools and reveals important insight into the distribution and phenotype of cells expressing neurogenesis markers in the adult human hippocampus.

ORGANISM(S): Homo sapiens

PROVIDER: GSE248545 | GEO | 2024/10/16

REPOSITORIES: GEO

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Project description:Mild exercise (ME) with an intensity below the lactate threshold (LT) is sufficient to enhance hippocampal function, while intense exercise (IE) above the LT negates such benefits. However, the question as to why ME more effectively enhances hippocampal function than does IE remains to be clarified. Here, we investigated adult hippocampal neurogenesis (AHN) as a mechanism of ME-induced cognitive improvement, and comprehensively delineated the transcriptomic profile of the hippocampus, using a rat whole-genome microarray approach through comparison with IE. Immunohistochemical results showed that less intense exercise (ME) is better suited to improve AHN, especially in regards to the survival and maturation of newborn neurons. DNA microarray analysis revealed that ME regulated more genes than did IE (ME: 604 genes, IE: 415 genes), and only 44 genes were modified with both exercise intensities. The identified molecular components did not comprise well-known factors related to exercise-induced AHN, such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF1), probably due to the timing of hippocampal tissue collection after the last training session and the technical feature of microarray. Rather, network analysis of the microarray data using Ingenuity Pathway Analysis algorithms revealed that the ME-influenced genes were principally related to lipid metabolism, protein synthesis and inflammatory response, which are recognized as associated with hippocampal neuroadaptations including AHN. In contrast, IE-influenced genes linked to immune response, a negative regulatory system of AHN and hippocampal function, were identified. Collectively, these results support our hypothesis that AHN could explain why ME enhances hippocampal function, and provide the ME-specific gene list that contain some potential regulators of this positive regulation. The list will become a foundation to elucidate the molecular pathway involving the ME-induced cognitive gain.

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Spatial transcriptomics analysis of adult hippocampal neurogenesis in the human brain

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