BRAIN BEHAVIOR AND IMMUNITY脑、行为与免疫
BRAIN BEHAVIOR AND IMMUNITY(英文缩写 BRAIN BEHAV IMMUN),ISSN 0889-1591,eISSN 1090-2139,中文译名:脑、行为与免疫 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 19.227 | Q1 |
| 2022 | 15.100 | Q1 |
| 2023 | 8.800 | Q1 |
| 2024 | 7.600 | Q1 |
| 2025 | 7.500 | Q1 |
BRAIN BEHAVIOR AND IMMUNITY 最新收录文献
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7. Clarifying TriNetX and NHIRD methodology in a study of syphilis infection and incident dementia.
PMID:日期:2026-10-01该文献暂无摘要。
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8. Bifidobacterium bifidum TMC3115-RAW264.7 cell conditioned mediums promote the synaptic development of primary hippocampal neuron via activating IL-6/JAK2/STAT3 signaling pathway.
PMID:日期:2026-10-01Immunomodulation represents a key mechanism through which the microbiota-gut-brain axis exerts its effects. While probiotics can promote central nervous system (CNS) development via this axis, current in vitro models hard to recapitulate the process whereby probiotics activate local immunity and subsequently deliver immune mediators to the CNS through systemic circulation. To address this gap, we established a probiotic-RAW264.7 cell-primary hippocampal neuron system for investigation of how live and heat-inactivated Bifidobacterium bifidum TMC3115 promotes hippocampal neuron development via macrophage-conditioned media. We found that the peptidoglycan (PGN) induced relatively low levels of IL-6, IL-1β, IL-10, and TNF-α secretion, whereas lipopolysaccharide (LPS) elicited markedly higher levels of IL-6, IL-1β, and IL-10, as measured by Enzyme-Linked Immunosorbent Assay (ELISA). In contrast, both live and heat-inactivated TMC3115 induced only moderate cytokine secretion. Conditioned mediums (CMs) derived from PGN and LPS treated macrophages inhibited synaptic and morphological development of primary hippocampal neurons, whereas CMs from both live and heat-inactivated TMC3115-RAW264.7 significantly enhanced neuronal survival and upregulated the mRNA expression of Cellular Fos (c-Fos), Postsynaptic Density Protein 95 (PSD95), and Synaptophysin (SYP). Notably, CMs from live TMC3115 elicited stronger pro-neurodevelopmental effects than that from the heat-inactivated counterpart. Importantly, IL-6 depletion in both live and heat-inactivated TMC3115-RAW264.7 CMs suppressed the expression of neurodevelopmental genes and proteins and impaired neuronal morphological maturation. Mechanistically, CMs of both live and heat-inactivated TMC3115-RAW264.7 activated the IL-6/JAK2/STAT3 signaling pathway in neurons, as indicated by increased pJAK2/JAK2 and pSTAT3/STAT3 ratios. Consistently, pharmacological inhibition of JAK2 or STAT3 markedly impaired synaptic development in primary hippocampal neurons. In summary, our results demonstrate that both live and heat-inactivated TMC3115 strain-specifically induce RAW264.7 cells to secrete IL-6 at physiologically relevant concentration, which contributes to the synaptic and morphological development of primary hippocampal neurons and is partially mediated through activation of the IL-6/JAK2/STAT3 signaling pathway.
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9. STK40 contributes to neuropathic pain by modulating macrophagic glycogen metabolism and inflammatory responses through the AKT/GSK3β/GYS1 axis.
9. STK40通过调节巨噬细胞糖原代谢和AKT/GSK3β/GYS1轴的炎症反应，导致神经性疼痛PMID:日期:2026-10-01Neuropathic pain (NP) is a complex and debilitating condition characterized by persistent pain due to nerve injury, underscoring the urgent need for improved diagnostic and treatment strategies. Although the glycogen metabolic process (GMP) has been reported to play an important role in NP pathology, the underlying mechanisms remain unclear. We conducted a bioinformatic analysis of transcriptomic datasets of patients with NP in the GEO database and identified three GMP-related hub genes (STK40, PRKAG2, and PHKA1) with strong combined diagnostic potential, achieving an area under the curve (AUC) of 0.832. Subsequent experiments demonstrated that after chronic constriction injury (CCI), only STK40 was significantly upregulated in macrophages of the dorsal root ganglia (DRG). Microinjection-mediated silencing of STK40 in the DRG or conditional knockout of STK40 in DRG macrophages alleviated pain-related behaviors in CCI mice. Mechanistically, STK40 promotes macrophage inflammatory responses by inhibiting the conversion of UDP-glucose (UDPG) to glycogen through the AKT/GSK3β/GYS1 signaling axis. These findings reinforce the importance of GMP in NP and identify STK40 as a potential therapeutic target for NP.
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10. Ventral striatal neuroimmune signalling biases the expression of social memory in male mice.
PMID:日期:2026-10-01Social behaviours are highly sensitive to inflammatory states. However, the precise contribution of neuroinflammation in the ventral striatum to social memory remains unclear. Using a mouse model of recurrent herpes simplex virus-1 (HSV-1) infection and a complementary model of region-restricted inflammation induced by bilateral intra-ventral striatum lipopolysaccharide (LPS) injection, we show that ventral striatal inflammation impacts social memory expression. Both HSV-1-infected and LPS-treated mice failed to discriminate between old and novel conspecifics, with LPS-treated animals showing a slight preference for the known stimulus. In these animals, social memory alterations were associated with microglial activation, inflammatory signalling, and increased GluA2 expression in the ventral striatum and were not dependent on altered social novelty sensitivity. In both models, behavioural alterations were rescued by dexamethasone treatment. Finally, LPS-induced neuroinflammatory markers in the ventral striatum correlated with preference for the familiar social stimulus. Together, these findings identify ventral striatal inflammation as a key modulator of social memory expression.