时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
In summary, this cohort of Spanish-speaking MTLE patients demonstrate age-associated cognitive decline most significantly in fluid intelligence and visuospatial reconstruction and memory domains.Since fluid intelligence and visuospatial reconstruction and memory are domains that also decline with disease duration (Ammothumkandy et al., 2025b), we performed multiple linear regression analyses to determine whether age remained independently associated with these cognitive domains (Supplementary Table S5).；Collectively, these findings suggest that age may have a stronger adjusted association with fluid intelligence than disease duration.An increase in immature astroglia associates with aging and a decline in fluid intelligenceWe next investigated whether age-associated cognitive decline in MTLE patients was linked to a pathological Dcx + stellar immature astroglial cell that we had previously identified in surgical epileptic hippocampus resections (Ammothumkandy et al., 2022).；We also performed multiple linear regressions to determine whether Dcx + immature astroglia remained independently associated with age after adjusting for disease duration (Supplementary Table S6).
方法
These cognitive studies in mice largely focus on spatial learning and memory, whereas human cognition encompasses additional domains such as intelligence, verbal learning and language that can have domain and species-specific cellular contributions (Ammothumkandy et al., 2025b).；However, a direct cellular association between pathological astroglia and decline in specific cognitive domains remains unexplored in humans.Cognitive decline is a comorbidity that occurs progressively in epilepsy patients.；Mesial Temporal Lobe Epilepsy (MTLE) is the most common form of adult epilepsy, and patients who do not respond to medications undergo surgical removal of epileptic hippocampal tissue as treatment (Engel, 2001).
核心结论
People with epilepsy demonstrate accelerated brain aging (Breuer et al., 2016; Hwang et al., 2020) and cognitive decline is especially pronounced in older individuals (Piazzini et al., 2006; Sen et al., 2018).；These findings highlight immature astroglia as an epilepsy-associated cellular feature corresponding to age-related cognitive decline and provides a basis for future mechanistic and translational studies.Methods and materialHuman participantsThe cognitive study was approved by University of Southern California Institutional Review Board approval number: HS-10-00162, and Rancho Los Amigos National Rehabilitation Center and the Rancho Research Institute’s Institutional (RRI) Review Board, approval number: RRI IRB # 195 with proper data use agreement.；In our previous study on human MTLE, we found that all Dcx+ stellar cells co-expressed GFAP and S100β, consistent with an immature astroglial phenotype, while lacking co-expression with markers of granule neurons (Prox1+), mossy cells (GluR2/3+), interneurons (Gad65/67+), microglia (Iba1+), and immature neurons (PSA-NCAM+) (Ammothumkandy et al., 2022).
局限
However, a direct cellular association between pathological astroglia and decline in specific cognitive domains remains unexplored in humans.Cognitive decline is a comorbidity that occurs progressively in epilepsy patients.；The number of Dcx + immature astroglial cells in MTLE hippocampus trended toward an increase with age; however, the significance of this phenotype and its association with cognitive decline was not investigated.；For fluid intelligence, however, the model including age and disease duration was significant (p = 0.0065).
对本项目的价值
中等价值：属「脑老化与神经退行」方向；脑老化 / 神经退行 / 认知栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.9/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 36,520 字符，题名指纹 0.82，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：人类流体智力的年龄相关下降与未成熟星形胶质细胞比例升高相对应
- 英文标题：An age-related decline in human fluid intelligence corresponds with immature astroglia prevalence.
- 期刊与标识：Frontiers in cellular neuroscience · PMID 42974419 · DOI 10.3389/fncel.2026.1926804 · PMC PMC13727376