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多发性硬化症斑块周围白质中的小胶质细胞激活取决于年龄和病变类型,但与少突胶质细胞丢失无关。

Microglia activation in periplaque white matter in multiple sclerosis depends on age and lesion type, but does not correlate with oligodendroglial loss.

机构信息

Institute of Neuropathology, University Hospital Münster, Pottkamp 2, 48149, Münster, Germany.

出版信息

Acta Neuropathol. 2023 Dec;146(6):817-828. doi: 10.1007/s00401-023-02645-2. Epub 2023 Oct 28.

Abstract

Multiple sclerosis (MS) is the most frequent inflammatory and demyelinating disease of the CNS. The disease course in MS is highly variable and driven by a combination of relapse-driven disease activity and relapse-independent disease progression. The formation of new focal demyelinating lesions is associated with clinical relapses; however, the pathological mechanisms driving disease progression are less well understood. Current concepts suggest that ongoing focal and diffuse inflammation within the CNS in combination with an age-associated failure of compensatory and repair mechanisms contribute to disease progression. The aim of our study was to characterize the diffuse microglia activation in periplaque white matter (PPWM) of MS patients, to identify factors modulating its extent and to determine its potential correlation with loss or preservation of oligodendrocytes. We analyzed microglial and oligodendroglial numbers in PPWM in a cohort of 96 tissue blocks from 32 MS patients containing 100 lesions as well as a control cohort (n = 37). Microglia activation in PPWM was dependent on patient age, proximity to lesion, lesion type, and to a lesser degree on sex. Oligodendrocyte numbers were decreased in PPWM; however, increased microglia densities did not correlate with lower oligodendroglial cell counts, indicating that diffuse microglia activation is not sufficient to drive oligodendroglial loss in PPWM. In summary, our findings support the notion of the close relationship between focal and diffuse inflammation in MS and that age is an important modulator of MS pathology.

摘要

多发性硬化症(MS)是中枢神经系统最常见的炎症性和脱髓鞘疾病。MS 的疾病进程高度多变,由复发驱动的疾病活动和复发无关的疾病进展共同驱动。新的局灶性脱髓鞘病变的形成与临床复发有关;然而,导致疾病进展的病理机制尚不清楚。目前的概念表明,中枢神经系统内持续的局灶性和弥漫性炎症以及与年龄相关的代偿和修复机制的失败,共同导致了疾病的进展。我们的研究旨在描述 MS 患者斑块周围白质(PPWM)中的弥漫性小胶质细胞激活,确定调节其程度的因素,并确定其与少突胶质细胞丢失或保留的潜在相关性。我们分析了来自 32 名 MS 患者的 96 个组织块的 PPWM 中的小胶质细胞和少突胶质细胞数量,这些组织块包含 100 个病变以及一个对照组(n=37)。PPWM 中的小胶质细胞激活依赖于患者年龄、与病变的距离、病变类型,在较小程度上还依赖于性别。PPWM 中的少突胶质细胞数量减少;然而,增加的小胶质细胞密度与较低的少突胶质细胞计数没有相关性,表明弥漫性小胶质细胞激活不足以导致 PPWM 中的少突胶质细胞丢失。总之,我们的发现支持了 MS 中局灶性和弥漫性炎症密切相关的观点,并且年龄是 MS 病理学的一个重要调节因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d6d/10628007/edb55591ff55/401_2023_2645_Fig1_HTML.jpg

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