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Notwithstanding their utility, these established methods exhibit inherent limitations in fully elucidating the complex histopathological transformations characteristic of MS. Specifically, they encounter difficulties in precisely quantifying and standardizing patient-specific pathological features, and often lack the requisite precision to delineate the disease's nuanced pathological hallmarks. Recent advancements in neuroimaging, biomarker discovery, and genomic profiling have yielded substantial evidence implicating glial cell activation as a central pathogenic mechanism in MS. In particular, the activation of astrocytes and microglia has been shown to play a pivotal role in disease progression, precipitating a cascade of events that culminate in neuronal axonal demise. The identification of distinct glial cell subsets represents a critical step towards the development of targeted therapeutic strategies. 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