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Persistent neuroinflammation may disrupt the 5-hydroxytryptamine (5-HT) signaling pathway, exacerbate neural dysfunction, and, through a positive feedback mechanism, impair neural circuit remodeling and synaptic plasticity, thereby contributing to the comorbid progression of both disorders
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Future studies should focus on whether these effects are long lasting with a deeper assessment of how they may correlate clinically, given that cognition is impaired in 40–70% of patients with MS ( There are limited studies evaluating cerebral glucose metabolism in relation to cognitive impairment in MS patients
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