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In recent years, the importance of hypoxic microenvironment in the pathogenesis of RA has gradually attracted attention

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The necessity for comprehensive mechanistic investigations addressing these interactions is highlighted by this complexity, which may help to explain the uneven clinical outcomes seen [49]

Although brain uptake is modest early on, tracer binding in motor cortex and brainstem increases as disease advances, mirroring human ALS neuroinflammation and expanding diagnostic reach to neuromuscular involvement (142, 146, 147)