Cognitive and affective disturbances are increasingly recognized as important extra-thyroidal manifestations of Hashimoto’s thyroiditis (HT). These neurological symptoms can occur even when systemic thyroid hormone levels remain within the normal range, suggesting that mechanisms beyond thyroid hormone deficiency contribute to CNS dysfunction.
In autoimmune thyroiditis, cognitive impairment was associated with a coordinated inflammatory response in the hippocampus and cortex, two regions essential for memory and higher-order cognitive processing.
Emerging evidence points to HMGB1 as a critical molecular link between peripheral thyroid autoimmunity and neuroinflammation. Moreover, associated signals are closely linked to activated microglia.
This places HMGB1 at a particularly important point in the disease mechanism—not simply as a marker released during inflammation, but as a potential amplifier connecting peripheral autoimmunity with central nervous system dysfunction.
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