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Conceptual review outlines thyroid hormone dysregulation in Alzheimer's disease, suggesting intersecting pathways of inflammation and altered signaling drive clinical heterogeneity.
An expanding body of evidence suggests that thyroid dysfunction may be clinically relevant in Alzheimer's disease (AD), although the significance of this association remains unsettled. Rather than reflecting a single biological pathway, thyroid hormone alterations in AD may involve downstream systemic adaptations related to inflammation and frailty, central dysregulation of thyroid hormone bioavailability and signaling, and upstream vulnerability mechanisms. Clarifying how these pathways intersect with cognitive and functional decline may help refine the biological interpretation of clinical heterogeneity in patients with AD.
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Ilardi et al. (2026) studied this question.
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