This describes the essential role of thyroid hormones, specifically triiodothyronine and thyroxine, in supporting and regulating the neural processes responsible for optimal cognitive performance, including attention, processing speed, and memory. Both hypothyroidism, a deficiency, and hyperthyroidism, an excess, can profoundly impair brain function. Maintaining euthyroid status is a non-negotiable requirement for cognitive health across all life stages.
Origin
The link between the thyroid gland and cognition has been recognized clinically for centuries, with the severe intellectual disability associated with congenital hypothyroidism being a historical benchmark. Modern endocrinology and neuroscience have since mapped the distribution of thyroid hormone receptors in the brain, particularly in the hippocampus and cortex. This understanding provides the foundation for diagnosing and treating thyroid-related cognitive symptoms.
Mechanism
Thyroid hormones act by binding to nuclear receptors in brain cells, regulating the expression of genes critical for neuronal differentiation, myelination, and neurotransmitter synthesis. T3, the active form, directly influences mitochondrial function and oxygen consumption in the brain, ensuring adequate energy supply for neural activity. Any disruption in the hypothalamic-pituitary-thyroid axis can lead to altered cerebral metabolism and subsequent cognitive slowing or impairment.
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