This describes the direct and indirect influence of the primary stress hormone, cortisol, on cognitive functions, including memory, executive function, and attention. While acute, transient increases in cortisol can enhance certain aspects of memory consolidation, chronic hypercortisolemia is clinically linked to detrimental effects on the hippocampus and prefrontal cortex, leading to impaired memory retrieval and cognitive flexibility.
Origin
This field of study originates from neuroendocrinology, specifically the research on the Hypothalamic-Pituitary-Adrenal (HPA) axis and its glucocorticoid output. The connection was established through the identification of high concentrations of glucocorticoid receptors in the hippocampus, a brain region critical for memory. The longevity perspective focuses on mitigating the cumulative, long-term neurotoxic effects of chronic stress-induced cortisol elevation.
Mechanism
Cortisol exerts its effect by binding to mineralocorticoid and glucocorticoid receptors in the brain. Chronic, elevated cortisol levels can lead to dendritic retraction and atrophy in hippocampal neurons, reducing synaptic plasticity and impairing the formation of new memories. Furthermore, sustained high cortisol contributes to systemic insulin resistance and chronic neuroinflammation, both of which indirectly compromise the brain’s metabolic and structural integrity, accelerating cognitive aging.
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