Adiposity Impact on Cognition refers to the clinically established correlation where excessive or dysfunctional adipose tissue, particularly visceral fat, negatively influences executive function, memory, and overall cognitive health. This impact arises because adipose tissue is not merely a passive energy store but an active endocrine organ that secretes adipokines and pro-inflammatory cytokines. These systemic inflammatory factors are directly implicated in driving neuroinflammation and vascular changes within the central nervous system. The consequence is a measurable impairment in the brain’s ability to process information efficiently.
Origin
This concept stems from the convergence of endocrinology, metabolic research, and neuroscience, acknowledging that body fat distribution is a key determinant of systemic inflammation and hormonal dysregulation. “Adiposity” comes from the Latin adeps meaning fat, and the impact on “cognition” highlights the functional consequence on the brain’s ability to process information. This integrated view is now central to understanding age-related cognitive decline and metabolic syndrome.
Mechanism
Dysfunctional adipocytes release inflammatory mediators, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which can traverse the blood-brain barrier. This chronic low-grade inflammation disrupts neuronal signaling, impairs synaptic plasticity, and promotes insulin resistance within the brain, particularly in the hippocampus, a region vital for memory. Concurrently, altered hormone profiles, including leptin and cortisol, contribute to the neuroendocrine imbalance that underlies the observed cognitive deficits.
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