Age-Related Cognition refers to the typical, non-pathological alterations in cognitive abilities that occur across the human lifespan, particularly noticeable in later decades. This physiological phenomenon often includes a subtle decline in processing speed, certain aspects of memory retrieval, and executive functions, while crystallized intelligence generally remains stable or improves. These changes are intricately linked to cumulative cellular senescence and shifts in neuroendocrine signaling, which impact synaptic integrity and neuronal network efficiency.
Origin
The term is descriptive, originating from geriatric medicine and neuropsychology to categorize the predictable functional changes observed as a function of chronological age. Its clinical relevance grew as researchers sought to differentiate normal physiological aging from pathological neurodegenerative diseases, emphasizing the role of biological aging mechanisms. The concept acknowledges the pervasive influence of time on the structural and functional capacity of the central nervous system.
Mechanism
The underlying mechanism involves a confluence of factors, including reduced neurotrophic support, mitochondrial dysfunction, and alterations in the hypothalamic-pituitary-adrenal (HPA) axis regulation. Specifically, age-related declines in hormones like estrogen and testosterone can reduce synaptic density and impair neuronal communication in key brain regions like the hippocampus. This cumulative biological wear, often exacerbated by chronic low-grade inflammation, compromises the brain’s ability to maintain optimal cognitive performance over time.
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