Age Related Neurological Senescence describes the gradual, intrinsic decline in the structural integrity and functional capacity of the central nervous system that occurs as a natural consequence of chronological aging. This physiological process is characterized by progressive alterations in neuronal and glial cell function, impacting cognitive and motor output. It is a fundamental component of human longevity, influencing the overall quality of healthspan. Understanding this senescence is crucial for developing interventions that support neuroendocrine health and cognitive vitality throughout life.
Origin
The term draws its roots from clinical neurology and gerontology, combining “age related” for chronological context, “neurological” referring to the nervous system, and “senescence” from the Latin senescere, meaning “to grow old.” Within endocrinology, its origin relates to the declining neurohormonal support, such as reduced neurosteroid synthesis and altered hypothalamic-pituitary axis signaling, which contributes to the brain’s aging phenotype. This framework helps clinicians contextualize age-associated changes in brain function as a complex interplay of systemic and localized decline.
Mechanism
The mechanism involves several cellular hallmarks of aging, including telomere attrition, mitochondrial dysfunction, and increased oxidative stress within neural tissue. A key element is the progressive reduction in synaptic plasticity and neurogenesis, often exacerbated by chronic low-grade neuroinflammation. Furthermore, diminished hormonal feedback loops, particularly those involving sex steroids and growth factors, impair the brain’s ability to maintain homeostasis and repair cellular damage. These combined molecular and physiological changes ultimately lead to the observed functional decline in memory, processing speed, and executive function.
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