The measurable deterioration of cognitive functions, such as memory, executive function, and processing speed, observed in some aging males concurrent with the physiological decline in androgen levels, particularly testosterone. This clinical manifestation is directly linked to the neurobiological impact of hypogonadism, differentiating it from other causes of age-related cognitive change. It represents a significant area of concern in male hormonal health, highlighting the systemic influence of sex steroids on central nervous system integrity.
Origin
The term combines “Andropause,” derived from the Greek andros (man) and pausis (cessation, referring to the male equivalent of menopause, though less abrupt), with the clinical descriptor “Cognitive Decline.” Its conceptual origin lies within the field of endocrinology and gerontology, where the relationship between declining hormone bioavailability and neurological health has been extensively studied. This lexicon entry places the condition firmly within the domain of age-related hormonal insufficiency.
Mechanism
The primary mechanism involves the reduced neuroprotective and neuromodulatory effects of testosterone and its metabolites, like estradiol, within the brain. Androgen receptors are abundant in key cognitive areas such as the hippocampus and frontal cortex; their diminished activation impairs synaptic plasticity and neuronal survival. Furthermore, low testosterone is associated with increased inflammatory markers and metabolic dysregulation in the brain, contributing to the pathological substrate of cognitive impairment.
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