The progressive decline in the efficiency or amplitude of endocrine or paracrine signaling cascades associated with chronological aging. This deficit often manifests as reduced receptor sensitivity or attenuated downstream effector responses, impacting homeostasis. Clinically, it reflects a diminished physiological capacity to respond robustly to homeostatic challenges.
Origin
This lexicon entry arises from observing age-related shifts in endocrine output and target tissue responsiveness, fundamentally rooted in endocrinology and gerontology. The term combines the concept of aging (“Age-Related”) with the core physiological principle of communication (“Signal”) and its subsequent decline (“Deficit”). Understanding this origin helps frame interventions aimed at restoring youthful signaling fidelity.
Mechanism
The mechanism often involves alterations in gene expression profiles within target cells or changes to intracellular second messenger systems. For example, diminished efficacy of steroid hormone receptors or reduced downstream kinase activity can characterize this process. Correcting this often requires optimizing the cellular environment to support robust signal transduction.
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