Age-Related Signaling Decline is the inevitable, progressive compromise in the precision, speed, and magnitude of intercellular and intracellular communication pathways that accompanies biological aging. This phenomenon impacts vital regulatory networks, including those mediated by hormones, growth factors, and key metabolic sensors, leading to blunted and often inappropriate physiological responses. Impaired signal fidelity is a major driver of systemic dyshomeostasis and the development of chronic, age-related diseases.
Origin
Rooted in molecular biology and endocrinology, this term focuses on the breakdown of communication as a core feature of aging, rather than solely on structural decay. It underscores that the body’s control systems lose their efficiency over time, impacting the ability of cells to coordinate and respond effectively to stimuli. This concept provides a molecular target for interventions aimed at restoring youthful cellular responsiveness.
Mechanism
Mechanistically, this decline is driven by several factors, including a reduction in the number or affinity of cell surface receptors for hormones and growth factors, and structural defects in the post-receptor signaling cascades. For example, key kinases and secondary messengers may become less responsive to activation. Furthermore, chronic inflammation and oxidative stress can directly damage signaling molecules, creating a state of pervasive ‘noise’ that interferes with the accurate transmission of biological instructions across the organism.
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