A Unifying Hypothesis: The Investing Fascia as a Mechanical Hub in Neurodegenerative Diseases—A Theoretical Framework Integrating the "Eight-Tier Evidence Pyramid" and "Six-System Interplay"
Abstract
The present study draws on available evidence to propose the "cervicogenic investing fascia mechanical constraint" hypothesis, employing an integrated argumentative framework with the "Eight-Tier Evidence Pyramid" as its structural backbone and the "Six-System Interplay" as its mechanistic core. The hypothesis posits that chronic forward head posture and aging drive fibrotic remodeling of the posterior cervical investing fascia. Following the loss of elastic buffering capacity, abnormal shear stresses generated by routine head-and-neck micromotions—such as turning, nodding, and arterial pulsation—are rigidly transmitted through the three-layer network of the deep cervical fascia to the carotid sheath, a critical anatomical hub. This single mechanical source simultaneously compromises six systems: arterial compression reduces cerebral perfusion; venous compression impairs intracranial venous return; lymphatic compression impedes immune-metabolic waste clearance; the glymphatic system's driving force is diminished, leading to retention of neurotoxic proteins including Aβ, tau, and α-synuclein; sympathetic nerve irritation results in overactivation; and vagal nerve compression reduces parasympathetic tone, disabling the cholinergic anti-inflammatory pathway. These six pathways do not operate in isolation but are mutually amplified through multiple positive feedback loops—arterial hypoperfusion exacerbates glymphatic clearance impairment, glymphatic dysfunction elevates intracranial pressure, which further compresses veins, and sympathetic-parasympathetic imbalance aggravates vasomotor dysregulation, culminating in a self-reinforcing six-system positive feedback vicious cycle. This framework provides a unified pathophysiological explanation for the differential responses of Alzheimer's disease, Parkinson's disease, and Parkinson-plus syndromes to the same mechanical intervention. The present study further proposes testable predictions based on shear-wave elastography and glymphatic functional imaging, offering a novel theoretical framework for early detection and mechanically targeted intervention in neurodegenerative diseases. The goal of this framework is to delay disease progression and secure a "neurological window of opportunity" for patients, rather than to reverse already-established neurodegenerative changes.
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Authors: Xuefeng Huang