Parkinson's Disease as Early Latent Bistability: An Ecological Homeostasis Working Model

Abstract Conventional approaches to Parkinson's disease (PD) seek proximal causes — misfolded proteins,mitochondrial defects, environmental toxins — and often implicitly assume a roughly monotonictrajectory from health to degeneration. In contrast, the Ecological Homeostasis (EH) framework treatsPD as a failure of multi-scale regulatory systems to maintain viable neural–immune–metabolic dynamicswithin a bounded region of state space under persistent perturbation. Neurodegeneration is interpretednot as linear decay but as a change in the residence time of the system within competing regimes ofactivity, driven by slow parameter drift and noise.We formalise this perspective using Itô stochastic differential equations (SDEs) to define a viabilityenvelope V(p), a soft constraint region S_ε(p), and a set-valued attractor A(p) under parametervector p. Within this framework, PD is characterised as an Early Latent Bistability (ELB) regime: thesystem's dynamics are compatible with both a dopaminergic-coherent regime and a pathologicalinflammatory–oxidative regime, but control parameters still allocate most residence time to thehealthy-like regime. ELB is explicitly defined as a model class whose topology includes, as special cases,both true bistability and critical slowing near a single, deforming attractor.We define the EH Triad: (i) Geometry — distance Δ(x;p) to regulatory boundaries; (ii) Resilience —stochastic stability ratio α/β, where α measures corrective regulatory strength and β the effective noisefloor; and (iii) Capacity — mean exit time E[τ] from the healthy viability region. We instantiate theseconstructs in a mechanistic PD case study focused on a chronic inflammation → iron dysregulation →oxidative variance → resilience erosion cascade. We then propose a hierarchical, person-specificCoherence Index (CI) for longitudinal studies. The EH framework shifts research questions from 'Whatcauses PD?' to 'Under what conditions is dopaminergic coherence viably maintainable, for whichindividuals, and for how long?'

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Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2026-02-21
DOI
https://doi.org/10.5281/zenodo.18719660
Primary Topic
Parkinson's Disease Mechanisms and Treatments
Type
article
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article

Parkinson's Disease as Early Latent Bistability: An Ecological Homeostasis Working Model

SHAI / HATI, John Richard Smith
Zenodo (CERN European Organization for Nuclear Research)
Parkinson's Disease Mechanisms and Treatments
article

Parkinson's Disease as Early Latent Bistability: An Ecological Homeostasis Working Model

SHAI / HATI, John Richard Smith
article en

Abstract

Abstract Conventional approaches to Parkinson's disease (PD) seek proximal causes — misfolded proteins,mitochondrial defects, environmental toxins — and often implicitly assume a roughly monotonictrajectory from health to degeneration. In contrast, the Ecological Homeostasis (EH) framework treatsPD as a failure of multi-scale regulatory systems to maintain viable neural–immune–metabolic dynamicswithin a bounded region of state space under persistent perturbation. Neurodegeneration is interpretednot as linear decay but as a change in the residence time of the system within competing regimes ofactivity, driven by slow parameter drift and noise.We formalise this perspective using Itô stochastic differential equations (SDEs) to define a viabilityenvelope V(p), a soft constraint region S_ε(p), and a set-valued attractor A(p) under parametervector p. Within this framework, PD is characterised as an Early Latent Bistability (ELB) regime: thesystem's dynamics are compatible with both a dopaminergic-coherent regime and a pathologicalinflammatory–oxidative regime, but control parameters still allocate most residence time to thehealthy-like regime. ELB is explicitly defined as a model class whose topology includes, as special cases,both true bistability and critical slowing near a single, deforming attractor.We define the EH Triad: (i) Geometry — distance Δ(x;p) to regulatory boundaries; (ii) Resilience —stochastic stability ratio α/β, where α measures corrective regulatory strength and β the effective noisefloor; and (iii) Capacity — mean exit time E[τ] from the healthy viability region. We instantiate theseconstructs in a mechanistic PD case study focused on a chronic inflammation → iron dysregulation →oxidative variance → resilience erosion cascade. We then propose a hierarchical, person-specificCoherence Index (CI) for longitudinal studies. The EH framework shifts research questions from 'Whatcauses PD?' to 'Under what conditions is dopaminergic coherence viably maintainable, for whichindividuals, and for how long?'

Zenodo (CERN European Organization for Nuclear Research)
Openalex Percentile: Top 52%
Parkinson's Disease Mechanisms and Treatments
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