Timelike Symmetry Breaking, Topological Instability, and Neurodegenerative Senescence Induced by Brain–Computer Interfaces: A Critique of Biological Ontology Based on the PFUSRC Framework
Year: 2026
Type: article
Abstract: Brain–Computer Interfaces (BCIs) demonstrate clear clinical value in neurorehabilitation and functional recovery. However, deep invasive BCIs for cognitive enhancement in healthy individuals represent a systematic violation of life’s inherent ontological structure. Based on PFUSRC universal topological axioms, time‑crystal‑like dynamics, noetic ontology, neuroenergetic homeostasis, and coupling interface gap dynamics, this paper proves that individual temporal sequence, noetic‑origin spatial topology, and neural flexible tolerance margins constitute three irreducible, non‑modifiable intrinsic structures of life. Without full‑spectrum temporal mapping, precise noetic anchor localization, and complete global neural dynamics modeling, deep BCI coupling imposes exogenous clocks, disrupts time‑crystal periodicity, invades neural topology, compresses tolerance intervals, and triggers pathological responses at the coupling interface. These effects inevitably lead to neurodegenerative senescence, predictive coding failure, cognitive ownership dissociation, and self‑consciousness collapse. Cognitive industrialization and intelligence commodification erase population‑level cognitive heterogeneity and cause irreversible depletion of civilizational creativity. A strict safety boundary is established: only superficial noise suppression and pathological functional repair are permitted; temporal rewriting, topological reconstruction, and cognitive overclocking in healthy brains are prohibited. This study concludes that neural enhancement violating temporal self‑consistency and topological closure constitutes a multiscale, cross‑hierarchical systemic catastrophe.
Author: Wang, Zhenmin
Language: English
Subfield: Cognitive Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7162552211
FWCI:
Cites:
Cited by:
Related to: