This theoretical paper presents Paper 20, which builds on the frameworks established in Papers 18 and 19 to propose a unified repair hypothesis. It explores how systemic repair failure—linked to platelet dysfunction and non-coding RNA dysregulation—may serve as a shared upstream mechanism contributing to the pathogenesis and progression of systemic lupus erythematosus (SLE), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson’s disease (PD). The model offers a complementary perspective to traditional disease-specific theories, aiming to stimulate further exploratory research into common biological pathways and potential cross-disease therapeutic approaches.
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FOO SENG ANG
Newcastle University Medicine Malaysia
Raffles University Iskandar
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FOO SENG ANG (Mon,) studied this question.
www.synapsesocial.com/papers/69e866416e0dea528ddeab02 — DOI: https://doi.org/10.5281/zenodo.19657566