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.
FOO SENG ANG (2026) studied this question.