Chronic Fatigue Syndrome (CFS), also known as Myalgic Encephalomyelitis (ME), is a complex disorder characterized by long-lasting fatigue, cognitive dysfunction, and sleep disturbances. Despite its widespread prevalence, the underlying biological mechanisms remain poorly defined, and no definitive diagnostic markers currently exist.
In this study, high-throughput RNA sequencing was performed on blood samples from 85 CFS patients and 80 healthy controls to identify molecular signatures associated with disease pathology. Results revealed three key clusters of dysregulated genes. The first cluster exhibited significant upregulation of pro-inflammatory cytokines and T-cell activation markers, suggesting a state of persistent low-grade immune activation. The second cluster demonstrated downregulation of mitochondrial genes involved in oxidative phosphorylation and ATP synthesis, indicating impaired energy metabolism at the cellular level. The third cluster included genes linked to neuronal signaling and neuroinflammation, which may explain the cognitive and neurological symptoms commonly seen in CFS.
Pathway enrichment analysis further highlighted disturbances in the AMPK and mTOR pathways, both of which are central regulators of energy balance and autophagy. Additionally, oxidative stress-related genes were found to be altered, pointing to mitochondrial dysfunction as a core component of disease pathology.
These findings collectively support the hypothesis that CFS is a multi-system disorder driven by immune dysregulation and metabolic impairment. Understanding these molecular mechanisms will pave the way for more accurate diagnostic biomarkers and targeted therapeutic strategies. Further longitudinal studies are required to validate these signatures and explore their clinical applicability in early detection and personalized treatment of CFS.
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