Kowalski, Antoni, Rebas, Elzbieta, Zylińska, Ludmiła · Postepy biochemii · 2007
Your brain uses a chemical messenger called GABA to calm nerve signals and prevent them from becoming overactive. When three key enzymes that control GABA levels don't work properly, it can cause various neurological problems including chronic fatigue syndrome, anxiety, seizures, and stiff-person syndrome. This article reviews what happens when GABA metabolism breaks down and how it affects the nervous system.
This study identifies impaired GABA metabolism as a potential biological mechanism in ME/CFS, providing a neurochemical framework for understanding fatigue and neurological symptoms. Understanding GABA dysfunction could guide future research into biomarkers and therapeutic targets specific to ME/CFS pathophysiology.
This review does not prove that GABA metabolism abnormalities are the primary cause of ME/CFS or demonstrate the prevalence of GABA enzyme dysfunction in ME/CFS patients. It does not establish whether GABA dysmetabolism is specific to ME/CFS or is a consequence versus a cause of the condition. The review cannot determine causation and represents theoretical synthesis rather than empirical evidence in ME/CFS populations.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
Spotted an error in this entry? Report it →