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Objective: Glutathione in its reduced form (GSH) is the most important free radical scavenging compound in the mammalian nervous system that prevents membrane lipid peroxidation. It is suspected that epileptic seizures are accompanied by a massive production of reactive oxygen species, i.e., oxidative stress. Methods: Using an 1 H MRS technique developed at the authors’ site, the authors measured glutathione levels in a volume of interest (VOI) of 25 × 25 × 25 mm placed in structurally normal-appearing tissue in the parietooccipital region of each hemispheres in patients with and without active epilepsy, and in a age-matched control group. Results: The GSH/water ratio in patients with epilepsy was significantly reduced in the parietooccipital region of both hemispheres (1.6 ± 1.0 × 10 − 5 ) compared to the GSH/water ratio in healthy controls (2.4 ± 1.1 × 10 − 5 ). There was no significant difference between the hemisphere with epileptogenic focus and the hemisphere without epileptogenic focus. The GSH/water ratios of the patients without active epilepsy were not different from the GSH/water ratios of patients with active epilepsy. Conclusion: The authors found evidence for a widespread impairment of the glutathione system in patients with epilepsy independent from seizure activity.

If the current rates of growth of the senior population and prevalence of Alzheimer disease (AD) continue, the number of individuals worldwide affected by this disabling disease will double from 24.3 to 42.3 million by 2020.1 Given the devastating impact of AD on patient, family, community, and society, considerable efforts are underway to unravel its pathophysiologic mechanisms, with the aim of developing safe and effective disease-modifying therapies. Such therapies will probably be most efficacious in the early symptomatic or ideally pre-symptomatic stages of the disease.2 An accurate diagnosis of AD in the early symptomatic stage is extremely challenging despite the development of useful clinical constructs like mild cognitive impairment (MCI), which enables the identification of individuals who may be in an early clinical phase of AD. Future diagnostic approaches toward early symptomatic and presymptomatic AD will almost certainly hinge upon biomarkers. In fact, new diagnostic criteria were recently proposed that operationalize the pre-dementia diagnosis of AD and include imaging and CSF biomarkers as supportive evidence.3 Beyond their use in diagnostics, imaging and other biomarkers will likely serve important roles in monitoring effects of …