ArticleMetabolites2022
Traumatic Brain Injury Triggers Neurodegeneration in a Mildly Symptomatic MELAS Patient: Implications on the Detrimental Role of Damaged Mitochondria in Determining Head Trauma Sequalae in the General Population.
Article in Metabolites, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- Advances in Cardiolipin Analysis: Applications in Central Nervous System Disorders and Nutrition Interventions.Biomolecules · 2026Review
- Mitochondrial dysfunction and NLRP3 inflammasome activation in drug-resistant epilepsy: emerging insights and mitochondrial-targeted therapeutic strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
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3 authors at 1 institution in 1 country.
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Abstract
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a maternally inherited genetic mitochondrial disease with a typical onset in the first two decades of life and a major involvement of central nervous system (CNS). We present the case of a man affected with an oligosymptomatic, genetically determined MELAS syndrome, whose clinical picture dramatically and irreversibly worsened following a mild head injury. We hypothesize that the CNS metabolic stress induced by the brain injury activated an irreversible cascade of events leading to progressive neurodegeneration because damaged mitochondria were unable to restore the balance between energy requirements and availability.
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