Melania González-Torres

The paper identifies PKR as a critical mediator of mitochondrial neuropathology in a mouse model of Leigh syndrome, showing its role in neuroinflammation and disease progression.

This study investigates sex-specific hypothalamic microinflammation and microglial polarization in response to high-fat diet, identifying JNK3 as a key regulator of these processes in males.

This study identifies dysfunctional pallido-subthalamic projections as a mediator of epilepsy in a mouse model of Leigh Syndrome and suggests STN inhibition as a potential therapeutic target.

The paper uses a novel viral tool to isolate mitochondria from affected neurons in a mouse model of Leigh Syndrome, revealing proteomic and acetylomic changes associated with mitochondrial dysfunction.