Elisenda Sanz

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 shows that chronic central IL-6 overexpression in Tg2576 mice worsens amyloidosis-related neuropathology and alters cortical and hippocampal gene expression, with sex-dependent effects.

This study investigates how mitochondrial dysfunction and immune activation contribute to retinal ganglion cell degeneration in optic neuropathy using transgenic models.

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 examines sex steroid receptor expression in Otp glutamatergic neurons of the medial extended amygdala and finds sex differences in receptor expression and neuronal morphology.

The paper compares regeneration mechanisms in four peripheral neuron types after nerve injury, finding distinct regenerative capacities and identifying MED12 as a key regulator in proprioceptors.

The paper characterizes PBN neuron subclusters using single-cell RNA sequencing and maps their axonal projections, identifying 21 subclusters and two major ascending pathways.

The paper identifies CCK-expressing vestibular neurons as key drivers of motion-induced malaise and shows their role in inducing conditioned taste aversion through parabrachial nucleus activation.

The paper shows that male mice have nearly as many Kiss1RP3V neurons as females, which can stimulate testosterone synthesis when activated.

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.

The paper identifies two genetically-defined neuronal populations in Ndufs4KO mice that drive distinct pathological features of Leigh Syndrome.