Albert Quintana

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 astrocytic PI3Kα supports synaptic plasticity and cognitive function by regulating serine metabolism and D-serine levels necessary for NMDA receptor activation during long-term potentiation.

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

The paper generates and characterizes the first mouse model with a dominant-negative glycine substitution in collagen VI alpha chains, showing key disease features for therapeutic research.

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 profiles the translatome of dorsal striatum PV interneurons, identifying molecular signatures and gene expression changes linked to psychostimulant exposure and reward behaviors.

This study shows that maltodextrin improves lifespan and reduces microglial reaction in Ndufs4KO mice, a model of mitochondrial disease, but does not improve locomotion or respiratory function.

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.