Juan Pedro Bolaños

The paper identifies a female-specific microglial redox program that influences susceptibility to obesity by modulating metabolic resilience and mTORC1 signaling.

This study shows that mitochondrial pyruvate import in astrocytes is essential for maintaining neurotransmitter homeostasis and seizure resistance, rather than primarily for bioenergetic purposes.

This study identifies glial-specific mitochondrial failure and redox imbalance as drivers of regional vulnerability in Friedreich ataxia using a mouse model.

This study identifies Pfkfb3 as essential for astrocytic glycolysis, which preserves cognition by reducing mitochondrial efficiency and redirecting pyruvate to neurons.

This study shows TET3 regulates terminal differentiation by affecting mitochondrial metabolic maturation and oxidative phosphorylation in intestinal epithelial cells.

The paper shows lactate-dependent glycolysis shifts produce D-serine, linking astrocyte metabolism to synaptic and cognitive functions through CB1 receptor activation.

This study identifies a metabolic shift driven by PFKFB3 in CLN7 disease, showing that targeting glycolysis can alleviate disease hallmarks in a mouse model and patient-derived cells.

This study shows that inhibiting PFKFB3 in neurons prevents redox stress and neuronal death in ischemia-reperfusion injury, and reduces brain damage in mice.

This study shows that Aβ25-35 activates Cdk5, leading to p53 phosphorylation and stabilization, which causes neuronal damage and can be prevented by inhibiting Cdk5 or p53.