Éva M. Szegő

Metabolic reprogramming and altered ATP content impair neuroprotective functions of microglia in β-glucocerebrosidase deficiency models

This study shows that GCase deficiency in microglia leads to metabolic changes and ATP depletion, impairing their neuroprotective functions and increasing neuronal vulnerability in Parkinson's disease.

Tissue inflammation induced by constitutively active STING is mediated by enhanced TNF signaling

This study shows that constitutive STING activation in mice causes SAVI, and TNF signaling mediates its pathogenesis, with TNFR1/2 inhibition improving disease symptoms.

Mitochondrial oxidant stress promotes alpha-synuclein aggregation and spreading in mice with mutated glucocerebrosidase

This study shows that GBA1 mutations increase mitochondrial oxidative stress, leading to alpha-synuclein aggregation and spreading in a mouse model of Parkinson's disease.

Constitutively active STING causes neuroinflammation and degeneration of dopaminergic neurons in mice

This study shows that constitutively active STING in mice leads to neuroinflammation and dopaminergic neuron degeneration, suggesting therapeutic targeting of this pathway.