Martha L. Escobar Galvis

This study shows that neuroinflammation occurs early in a mouse model of prodromal Parkinson's disease before neuronal loss, linking Syn pathology to olfactory dysfunction.

This study profiles DNA methylation in COVID-19 patients and finds hypomethylation linked to neurological pathways in severe cases.

This study shows that -synuclein aggregation disrupts cortico-amygdala connectivity, leading to social behavior deficits in synucleinopathies, and that restoring this connection can rescue the behavior.

The paper identifies that Tet2 loss promotes ciliogenesis and reduces α-synuclein pathology in Parkinson's disease models.

The paper shows that metabolite extracts contain active enzymes and demonstrates a new workflow to remove proteins for improved metabolomics.

This study integrates metabolomics and RNAseq from the same liver samples to show that prior metabolite extraction does not harm RNAseq quality and reveals pyrimidine metabolism as a key pathway in acute viral infection.

This study investigates how alpha-synuclein aggregation in the basolateral amygdala affects glutamatergic transmission, finding that it selectively disrupts cortico-BLA synapses.

The paper shows that experimental colitis increases alpha-synuclein accumulation in the gut and brain, linking intestinal inflammation to Parkinson's disease pathology.

This study shows that T cells reduce phosphorylated α-synuclein pathology in a mouse model of α-synucleinopathy.

This study shows alpha-synuclein is required for interferon-stimulated gene expression in neurons during RNA virus infection and links it to phosphorylated S129-asyn pathology.

This study shows that loss of one Engrailed1 allele in mice increases α-synuclein aggregation after PFF injection, suggesting a role for En1 in PD pathology.