Elisa Navarro

This study identifies cholesterol accessibility as a key driver of TLR4-dependent microglial activation, showing that SR-B1 mediates LPS-induced cholesterol uptake and regulates TLR4 signaling and inflammatory responses.

This study shows the G2019S LRRK2 mutation alters transcriptomes of myeloid cells under proinflammatory conditions, affecting lipid metabolism and phagocytic function.

This study shows that combining Nrf2 activation with microglial repopulation after PLX5622 treatment improves cognitive deficits, neuronal loss, and mitochondrial function in a tauopathy model.

The paper identifies integrated stress response (ISR) signatures and proteostasis defects in monocytes from GBA1- and LRRK2-linked Parkinson's disease, linking them to immune dysfunction.

The paper analyzes RNA editing in myeloid cells under inflammatory stimulation, finding that C-to-U editing has a larger effect on proteome recoding compared to A-to-I editing.

The paper presents a long-read RNA-seq atlas of microglia isoforms, identifying novel isoforms and their associations with genetic risk loci in Alzheimer's and Parkinson's disease.

This study shows that NCLX is necessary for HIF-1 stabilization and transcriptional activity during hypoxia, linking acute and medium-term hypoxic responses through mitochondrial signaling.

The paper identifies transcriptomic changes in monocytes from GBA mutation carriers with Parkinson's disease, highlighting dysregulated pathways related to alpha-synuclein degradation and lysosomal function.

The paper analyzes the transcriptome of human microglia across brain regions, aging, and disease to identify genetic effects on gene expression and splicing, linking them to neurological disorders.

The paper identifies discordant mitochondrial gene expression patterns in PD monocytes and microglia, revealing distinct transcriptomic alterations in these myeloid cell types.

The paper identifies neurodegenerative disease-specific trans-eQTLs by analyzing gene expression in stimulated monocytes and macrophages using tensor decomposition.