Klébea Carvalho

Pharmacologic inhibition of C5aR1 suppresses disease-enhancing processes and promotes disease mitigating pathways in an aggressive model of Alzheimer's disease.

Long-read sequencing of 81 human and mouse samples yields 200,000 full-length transcripts plus a triplet framework that separates promoter choice, splicing and 3' end use across tissues.

The paper shows that C5aR1 antagonism reduces amyloid load and dystrophic neurites in a mouse model of Alzheimer's disease, shifting microglial polarization toward a neuroprotective phenotype.

This study shows that modulating C5a-C5aR1 signaling in Alzheimer's disease models affects cognitive decline and gene expression related to inflammation and astrocyte activation.

The paper uses single-cell and nucleus RNA-seq to analyze glial subpopulations in AD mouse models, finding differences in astrocyte activation and microglia subtypes between 3xTg-AD and 5xFAD models.

The paper identifies gene regulatory networks driving macrophage polarization using bulk and single-cell RNA-seq and ATAC-seq data from HL-60-derived macrophages.