Clare Pridans

This study shows that non-mutated human tau causes neurodegeneration in a microglia-dependent manner in a mouse model of Alzheimer's disease.

The paper shows that wild-type bone marrow-derived microglia-like cells reduce strain-dependent neuropathology in Csf1r mutant mice by preventing thalamic calcification.

This study shows that microglia are essential for excitatory synapse formation in the nucleus accumbens during early development, impacting threat avoidance behaviors in adulthood.

This study shows that neurodevelopmental processes in the cortex and thalamus can occur normally without microglia, using a genetically modified mouse model.

This study shows microglia initially seed amyloid plaques in Alzheimer's disease but later help compact them, with genetic and pharmacological manipulation affecting plaque formation.

This study examines the impact of a heterozygous Csf1r mutation on brain development and neuropathology in mice, showing reduced microglial abundance and altered gene expression in disease models.

This study shows microglia regulate cerebral blood flow through CD39-mediated ATP breakdown, affecting neurovascular coupling and CBF reactivity.

This study shows microglia promote beta-amyloid plaque formation but are not required for subsequent pathological changes in Alzheimer's disease.

This study shows that complete microglia deficiency accelerates CNS prion disease without increasing prion accumulation, suggesting microglia protect against astrocyte-driven pathology rather than clearing prions.

This study investigates a kinase-dead Csf1r mutation in mice, showing it causes dominant-negative effects on CSF1R signaling and impacts macrophage development and brain microglia.

This study shows that Csf1r mutation in mice, rats, and humans causes developmental defects, and bone marrow transfer can reverse some phenotypes by restoring macrophages.

This paper develops a CSF1R-FRed transgenic mouse that specifically labels mononuclear phagocyte system cells, showing high expression in monocytes, macrophages, and dendritic cells while excluding other lineages.

The paper reports a CRISPR-Cas9-induced deletion and reinsertion event in the mouse Csf1r promoter, highlighting the need for copy number analysis to confirm genomic edits.

Maternal tamoxifen treatment in early mouse embryos causes a 4-5-fold expansion of the macrophage population by 10.5dpc.

This paper presents a high-resolution gene expression atlas for sheep, identifying transcriptional signatures and functional annotations across tissues and developmental stages.