Benoit Lehallier

This study identifies molecular foci of brain aging in mice using spatiotemporal RNA-seq, showing accelerated glial aging in white matter and differential gene expression linked to neurodegenerative diseases.

This study uses single-cell RNA-sequencing to analyze cell type-specific responses to young or aged blood in heterochronic parabiosis, identifying mitochondrial function as a key factor in rejuvenation.

The paper identifies lipid droplet-accumulating microglia (LAM) as a dysfunctional, pro-inflammatory state in aging brains, linked to neurodegeneration.

Profiling 2,925 plasma proteins in 4,331 people aged 18-95 reveals non-linear aging: protein waves crest at 34, 60 and 78 years, later waves overlapping disease proteomes.

The paper shows that plasma from exercising mice reduces brain inflammation and improves memory, with clusterin as a key anti-inflammatory factor also elevated in human exercisers.

The paper analyzes aging dynamics across 17 organs and plasma proteomics in mice, revealing consistent gene expression trajectories with organ-specific timing and amplitude.

This study uses single-cell RNA sequencing to show that brain endothelial cells respond to circulatory cues of aging, with aged plasma inducing aging transcriptomes and young plasma reversing them.

The paper creates a single-cell transcriptomic atlas of 20 mouse organs and tissues, providing a resource for studying gene expression across cell types.

This study shows aged blood reduces hippocampal neurogenesis and activates microglia via VCAM1 at the BBB, and blocking VCAM1 reverses these effects.