Amandine Grimm

This study shows abnormal tau protein increases mitochondrial transfer from astrocytes to neurons via contact-dependent mechanisms, affecting mitochondrial function in tauopathies.

This study shows that iPSCs from aged donors retain mitochondrial aging features like impaired bioenergetics and increased reactive oxygen species, suggesting they can model mitochondrial aging for drug screening.

This study compares aging-related mitochondrial characteristics in iPSC-derived neurons and direct conversion neurons, finding both retain age-associated phenotypes but differ in metabolic responses.

This study shows that mutant huntingtin spreads across neuromuscular junctions, causing muscle pathology in human cells and mice, suggesting transmission as a therapeutic target for neurodegenerative diseases.