Albee Messing

This study identifies GFAP as a novel mediator of mitochondrial fission by surrounding fission sites and modulating Drp1 recruitment, revealing a new mechanism in mitochondrial plasticity.

This paper introduces a new rat model of Alexander disease that exhibits key pathological features and motor impairment, demonstrating that antisense oligonucleotide therapy can reverse GFAP pathology and white matter deficits.