57.7
Shabab B. Hannan
Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen
Shabab B. Hannan has made significant contributions to our understanding of mitochondrial dysfunction and neurodegeneration through a series of studies on molecular pathways and model organisms. Research on bcas3 loss-of-function variants identified a syndromic neurodevelopmental disorder, highlighting the critical role of this gene in human health. In Drosophila models, autophagy inhibition rescued defects caused by mitochondrial chaperone Hsc70-5, while inhibition also alleviated structural and functional deficits associated with its loss. The kif1a homolog Unc-104 was found essential for spontaneous release, postsynaptic density maturation, and perisynaptic scaffold organization in synapses, underscoring its importance in neuronal development and function. These findings have broader implications for our understanding of tauopathies, where impaired retrograde transport by the dynein/dynactin complex contributes to disease progression.