Proteins of the reticulon and REEP families, homologous to the products of human Hereditary Spastic Paraplegia disease genes, contribute to shaping and continuity of the axonal endoplasmic reticulum network in Drosophila.

The pseudoenzyme CPT1C is able to sense changes in intracellular malonyl-CoA levels caused by nutrients or energy stress and regulate late endosomes/lysosomes anterograde transport, necessary for proper axon growth.

Transportomic analysis of the changes underlying neurodegeneration reveals the importance of Kif5a for neuronal survival and highlights the need to restore specific anterograde cargo transport to for regeneration.

Studies in mice and neurons reveal how modulation of the axonal transport of synaptic vesicles via huntingtin phosphorylation influences the number of vesicles accumulating at the synapse, subsequent glutamate release, and behavior in mice.

Drosophila model reveals that NTE/SWS-associated neurodegeneration is a lysosomal storage disorder accompanied by a leaky brain permeability barrier, abnormal fatty acid metabolism, and inflammation.

Synaptic defects previously attributed to loss of kinesin function are found to be mediated by the Wnd/DLK axonal injury signaling pathway, which restrains the total levels of presynaptic proteins in response to their accumulation.

A comprehensive, quantitative, protein-protein interaction screen maps the network of interactions between human MIT domains and ESCRT-III C-terminal tails, and reveals MIT domain-containing protein cofactors for abscission and the 'No Cut' abscission checkpoint.

A potential medication has been found for the brain and muscle degenerative diseases caused by mutant forms of Valosin-Containing Protein.