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A study at the Centre for Molecular Cell Biology (Palacios lab in collaboration with Whitworth lab and Talisman Therapeutics Ltd, Cambridge, UK) demonstrates that the motor proteins kinesin-1 and kinesin-3 are required for the survival of both Drosophila and human neurons and shows that increasing their activity can alleviate neurodegenerative defects in a model of Alzheimer's disease (AD).

Neurons depend on efficient intracellular transport to move organelles and other cargoes across their long cellular processes. Defects in this transport system have been linked to several neurodegenerative disorders. Using both Drosophila and human iPSC-derived neurons, the researchers found that reducing kinesin levels disrupts neuronal development and survival. The team then investigated whether boosting kinesin activity could protect neurons from neurodegeneration. Using a humanised Drosophila model expressing a pathogenic amyloid-β, associated with familial AD, they found that increasing levels of kinesin-1 or kinesin-3 restored normal neuronal morphology and improved age-dependent locomotor defects. These findings identify kinesins as promising targets for therapeutic intervention in neurodegenerative disease.

Building on this, the Palacios lab, in collaboration with the Bulgakova lab, has secured funding to identify small-molecule activators of kinesin-1 (from MRC–AstraZeneca).

Reference:

Deepthy Francis, Francesco Paonessa, Victoria L. Hewitt, Maria Southall, Isabel Peset, Alexander J. Whitworth, Frederick J. Livesey, Caroline C. G. Fabre, Isabel M. Palacios. Investigating how changes in the levels of kinesins impact neuronal health in Drosophila and human iPSC-derived neurons AD model. Open Biol 1 May 2026; 16 (5): 250319. https://doi.org/10.1098/rsob.250319