(+)-Discodermolide has also been found to be neuroprotective in recent Alzheimer research. The microtubule-stabilizing feature of (+)-discodermolide was used to restore neuron functions that have been disrupted by the amyloid induced sequestration. Tau protein is known to stabilize the microtubule network in healthy neurons. It served as the “railroad track” upon which actin, tubulin, mitochondria, neurotransmitter-related enzymes and vesicles carrying messenger proteins are delivered. The presence of Amyloid in the cell could lead to tau protein aggregation and microtubule numbers reduction.  In transgenic mouse model for human tauopathy, (+)-discodermolide stabilizes microtubules and restores fast axonal transport in cells, offsetting the loss of function caused by aggregation of tau protein. The motor-impaired mice exhibited a full restoration of normal movement with (+)-discodermolide treatment.