Trehalose improves the movement ability of AβarcDrosophila by restoring the damaged mitochondria.

Background: The deposition of Aβ₄₂ has been regarded as one of the important pathological features of Alzheimer's disease (AD). However, drug development for Aβ₄₂ toxicity has been progressed slowly.

Objective: Our aim was to introduce the effect and related mechanism of trehalose on an Aβ_arc (arctic mutant Aβ₄₂) Drosophila AD model.

Methods: The human Aβ_arc was expressed in Drosophila to construct the AD model. Trehalose was added to the culture vial. The movement ability was determined by detecting climbing ability and flight ability. Enzyme-linked immunosorbent assay was used to detect the levels of Aβ_arc, ATP, and lactate. Electron microscopy assay, mitochondrial membrane potential assay, and mitochondrial respiration assay were used to assess the mitochondrial structure and function.

Results: Trehalose strongly improved the movement ability of Aβ_arc Drosophila in a concentration gradient-dependent manner. Furthermore, trehalose increased the content of ATP and decreased the content of Aβ_arc and lactate both in the brain and thorax of Aβ_arc Drosophila. More importantly, the mitochondrial structure and function were greatly improved by trehalose treatment in Aβ_arc Drosophila.

Conclusion: Trehalose improves movement ability at least partly by reducing the Aβ_arc level and restoring the mitochondrial structure and function in Aβ_arc Drosophila.