Expression of β-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila

Axoplasmic transport Axon terminal
DOI: 10.1523/jneurosci.3699-09.2010 Publication Date: 2010-01-27T18:18:22Z
ABSTRACT
Alzheimer's disease (AD) is attributable to synapse dysfunction and loss, but the nature progression of presynaptic structural functional changes in AD are essentially unknown. We expressed wild-type or arctic form β amyloid 1-42 (Aβ) a small group neurons adult fly performed extensive time course analysis function structure both axon terminals at identified single-neuron level. Aβ accumulated intracellularly induced range age-dependent changes, including depletion mitochondria, slowdown bi-directional transports axonal decreased synaptic vesicles, increased large vacuoles, elevated fatigue. These correlated with deficit motor behavior. All these alterations were accelerated flies expressing Aβ. The mitochondria was earliest detected phenotype not caused by change transport mitochondria. Moreover, exhibited dramatic reduction number significant increase size aged Aβ-expressing flies, indicating global neuron an impairment fission. results suggest that accumulation depletes leading other deficits.
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