| Summary: | 碩士 === 國立清華大學 === 系統神經科學研究所 === 104 === Alzheimer’s disease (AD) is the well-known and leading cause of dementia. Amyloid beta (Aβ), one of AD’s early onset pathological hallmarks, has been studied in many different aspects including in vitro and in vivo researches. Some of those studies revealed that the oligomer form rather than the fibrils of Aβ is the major cause of its cytotoxicity. We know little about how two kinds of deposition formed during aging: intracellular and extracellular depositions. Which is the major deposition leading to neuron dysfunction? Aβ can destroy the balance between neuron excitatory and inhibitory. Glutamatergic neuron is the classic excitatory neurons whose excitotoxicity usually come up with Aβ deposits and gamma-aminobutyric acid (GABA) is the classic inhibitory neurotransmitter, both are necessary for learning and memory. Here, we used the model organism Drosophila with the adequately established GAL4-UAS system to express Aβ in glutamatergic and GABAergic neurons to explore its toxic effects. By using general Aβ antibody, we identified the existence and deposits of Aβ, which have not been done in early studies. We found the neuron loss induced by Aβ and these Aβ deposits emerged at a very early stage. Deposits are earlier and largely found in/or around the antennal lobe, indicating that olfactory system, the major part for Drosophila to sense and establish memory is the most affected which is full of glutamatergic and GABAergic neurons. Together, this study provided a great, direct evidence of Aβ plague-like deposition existence in Drosophila AD model, which can be useful for better utilization of this powerful model organism.
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