Alzheimers's disease is one of the alarming neurodegenerative disease and it is of global concern.The hallmarks of the disease are the amyloid beta (Aβ) aggregation and presence of neurofibrillary tangles (NFTs). The interaction of Aβ with macromolecular targets affects the normal cellular functions. The amyloid peptide interaction with cellular surfaces may trigger the intracellular cascades of signalling. Interaction of Aβ with mitochondria leads to the generation of free radicals. Many studies have suggested the involvement of mitochondrial dysfunction in Alzheimer's disease. Melatonin prevents mitochondria stress and by means of activating the antioxidant systems it protects the death of neurons. Although the study have been already conducted on Aβ42 infused or injury induced animal models but till date there is no reports of such studies on transgenic model of Drosophila melanogaster. In the present study, we have taken UAS/Gal4 system for the development of transgenic flies that overexpress Aβ42 in the brain of Drosophila. With the help of these transgenic flies we have analyse different experiments like behavioural parameters, oxidative stress parameters and protein expression through western blotting in the presence of melatonin. We have found that melatonin significantly ameliorated the toxicity caused by the Aβ42 overexpression. Thus the present study could be beneficial to find out the role of melatonin in transgenic flies overexpressing human Aβ42.
Keywords: Amyloid beta; Mitochondrial dysfunction; Neurofibrillary tangles; Transgenic flies.
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