Parkinson’s disease (PD) is the second most common neurodegenerative disease and it is characterized by degeneration of dopaminergic neurons in the substantia nigra of mid brain that lead to impairments of motor functions (Merve et al, 2017). The loss of dopaminergic neurons give rise to motor symptoms like bradykinesia, rest tremor, postural instability, and shuffling gait; non-motor symptoms like impaired olfaction, constipation, depression, increased daytime sleep, rapid eye movement sleep disorder, and behavioral deficits are also commonly observed (Saleem et al, 2012). Presently, the treatment strategies for PD include Deep Brain Stimulation and Levo-dopa therapy. However the medication is limited only to improve the progressing symptoms and that too with more of side effects (Zrinzo et al, 2012; Fahn et al, 2000) and there is no therapy available that will cure the disease. Developing a therapeutic strategy for neurodegenerative disease such as PD remains a challenge till date. While attempting to understand the PD progression researchers have developed several animal models including Drosophila. A suitable model for sporadic PD should show histopathologically characterizable progressive loss of dopamine neurons together with other neurons and significant reduction in dopamine level. Since PD is a late onset neurodegenerative disease, the symptoms depiction in the model organism should be in a stage of adulthood equivalent to the age where PD sets in. The model animal should also manifest disease in such a way that it would mimic the PD affected human motor symptoms. Numerous case studies have reported that the subjects having exposure to pesticides, herbicides showed symptoms similar to Parkinsonism. Laboratory exposure of model organisms to environmental toxins like PQ is therefore productively employed to study the disease progressions. Studies on post-mortem brains from PD patients have implicated the vi role of oxidative damage in the pathogenesis of PD (Yuan et al, 2016; Zeevalk et al, 2008; Bosco et al, 2006). Accumulation of free radicals and subsequent neurodegeneration in specific brain regions have been proposed as the underlying factors in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease (Halliwell, 2006) suggesting that oxidative modifications of enzymes and structural proteins play a significant role in their pathogenesis. Several researchers employ natural compounds with neuroprotective properties; try to explore ways for their therapeutic application. Curcumin, a natural active compound present in Curcuma Longa L (Turmeric) has been shown to possess potent neuroprotective properties. It is largely used in food as spices, coloring agent, and traditional medicines in India, China, Southeast Asia (Aggarwal et al, 2007) and properties of curcumin performing neuroprotective effect, anti-oxidant, anti-inflammatory and anti-cancer are well known. It crosses the blood-brain barrier and exerts protective action on neurons in central neurological disease (Lee et al, 2013). Through Drosophila model, curcumin have been shown to extend life span, sequester oxidative stress mediated free radicals, enhance locomotor ability and show chemo preventive property, improves characteristic symptoms associated with PD (Nguyen et al, 2018; Liu et al, 2013; Lee et al, 2010) suggesting its potential use in treatment applicability in higher organisms. However, all the available investigations were performed in young model organisms. It is reported that there exists significant change of about 23% in genome-wide transcript profiles with age in Drosophila (Pletcher et al, 2002) and genotropic drugs would be effective only during those life cycle stages wherein target molecules are available (Soh et al, 2013) suggesting that targets of genotropic compounds under study may well not be present in all life stages. However, no reports are available regarding the efficacy of vii curcumin in PD models during later phases of adult life. Therefore, it is necessary to understand the neuprotective efficacy of compounds at the adult phases like the transition phase in Drosophila, where the disease such as idiopathic PD sets in. Therefore, understanding the mechanistic insights of the disease and applying this knowledge, one can attempt to find the remedial measures that can be further validated in human.