Modeling of Parkinson's Disease in Different Models.

Parkinson's Disease (PD) is a progressive disorder worldwide and its etiology remains unidentified. Over the last few decades, animal models of PD have been extensively utilized to explore the development and mechanisms of this neurodegenerative condition. Toxic and transgenic animal models for PD possess unique characteristics and constraints, necessitating careful consideration when selecting the appropriate model for research purposes. Animal models have played a significant role in uncovering the causes and development of PD, including its cellular and molecular processes. These models suggest that the disorder arises from intricate interplays between genetic predispositions and environmental influences. Every model possesses its unique set of strengths and weaknesses. This review provides a critical examination of animal models for PD and compares them with the features observed in the human manifestation of the disease.

Resveratrol: Protective Agent Against Alzheimer's Disease.

Resveratrol is a biologically active natural phenolic plant product. It has several properties which make them useful to treat the disease. In this review, we have highlighted the neuroprotective effects of resveratrol. Several available animal models have been proven to help understand the disease pathway and mechanism of action by resveratrol. In this review, we have highlighted the neuroprotective activity of resveratrol in AD, which effectively counter the neurodegenerative disease by decreasing the formation of plaques. Resveratrol is a natural plant product that is easily available, cost-effective, and possesses neuroprotective activity, which is useful for treating neurodegenerative diseases. Resveratrol presents a promising avenue for AD treatment due to its diverse neuroprotective mechanisms. Given the ongoing global challenge in treating AD, researchers have increasingly focused on exploring the therapeutic potential of resveratrol.

Effect of Rotenone on the Neurodegeneration among Different Models.

Rotenone is a naturally occurring plant product used as an insecticide, pesticide and piscicide. It is lipophilic in nature and can cross the blood-brain barrier and induce the degeneration of neurons. It inhibits the mitochondrial respiratory chain complex I and stops the transfer of electrons. It induces ROS generation, which impairs mitochondrial activity. Rotenone is a toxic agent which causes the death of neurons. The present review describes the effect of rotenone on neurodegeneration with an emphasis on behavioral, pathological and neuropathological components carried out on various experimental models such as cell lines, Drosophila melanogaster, mice and rats.

Evaluation of the toxic potential of Bisphenol-A glycidylmethacrylate (BisGMA) on the third instar larvae of transgenic Drosophila.

Introduction: In the present study the cytotoxic and genotoxic effects of Bisphenol-A glycidyl methacrylate (BisGMA) was studied on the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ)Bg9. Materials and methods: The concentration of BisGMA i.e. 0.005, 0.010, 0.015 and 0.020 M were established in diet and the larvae were allowed to feed on it for 24 h. Results: A dose dependent significant increase in the activity of ß-galactosidase was observed compared to control. A significant dose dependent tissue damage was observed in the larvae exposed to 0.010, 0.015 and 0.020 M of BisGMA compared to control. A dose dependent significant increase in the Oxidative stress markers was observed compared to control. BisGMA also exhibit significant DNA damaged in the third instar larvae of transgenic D. melanogaster (hsp70-lacZ)Bg9 at the doses of 0.010, 0.015 and 0.020 M compared to control. Conclusion: BisGMA at 0.010, 0.015 and 0.020 M was found to be cytotoxic for the third instar larvae of transgenic D. melanogaster (hsp70-lacZ) Bg9.

Evaluation of Bis(2-ethylhexyl) phthalate toxicity on the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ) Bg9.

Bis(2-ethylhexyl) phthalate, generally known as DEHP is a synthetic compound mainly used as a plasticizer to make polyvinyl chloride products flexible and soft. The present work aimed to study the toxicity of Bis(2-ethylhexyl) phthalate on the third instar larvae of transgenic Drosophila melanogaster(hsp70-lacZ) Bg9. The hsp70 gene is associated with the ß-galactosidase in our present transgenic strain therefore, the more activity of ß-galactosidase will indirectly correspond to hsp70 expression. The third instar larvae were allowed to feed on the diet for 24 h having 0.001, 0.005, 0.01, and 0.02 M of Bis(2-ethylhexyl) phthalate at the final concentration. After the exposure of 24hrs, the larvae were subjected to ONPG assay, X-gal staining, trypan blue exclusion test, oxidative stress markers assays, and comet assay. A dose-dependent increase in hsp70 expression, tissue damage, Glutathione-S-transferase (GST) activity, lipid peroxidation, monoamine oxidase, caspase-9 & 3, protein carbonyl content (PCC), DNA damage and decrease in the glutathione (GSH) content, delta-aminolevulinic acid dehydrogenase (ẟ-ALD-D) and acetylcholinesterase activity were observed in the larvae exposed to 0.005, 0.01, 0.02 M of Bis-(2-ethylhexyl) phthalate. The dose of 0.001 M of Bis(2-ethylhexyl) phthalate did not showed any toxic effects and hence can be considered as No Observed Adverse Effect Level (NOAEL) for Bis(2-ethylhexyl) phthalate. The study supports the use of Drosophila for the evaluation of possible toxic effects associated with synthetic compounds.

Beneficial effects of apigenin on the transgenic Drosophila model of Alzheimer's disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder. The available drugs improve the symptoms but do not play role in modifying disease effects. Currently, the treatment strategies focus on inhibiting the production of Aß-42 aggregates and tau filaments. In this context the natural plant products could act as a potent candidate. Therefore, we decided to study the effect of apigenin on the transgenic Drosophila model of AD i.e., expressing Aß-42 in the neurons. The AD flies were allowed to feed on the diet having 25, 50, 75 and 100 µM of apigenin for 30 days. The exposure of AD flies to apigenin showed a dose dependent significant decrease in the oxidative stress and delay in the loss of climbing ability. Apigenin also inhibits the activity of acetylcholinesterase. The immunostaining and molecular docking studies suggest that apigenin inhibits the formation of Aß-42 aggregates. Apigenin is potent in reducing the AD symptoms being mimicked in the transgenic Drosophila model of AD.

Modulation of Huntington's Disease in Drosophila.

Huntington's disease (HD) is a progressive neurodegenerative disorder which deteriorates the physical and mental abilities of the patients. It is an autosomal dominant disorder and is mainly caused by the expansion of a repeating CAG triplet. A number of animal models ranging from worms, fruit flies, mice and rat, pig, sheep and monkeys are available, which have been helpful in understanding various pathways involved during the progression of the disease. Drosophila is one of the most commonly used model organisms for biomedical science, due to low cost maintenance, short life span and easy implications of genetic tools. The present review provides a brief description of HD and the studies carried out for HD to date, taking Drosophila as a model.