scholarly journals Protective effect of curcumin in transgenic Drosophila melanogaster model of Parkinson’s disease

2012 ◽  
Vol 2 (1) ◽  
pp. 3 ◽  
Author(s):  
Yasir Hasan Siddique ◽  
Gulshan Ara ◽  
Smita Jyoti ◽  
Mohammad Afzal

Studies on model organisms have been found to be invaluable in clarifying the cellular and molecular basis of normal cellular processes and disease pathogenesis. Drosophila mutants and transgenes have provided a platform to understand the mechanisms associated with degenerative disease. Studies on the role of polyphenols in protecting against neurodegenerative diseases are limited. In the present study, the effect of curcumin at various doses was studied on the climbing ability of the transgenic <em>Drosophila melanogaster </em>that expresses normal human α-synuclein in the neurons. A significant dose-dependent protection against loss of climbing ability was observed. The results suggest that curcumin can strongly improve the climbing ability of Parkinson’s disease model flies and also supports the utility of this model in studying the symptoms of Parkinson’s disease.

2020 ◽  
Vol 11 (24) ◽  
pp. 4416-4425
Author(s):  
Saba Ubaid ◽  
Mohammad Rumman ◽  
Babita Singh ◽  
Mohd. Sohail Akhtar ◽  
Abbas A. Mahdi ◽  
...  

2021 ◽  
Author(s):  
Jade Parker-Character ◽  
David R. Hager ◽  
Tanner B. Call ◽  
Zachary S. Pickup ◽  
Scott A. Turnbull ◽  
...  

Abstract It is well-established that there are differences in the fecal microbiota composition between Parkinson’s disease (PD) patients and control populations, but the mechanisms underlying these differences are not yet fully understood. To begin to close the gap between description and mechanism we studied the relationship between the microbiota and PD in a model organism, Drosophila melanogaster. First, fecal transfers were performed with a D. melanogaster model of PD that had a mutation in the parkin (park25) gene. Results indicate that the PD model feces had a negative effect on both pupation and eclosion in both control and park25 flies, with a greater effect in PD model flies. Analysis of the microbiota composition revealed differences between the control and park25 flies, consistent with many human studies. Conversely, gnotobiotic treatment of axenic embryos with feces-derived bacterial cultures did not affect eclosure. We speculate this result might be due to similarities in bacterial prevalence between mutant and control feces. Further, we confirmed a bacteria-potentiated impact on mutant and control fly phenotypes by measuring eclosure rate in park25flies that were mono-associated with members of the fly microbiota. Both the fecal transfer and the mono-association results indicate a host genotype-microbiota interaction. Overall, this study concludes functional effects of the fly microbiota on PD model flies, providing support to the developing body of knowledge regarding the influence of the microbiota on PD.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jade Parker-Character ◽  
David R. Hager ◽  
Tanner B. Call ◽  
Zachary S. Pickup ◽  
Scott A. Turnbull ◽  
...  

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease, besides Alzheimer’s Disease, characterized by multiple symptoms, including the well-known motor dysfunctions. It is well-established that there are differences in the fecal microbiota composition between Parkinson’s disease (PD) patients and control populations, but the mechanisms underlying these differences are not yet fully understood. To begin to close the gap between description and mechanism we studied the relationship between the microbiota and PD in a model organism, Drosophila melanogaster. First, fecal transfers were performed with a D. melanogaster model of PD that had a mutation in the parkin (park25) gene. Results indicate that the PD model feces had a negative effect on both pupation and eclosion in both control and park25 flies, with a greater effect in PD model flies. Analysis of the microbiota composition revealed differences between the control and park25 flies, consistent with many human studies. Conversely, gnotobiotic treatment of axenic embryos with feces-derived bacterial cultures did not affect eclosure. We speculate this result might be due to similarities in bacterial prevalence between mutant and control feces. Further, we confirmed a bacteria-potentiated impact on mutant and control fly phenotypes by measuring eclosure rate in park25 flies that were mono-associated with members of the fly microbiota. Both the fecal transfer and the mono-association results indicate a host genotype-microbiota interaction. Overall, this study concludes functional effects of the fly microbiota on PD model flies, providing support to the developing body of knowledge regarding the influence of the microbiota on PD.


Data in Brief ◽  
2021 ◽  
pp. 107535
Author(s):  
Gayathree Karthikkeyan ◽  
Ashwini Prabhu ◽  
Ravishankar Pervaje ◽  
Sameera Krishna Pervaje ◽  
Prashant Kumar Modi ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 407
Author(s):  
Andrei Surguchov

Parkinson’s disease (PD) is the second most common neurodegenerative disease, afflicting ~10 million people worldwide. Although several genes linked to PD are currently identified, PD remains primarily an idiopathic disorder. Neuronal protein α-synuclein is a major player in disease progression of both genetic and idiopathic forms of PD. However, it cannot alone explain underlying pathological processes. Recent studies demonstrate that many other risk factors can accelerate or further worsen brain dysfunction in PD patients. Several PD models, including non-mammalian eukaryotic organisms, have been developed to identify and characterize these factors. This review discusses recent findings in three PD model organisms, i.e., yeast, Drosophila, and Caenorhabditis elegans, that opened new mechanisms and identified novel contributors to this disorder. These non-mammalian models share many conserved molecular pathways and cellular processes with humans. New players affecting PD pathogenesis include previously unknown genes/proteins, novel signaling pathways, and low molecular weight substances. These findings might respond to the urgent need to discover novel drug targets for PD treatment and new biomarkers for early diagnostics of this disease. Since the study of neurodegeneration using simple eukaryotic organisms brought a huge amount of information, we include only the most recent or the most important relevant data.


2004 ◽  
Vol 18 (3) ◽  
pp. 589-591 ◽  
Author(s):  
Wei Zhang ◽  
Tongguang Wang ◽  
Liya Qin ◽  
Hui‐Ming Gao ◽  
Belinda Wilson ◽  
...  

2020 ◽  
Vol 21 (7) ◽  
pp. 2464 ◽  
Author(s):  
Shyh Jenn Chia ◽  
Eng-King Tan ◽  
Yin-Xia Chao

Parkinson’s disease (PD) is the most common movement disorder with motor and nonmotor signs. The current therapeutic regimen for PD is mainly symptomatic as the etio-pathophysiology has not been fully elucidated. A variety of animal models has been generated to study different aspects of the disease for understanding the pathogenesis and therapeutic development. The disease model can be generated through neurotoxin-based or genetic-based approaches in a wide range of animals such as non-human primates (NHP), rodents, zebrafish, Caenorhabditis (C.) elegans, and drosophila. Cellular-based disease model is frequently used because of the ease of manipulation and suitability for large-screen assays. In neurotoxin-induced models, chemicals such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat are used to recapitulate the disease. Genetic manipulation of PD-related genes, such as α-Synuclein(SNCA), Leucine-rich repeat kinase 2 (LRRK2), Pten-Induced Kinase 1 (PINK1), Parkin(PRKN), and Protein deglycase (DJ-1) Are used in the transgenic models. An emerging model that combines both genetic- and neurotoxin-based methods has been generated to study the role of the immune system in the pathogenesis of PD. Here, we discuss the advantages and limitations of the different PD models and their utility for different research purposes.


2017 ◽  
Vol 381 ◽  
pp. 1046-1047
Author(s):  
X.Q. Zhang ◽  
F. Wang ◽  
C.J. Mao ◽  
D.J. Lv ◽  
Y.P. Yang ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document