Folic acid supplementation rescues anomalies associated with knockdown of parkin in dopaminergic and serotonergic neurons in Drosophila model of Parkinson's disease

Singh, Sandeep Kumar; Yadav, Ankita; Srikrishna, Saripella

doi:10.1016/j.bbrc.2015.03.106

Cited by 18 publications

(18 citation statements)

References 29 publications

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“…Protects against mitochondrial-induced oxidative damage and neuronal death PD [150] Nesfatin-1 Attenuates rotenone-induced mitochondrial membrane potential collapse, ROS production and the subsequent caspase-3 activation and restore the function of mitochondrial respiratory chain complex I PD [151] Folic acid Alleviates the behavioral defects, oxidative stress, and represses mitochondrial dysfunction as well PD [152] Lutein…”

Section: Methazolamide (Mtz)mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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Section: Methazolamide (Mtz)mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Other investigations [129,130] focused on the role of fly microbiota in providing essential folates and vitamin B 1 to their host when those are scarce in the diet. Another study [131] showed that folate supplementation was able to alleviate mitochondrial dysfunction in a Parkinson fly model. However, to our knowledge, only vitamin B 6 has been studied in detail in a Drosophila model with the aim to understand cellular and molecular mechanisms at the basis of its beneficial effect on human diseases [132][133][134][135].…”

Section: Drosophila As a Model System To Study The Effects Of B 6 Depmentioning

confidence: 99%

The multifaceted role of vitamin B ₆ in cancer: Drosophila as a model system to investigate DNA damage

et al. 2020

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A perturbed uptake of micronutrients, such as minerals and vitamins, impacts on different human diseases, including cancer and neurological disorders. Several data converge towards a crucial role played by many micronutrients in genome integrity maintenance and in the establishment of a correct DNA methylation pattern. Failure in the proper accomplishment of these processes accelerates senescence and increases the risk of developing cancer, by promoting the formation of chromosome aberrations and deregulating the expression of oncogenes. Here, the main recent evidence regarding the impact of some B vitamins on DNA damage and cancer is summarized, providing an integrated and updated analysis, mainly centred on vitamin B 6 . In many cases, it is difficult to finely predict the optimal vitamin rate that is able to protect against DNA damage, as this can be influenced by a given individual's genotype. For this purpose, a precious resort is represented by model organisms which allow limitations imposed by more complex systems to be overcome. In this review, we show that Drosophila can be a useful model to deeply understand mechanisms underlying the relationship between vitamin B 6 and genome integrity.

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“…Adults with a reduced amount of Rpt2 in the dopaminergic neurons have a very significant reduction of their half-life (18 days vs 27 days in controls). Importantly, a similar effect has been found using the same TH-Gal4 driver to reduce Parkin expression using an RNAi against Parkin or by overexpression of human α-synuclein in adults ( Srivastav et al, 2015 ; Hernández-Vargas et al, 2011 ). Unlike the other phenotypes measured in this work, negative geotaxis decays similarly both in the experimental and control lines; however, it has been reported that induced locomotion is mostly controlled by the PAM dopaminergic cluster which incidentally, is where the expression of the TH-Gal4 driver is weakest ( Friggi-Grelin et al, 2003a , 2003b ).…”

Section: Discussionmentioning

confidence: 59%

Rpt2 proteasome subunit reduction causes Parkinson's disease like symptoms in Drosophila

et al. 2020

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Folic acid supplementation rescues anomalies associated with knockdown of parkin in dopaminergic and serotonergic neurons in Drosophila model of Parkinson's disease

Cited by 18 publications

References 29 publications

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

The multifaceted role of vitamin B ₆ in cancer: Drosophila as a model system to investigate DNA damage

Rpt2 proteasome subunit reduction causes Parkinson's disease like symptoms in Drosophila

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Folic acid supplementation rescues anomalies associated with knockdown of parkin in dopaminergic and serotonergic neurons in Drosophila model of Parkinson's disease

Cited by 18 publications

References 29 publications

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

The multifaceted role of vitamin B 6 in cancer: Drosophila as a model system to investigate DNA damage

Rpt2 proteasome subunit reduction causes Parkinson's disease like symptoms in Drosophila

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The multifaceted role of vitamin B ₆ in cancer: Drosophila as a model system to investigate DNA damage