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[
Curr Aging Sci,
2021]
BACKGROUND: The antidepressant mianserin has been shown to extend the lifespan of Caenorhabditis elegans (C. elegans), a well-established model organism used in aging research. The extension of lifespan in C. elegans was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegans in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. OBJECTIVE: To investigate the effect of glucose added to the diet of C. elegans on the lifespan-extension effect of mianserin. METHODS: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 M mianserin, (G) 73 mM glucose, and (M50G) 50 M mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. RESULTS: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. CONCLUSION: The addition of glucose to the diet of C. elegans abolishes the lifespan-extension effects of mianserin.
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[
International Worm Meeting,
2019]
Oxidative stress and inflammation are critical components in the development of obesity. Culinary herbs and spices, abundant in anti-oxidant and anti-inflammatory phytochemicals, may be useful in the prevention of obesity. In the present study, we report strong anti-obesity properties of culinary spices. Wild-type Bristol N2 strain (Caenorhabditis Genetics Centre) were grown on NGM plates seeded with E. coli (OP50). Worms were exposed to extract (1mg of dry powder per 1ml of NGM) of red chilli, black pepper, ginger, and turmeric. Fat content was determined on day 5 (adult stage) by staining with Oil-Red O. Compared to control group, chilli, ginger and pepper reduced the fat content of the worms by 92, 89 and 57% respectively. Turmeric had no effect on the fat content of C elegans. In conclusion, culinary herbs and spices may be useful in the prevention of obesity and C. elegans is a useful model for screening the anti-obesity properties of culinary spices.
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[
Saudi Pharm J,
2021]
The use of many psychotropic drugs (PDs) is associated with increased caloric intake, significant weight gain, and metabolic disorders. The nematode <i>Caenorhabditis elegans (C. elegans)</i> has been used to study the effects of PDs on food intake. However, little is known about PDs effects on the body fat of <i>C. elegans</i>. In <i>C. elegans</i>, feeding behavior and fat metabolism are regulated through independent mechanisms. This study aims to evaluate the body fat and food intake of <i>C. elegans</i> in response to treatment olanzapine and fluoxetine. Here we report that, with careful consideration to the dosage used, administration of fluoxetine and olanzapine increases body fat and food intake in <i>C. elegans</i>.
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[
International Worm Meeting,
2019]
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the most common cause of dementia worldwide. Amyloid-? (A?) induced oxidative stress and toxicity are believed to be behind the pathogenesis of AD. Currently there is no pharmaceutical intervention that has been shown to cure or treat AD. Polyphenol rich food are of great interest in both nutrition and medicine for their potential to improve human health. In particular, the consumption of flavonoid rich cocoa is reported to have several health-promoting effects relating to its antioxidant capacity, which include reducing the risk for cardiovascular disease, cancer, and protection against neurotoxicity. The objective of this study was to determine the long-term effects of cocoa supplementation on A? toxicity in a transgenic model of C. elegans. Control (GRU101) and the transgenic strain (GRU102) expressing constitutive pan-neuronal A?1-42 were grown on Nematode Growth Medium (NGM) plates with Escherichia coli (E. coli) OP50 diet. Cocoa powder suspended in M9 buffer (5mg/ml for motility assay and 1mg/ml, 2 mg/ml and 3mg/ml for lifespan assay) was spread on the lawn of E. coli. Measurements included growth, motility and lifespan. GRU102 strain exhibited a lower growth rate, reduced motility and a 13% reduction in mean lifespan. Cocoa supplementation increased growth rate and increased motility of GRU102 strain to reach similar levels to the GRU101 strain. In addition, cocoa supplementation increased the lifespan of GRU102 in a dose dependent manner. Cocoa supplementation appears to reverse the symptoms relating to A? toxicity in GRU102 worms.
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[
Nutr Metab Insights,
2021]
Background: when supplemented starting from L1 stage. Aim: . Methods: were supplemented with cocoa starting from L1 stage till the death. Survival curves were plotted, and mean lifespan was reported. Results: mutants. Conclusion: Early-start supplementation is essential for cocoa-mediated lifespan extension which is dependent on insulin/IGF-1 signaling pathway and mitochondrial respiration.
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Pennington PR, Heistad RM, Nyarko JNK, Barnes JR, Bolanos MAC, Parsons MP, Knudsen KJ, De Carvalho CE, Leary SC, Mousseau DD, Buttigieg J, Maley JM, Quartey MO
[
Sci Rep,
2021]
The pool of -Amyloid (A) length variants detected in preclinical and clinical Alzheimer disease (AD) samples suggests a diversity of roles for A peptides. We examined how a naturally occurring variant, e.g. A(1-38), interacts with the AD-related variant, A(1-42), and the predominant physiological variant, A(1-40). Atomic force microscopy, Thioflavin T fluorescence, circular dichroism, dynamic light scattering, and surface plasmon resonance reveal that A(1-38) interacts differently with A(1-40) and A(1-42) and, in general, A(1-38) interferes with the conversion of A(1-42) to a -sheet-rich aggregate. Functionally, A(1-38) reverses the negative impact of A(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an A(1-42) phenotype in Caenorhabditis elegans. A(1-38) also reverses any loss of MTT conversion induced by A(1-40) and A(1-42) in HT-22 hippocampal neurons and APOE 4-positive human fibroblasts, although the combination of A(1-38) and A(1-42) inhibits MTT conversion in APOE 4-negative fibroblasts. A greater ratio of soluble A(1-42)/A(1-38) [and A(1-42)/A(1-40)] in autopsied brain extracts correlates with an earlier age-at-death in males (but not females) with a diagnosis of AD. These results suggest that A(1-38) is capable of physically counteracting, potentially in a sex-dependent manner, the neuropathological effects of the AD-relevant A(1-42).
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[
Worm Breeder's Gazette,
2003]
Wormgenes is a new resource for C.elegans offering a detailed summary about each gene and a powerful query system.
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[
Front Pharmacol,
2020]
Oligomeric assembly of Amyloid- (A) is the main toxic species that contribute to early cognitive impairment in Alzheimer's patients. Therefore, drugs that reduce the formation of A oligomers could halt the disease progression. In this study, by using transgenic <i>Caenorhabditis elegans</i> model of Alzheimer's disease, we investigated the effects of frondoside A, a well-known sea cucumber <i>Cucumaria frondosa</i> saponin with anti-cancer activity, on A aggregation and proteotoxicity. The results showed that frondoside A at a low concentration of 1 M significantly delayed the worm paralysis caused by A aggregation as compared with control group. In addition, the number of A plaque deposits in transgenic worm tissues was significantly decreased. Frondoside A was more effective in these activities than ginsenoside-Rg3, a comparable ginseng saponin. Immunoblot analysis revealed that the level of small oligomers as well as various high molecular weights of A species in the transgenic <i>C. elegans</i> were significantly reduced upon treatment with frondoside A, whereas the level of A monomers was not altered. This suggested that frondoside A may primarily reduce the level of small oligomeric forms, the most toxic species of A. Frondoside A also protected the worms from oxidative stress and rescued chemotaxis dysfunction in a transgenic strain whose neurons express A. Taken together, these data suggested that low dose of frondoside A could protect against A-induced toxicity by primarily suppressing the formation of A oligomers. Thus, the molecular mechanism of how frondoside A exerts its anti-A aggregation should be studied and elucidated in the future.
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[
International Journal of Developmental Biology,
1998]
Pleiotropy , a situation in which a single gene influences multiple phenotypic tra its, can arise in a variety of ways. This paper discusses possible underlying mechanisms and proposes a classification of the various phenomena involved.
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[
Curr Biol,
2011]
Recent work on a Caenorhabditis elegans transmembrane ATPase reveals a central role for the aminophospholipid phosphatidylethanolamine in the production of a class of extracellular vesicles.