Effects of linagliptin on glucose-induced neuronal damage on Caenorhabditis elegans

2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
K Wongchai ◽  
A Schlotterer ◽  
J Lin ◽  
M Morcos ◽  
T Klein ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Neuronal Damage

scholarly journals Effects of NAD+ in Caenorhabditis elegans Models of Neuronal Damage

Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 993
Author(s):  
Yuri Lee ◽  
Hyeseon Jeong ◽  
Kyung Hwan Park ◽  
Kyung Won Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Therapeutic Strategy ◽  
Axon Regeneration ◽  
Neuronal Damage ◽  
Biological Processes ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Neuronal Functions ◽  
Molecular Components

Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor that mediates numerous biological processes in all living cells. Multiple NAD+ biosynthetic enzymes and NAD+-consuming enzymes are involved in neuroprotection and axon regeneration. The nematode Caenorhabditis elegans has served as a model to study the neuronal role of NAD+ because many molecular components regulating NAD+ are highly conserved. This review focuses on recent findings using C. elegans models of neuronal damage pertaining to the neuronal functions of NAD+ and its precursors, including a neuroprotective role against excitotoxicity and axon degeneration as well as an inhibitory role in axon regeneration. The regulation of NAD+ levels could be a promising therapeutic strategy to counter many neurodegenerative diseases, as well as neurotoxin-induced and traumatic neuronal damage.

Airborne toluene exposure causes germline apoptosis and neuronal damage that promotes neurobehavioural changes in Caenorhabditis elegans

2020 ◽  
Vol 256 ◽  
pp. 113406 ◽  
Author(s):  
Marcell Valandro Soares ◽  
Mariele Feiffer Charão ◽  
Mauricio Tavares Jacques ◽  
Ana Laura Anibaletto dos Santos ◽  
Cristiane Luchese ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Neuronal Damage ◽  
Toluene Exposure

scholarly journals Behavioral and dopaminergic damage induced by acute iron toxicity in Caenorhabditis elegans

2015 ◽  
Vol 4 (4) ◽  
pp. 878-884 ◽  
Author(s):  
Daiandra de Almeida Fagundez ◽  
Daniela Freitas Câmara ◽  
Willian Goulart Salgueiro ◽  
Simone Noremberg ◽  
Robson Luiz Puntel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Neuronal Damage ◽  
Motor Impairment ◽  
Iron Toxicity ◽  
C Elegans ◽  
Biological Defects

Iron (Fe) exposure, results in multiple biological defects in C. elegans, including reproductive and motor impairment, which may be related to oxidative stress and neuronal damage.

Neuronal damage induced by nanopolystyrene particles in nematode Caenorhabditis elegans

2019 ◽  
Vol 6 (8) ◽  
pp. 2591-2601 ◽  
Author(s):  
Man Qu ◽  
Yan Kong ◽  
Yujie Yuan ◽  
Dayong Wang
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Neuronal Damage ◽  
Nematode Caenorhabditis Elegans

Our observations highlight the potential of nanoplastics in inducing damage on both development and functions of nervous system after long-term exposure.

Understanding Diabetic Polyneuropathy and Longevity: What Can We Learn from the Nematode Caenorhabditis Elegans?

2012 ◽  
Vol 120 (04) ◽  
pp. 182-183 ◽  
Author(s):  
M. Mendler ◽  
A. Schlotterer ◽  
M. Morcos ◽  
P. Nawroth
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Neuronal Damage ◽  
Insulin Signalling ◽  
Diabetic Polyneuropathy ◽  
Nematode Caenorhabditis Elegans ◽  
Ideal Model ◽  
Complex Interplay ◽  
Intrinsic Factors ◽  
System A

AbstractPathogenesis of late diabetic complications is influenced by a complex interplay of multiple exogenous and intrinsic factors. The well characterised nematode Caenorhabditis elegans is an ideal model to study causes of diabetic polyneuropathy because of its easily accessible nervous system. A repertoire of methods allows the assessment of both morphological and functional glucotoxic damages as well as reduction of lifespan, thereby helping to examine the influence of different pathways and mechanisms on neurodegeneration. Its insulin signalling system allows to directly visualize effects of insulin on high glucose induced neuronal damage, leading to a better understanding of diabetic polyneuropathy.

scholarly journals Neuroprotective Effects against Glutamate-Induced HT-22 Hippocampal Cell Damage and Caenorhabditis elegans Lifespan/Healthspan Enhancing Activity of Auricularia polytricha Mushroom Extracts

2021 ◽  
Vol 14 (10) ◽  
pp. 1001
Author(s):  
Chanin Sillapachaiyaporn ◽  
Panthakarn Rangsinth ◽  
Sunita Nilkhet ◽  
Alison T. Ung ◽  
Siriporn Chuchawankul ◽  
...  
Keyword(s):  
Linoleic Acid ◽  
Caenorhabditis Elegans ◽  
Antioxidant Enzyme ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Gas Chromatography Mass Spectrometry ◽  
Auricularia Polytricha ◽  
Ros Accumulation

Oxidative stress is associated with several diseases, particularly neurodegenerative diseases, commonly found in the elderly. The attenuation of oxidative status is one of the alternatives for neuroprotection and anti-aging. Auricularia polytricha (AP), an edible mushroom, contains many therapeutic properties, including antioxidant properties. Herein, we report the effects of AP extracts on antioxidant, neuroprotective, and anti-aging activities. The neuroprotective effect of AP extracts against glutamate-induced HT-22 neuronal damage was determined by evaluating the cytotoxicity, intracellular reactive oxygen species (ROS) accumulation, and expression of antioxidant enzyme genes. Lifespan and healthspan assays were performed to examine the effects of AP extracts from Caenorhabditis elegans. We found that ethanolic extract (APE) attenuated glutamate-induced HT-22 cytotoxicity and increased the expression of antioxidant enzyme genes. Moreover, APE promoted in the longevity and health of the C. elegans. Chemical analysis of the extracts revealed that APE contains the highest quantity of flavonoids and a reasonable percentage of phenols. The lipophilic compounds in APE were identified by gas chromatography/mass spectrometry (GC/MS), revealing that APE mainly contains linoleic acid. Interestingly, linoleic acid suppressed neuronal toxicity and ROS accumulation from glutamate induction. These results indicate that AP could be an exciting natural source that may potentially serves as neuroprotective and anti-aging agents.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain

2001 ◽  
Vol 13 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Vemuganti L. Raghavendra Rao ◽  
Aclan Dogan ◽  
Kellie K. Bowen ◽  
Kathryn G. Todd ◽  
Robert J. Dempsey
Keyword(s):  
Rat Brain ◽  
Neuronal Damage ◽  
Traumatic Injury ◽  
Glutamate Transporter ◽  
Glial Glutamate Transporter ◽  
Antisense Knockdown
Sign in / Sign up

Export Citation Format

Share Document