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2000
Volume 25, Issue 4
  • ISSN: 1871-5249
  • E-ISSN: 1875-6166

Abstract

A small, translucent nematode known as Caenorhabditis elegans, or C. elegans, is frequently utilized as a model organism in biomedical studies. These worms, which are around 1 mm long and feed on bacteria, are usually found in soil. For accessible and effective research on genetics, developmental biology, neuroscience, cell biology, and aging, C. elegans provide an ideal model. Its simplicity, which includes a translucent body and a nervous system with only 302 neurons, makes it possible to see cellular and developmental processes in great detail. Because of its special benefits, the worm Caenorhabditis elegans allows for a thorough characterization of the cellular and molecular processes causing age-related neurodegenerative diseases.

This is a general review of the life cycle, experimental methodologies, and the use of to model brain diseases, including those related to molecular and genetic factors that cause neurodegenerative diseases. Additionally, we go over how is a perfect model organism for studying neurons in instances of prevalent age-related neurodegenerative illnesses due to a combination of its biological traits and new analytical techniques.

The literature review process was carried out step-by-step using online search databases such as Web of Science, PubMED, Embase, Google Scholar, Medline, and Google Patents. In the first searches, keywords like , disease modelling, and neuroprotective activity were employed.

Because of 's physiological transparency, it is possible to track the development of neurodegeneration in aging organisms by using co-expressed fluorescent proteins. Importantly, a fully characterized connectome provides a unique ability to precisely connect cellular death with behavioural instability or phenotypic diversity , thus permitting a deep knowledge of the detrimental effect of neurodegeneration on wellbeing.

In addition, pharmacological therapies and both forward and reverse gene screening speed up the discovery of modifiers that change neurodegeneration. These chemical-genetic investigations work together to determine important threshold states that either increase or decrease cellular stress in order to unravel related pathways.

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References

  1. KonstantinidisG. TavernarakisN. Molecular Basis of Neuronal Autophagy in Ageing: Insights from Caenorhabditis elegans.Cells202110369410.3390/cells10030694 33800981
    [Google Scholar]
  2. ForslundK. SchreiberF. ThanintornN. SonnhammerE.L.L. OrthoDisease: Tracking disease gene orthologs across 100 species.Brief. Bioinform.201112546347310.1093/bib/bbr024 21565935
    [Google Scholar]
  3. KimY. ParkY. HwangJ. KwackK. Comparative genomic analysis of the human and nematode Caenorhabditis elegans uncovers potential reproductive genes and disease associations in humans.Physiol. Genomics201850111002101410.1152/physiolgenomics.00063.2018 30240344
    [Google Scholar]
  4. MarkakiM. TavernarakisN. Caenorhabditis elegans as a model system for human diseases.Curr. Opin. Biotechnol.20206311812510.1016/j.copbio.2019.12.011 31951916
    [Google Scholar]
  5. KipreosE.T. van den HeuvelS. Developmental control of the cell cycle: Insights from Caenorhabditis elegans.Genetics2019211379782910.1534/genetics.118.301643 30846544
    [Google Scholar]
  6. MarshE.K. MayR.C. Caenorhabditis elegans, a model organism for investigating immunity.Appl. Environ. Microbiol.20127872075208110.1128/AEM.07486‑11 22286994
    [Google Scholar]
  7. WenH. GaoX. QinJ. Probing the anti-aging role of polydatin in Caenorhabditis elegans on a chip.Integr. Biol.201461354310.1039/C3IB40191J 24305800
    [Google Scholar]
  8. CollinsJ.J. EvasonK. KornfeldK. Pharmacology of delayed aging and extended lifespan of Caenorhabditis elegans.Exp. Gerontol.200641101032103910.1016/j.exger.2006.06.038 16872777
    [Google Scholar]
  9. CaldwellK.A. WillicottC.W. CaldwellG.A. Modeling neurodegeneration in Caenorhabditis elegans.Dis. Model. Mech.20201310dmm04611010.1242/dmm.046110 33106318
    [Google Scholar]
  10. KormishJ.D. GaudetJ. McGheeJ.D. Development of the C. elegans digestive tract.Curr. Opin. Genet. Dev.201020434635410.1016/j.gde.2010.04.012 20570129
    [Google Scholar]
  11. StrangeK. An overview of C. elegans biology.Methods Mol. Biol.2006351111 16988422
    [Google Scholar]
  12. ParkH.E.H. JungY. LeeS.J.V. Survival assays using Caenorhabditis elegans.Mol. Cells2017402909910.14348/molcells.2017.0017 28241407
    [Google Scholar]
  13. WittkowskiP. Marx-StoeltingP. VioletN. FetzV. SchwarzF. OelgeschlägerM. SchönfelderG. VoglS. Caenorhabditis elegans As a Promising Alternative Model for Environmental Chemical Mixture Effect Assessment—A Comparative Study.Environ. Sci. Technol.20195321127251273310.1021/acs.est.9b03266 31536708
    [Google Scholar]
  14. LeeS.Y. KangK. Measuring the effect of chemicals on the growth and reproduction of caenorhabditis elegans.J. Vis. Exp.201712856437 29053679
    [Google Scholar]
  15. GjorgjievaJ. BironD. HaspelG. Neurobiology of Caenorhabditis elegans Locomotion: Where Do We stand?Bioscience201464647648610.1093/biosci/biu058 26955070
    [Google Scholar]
  16. LüersenK. GottschlingD.C. DöringF. Complex locomotion behavior changes Are induced in Caenorhabditis elegans by the lack of the regulatory leak K+ Channel TWK-7.Genetics2016204268370110.1534/genetics.116.188896 27535928
    [Google Scholar]
  17. KoelleM.R. HorvitzH.R. EGL-10 regulates G protein signaling in the C. elegans nervous system and shares a conserved domain with many mammalian proteins.Cell199684111512510.1016/S0092‑8674(00)80998‑8 8548815
    [Google Scholar]
  18. GardnerM. RosellM. MyersE.M. Measuring the effects of bacteria on C. elegans behavior using an egg retention assay.J. Vis. Exp.201380e51203 24192811
    [Google Scholar]
  19. HobertO. LoriaP. Uses of GFP in Caenorhabditis elegans.Methods Biochem. Anal.20064720322610.1002/0471739499.ch10 16335715
    [Google Scholar]
  20. BraeckmanB.P. SmoldersA. BackP. De HenauS. In Vivo Detection of Reactive Oxygen Species and Redox Status in Caenorhabditis elegans.Antioxid. Redox Signal.2016251057759210.1089/ars.2016.6751 27306519
    [Google Scholar]
  21. LabuschagneC.F. BrenkmanA.B. Current methods in quantifying ROS and oxidative damage in Caenorhabditis elegans and other model organism of aging.Ageing Res. Rev.201312491893010.1016/j.arr.2013.09.003 24080227
    [Google Scholar]
  22. MinH. LeeM. ChoK.S. LimH.J. ShimY.H. Nicotinamide supplementation improves oocyte quality and offspring development by modulating mitochondrial function in an aged Caenorhabditis elegans Model.Antioxidants202110451910.3390/antiox10040519 33810497
    [Google Scholar]
  23. HeY. MiaoL. YuL. ChenQ. QiaoY. ZhangJ-F. ZhouY. A near-infrared fluorescent probe for detection of exogenous and endogenous hydrogen peroxide in vivo.Dyes Pigments201916816016510.1016/j.dyepig.2019.04.055
    [Google Scholar]
  24. DudleyN.R. LabbéJ.C. GoldsteinB. Using RNA interference to identify genes required for RNA interference.Proc. Natl. Acad. Sci. USA20029974191419610.1073/pnas.062605199 11904378
    [Google Scholar]
  25. MaedaI. KoharaY. YamamotoM. SugimotoA. Large-scale analysis of gene function in Caenorhabditis elegans by high-throughput RNAi.Curr. Biol.200111317117610.1016/S0960‑9822(01)00052‑5 11231151
    [Google Scholar]
  26. KamathR. AhringerJ. Genome-wide RNAi screening in Caenorhabditis elegans.Methods200330431332110.1016/S1046‑2023(03)00050‑1 12828945
    [Google Scholar]
  27. KalettaT. HengartnerM.O. Finding function in novel targets: C. elegans as a model organism.Nat. Rev. Drug Discov.20065538739910.1038/nrd2031 16672925
    [Google Scholar]
  28. SifriC.D. BegunJ. AusubelF.M. The worm has turned – microbial virulence modeled in Caenorhabditis elegans.Trends Microbiol.200513311912710.1016/j.tim.2005.01.003 15737730
    [Google Scholar]
  29. KurzC.L. EwbankJ.J. Caenorhabditis elegans: An emerging genetic model for the study of innate immunity.Nat. Rev. Genet.20034538039010.1038/nrg1067 12728280
    [Google Scholar]
  30. SenGuptaT. PalikarasK. EsbensenY.Q. KonstantinidisG. GalindoF.J.N. AchantaK. KassahunH. StavgiannoudakiI. BohrV.A. AkbariM. GaareJ. TzoulisC. TavernarakisN. NilsenH. Base excision repair causes age-dependent accumulation of single-stranded DNA breaks that contribute to Parkinson disease pathology.Cell Rep.2021361010966810.1016/j.celrep.2021.109668 34496255
    [Google Scholar]
  31. KuwaharaT. KoyamaA. KoyamaS. YoshinaS. RenC.H. KatoT. MitaniS. IwatsuboT. A systematic RNAi screen reveals involvement of endocytic pathway in neuronal dysfunction in α-synuclein transgenic C. elegans.Hum. Mol. Genet.200817192997300910.1093/hmg/ddn198 18617532
    [Google Scholar]
  32. JinekM. ChylinskiK. FonfaraI. HauerM. DoudnaJ.A. CharpentierE. A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity.Science2012337609681682110.1126/science.1225829 22745249
    [Google Scholar]
  33. PaixA. FolkmannA. RasolosonD. SeydouxG. High efficiency, homology-directed Genome editing in Caenorhabditis elegans using CRISPR-Cas9 Ribonucleoprotein complexes.Genetics20152011475410.1534/genetics.115.179382 26187122
    [Google Scholar]
  34. PalikarasK. SenGuptaT. NilsenH. TavernarakisN. Assessment of dopaminergic neuron degeneration in a C. elegans model of Parkinson’s disease.STAR Protoc.20223210126410.1016/j.xpro.2022.101264 35403008
    [Google Scholar]
  35. Naranjo-GalindoF.J. AiR. FangE.F. NilsenH.L. SenGuptaT.C. elegans as an animal model to study the intersection of DNA Repair, aging and neurodegeneration.Front. Aging2022391611810.3389/fragi.2022.916118 35821838
    [Google Scholar]
  36. JungH. KimS.Y. Canbakis CecenF.S. ChoY. KwonS.K. Dysfunction of mitochondrial Ca2+ regulatory machineries in brain aging and neurodegenerative diseases.Front. Cell Dev. Biol.2020859979210.3389/fcell.2020.599792 33392190
    [Google Scholar]
  37. LautrupS. SinclairD.A. MattsonM.P. FangE.F. NAD+ in Brain Aging and Neurodegenerative Disorders.Cell Metab.201930463065510.1016/j.cmet.2019.09.001 31577933
    [Google Scholar]
  38. HartmanJ.H. Gonzalez-HuntC. HallS.M. RydeI.T. CaldwellK.A. CaldwellG.A. MeyerJ.N. Genetic defects in mitochondrial dynamics in Caenorhabditis elegans impact ultraviolet C radiation- and 6-hydroxydopamine-Induced Neurodegeneration.Int. J. Mol. Sci.20192013320210.3390/ijms20133202 31261893
    [Google Scholar]
  39. MachielaE. RudichP.D. TraaA. AnglasU. SooS.K. SenchukM.M. Van RaamsdonkJ.M. Targeting mitochondrial network disorganization is protective in C. elegans models of huntington’s disease.Aging Dis.20211271753177210.14336/AD.2021.0404 34631219
    [Google Scholar]
  40. LuzA.L. Lagido, C.; Hirschey, M.D.; Meyer, J.N. In Vivo Determination of Mitochondrial Function Using Luciferase-Expressing Caenorhabditis elegans: Contribution of Oxidative Phosphorylation, Glycolysis, and Fatty Acid Oxidation to Toxicant-Induced Dysfunction. Curr ProtocToxicol.,201669:25.8, 1-25.
    [Google Scholar]
  41. ChenY. ScarcelliV. LegouisR. Approaches for studying autophagy in Caenorhabditis elegans.Cells2017632710.3390/cells6030027 28867808
    [Google Scholar]
  42. HallD.H. HartwiegE. NguyenK.C.Q. Modern electron microscopy methods for C. elegans.Methods Cell Biol.20121079314910.1016/B978‑0‑12‑394620‑1.00004‑7 22226522
    [Google Scholar]
  43. TianY. LiZ. HuW. RenH. TianE. ZhaoY. LuQ. HuangX. YangP. LiX. WangX. KovácsA.L. YuL. ZhangH.C. elegans screen identifies autophagy genes specific to multicellular organisms.Cell201014161042105510.1016/j.cell.2010.04.034 20550938
    [Google Scholar]
  44. PalmisanoNJ Meléndez A Detection of autophagy in caenorhabditis elegans by western blotting analysis of LGG-1. Cold Spring Harb Protoc.20162
    [Google Scholar]
  45. Al RawiS. Louvet-ValléeS. DjeddiA. SachseM. CulettoE. HajjarC. BoydL. LegouisR. GalyV. Postfertilization autophagy of sperm organelles prevents paternal mitochondrial DNA transmission.Science201133460591144114710.1126/science.1211878 22033522
    [Google Scholar]
  46. LabbadiaJ. MorimotoR.I. The biology of proteostasis in aging and disease.Annu. Rev. Biochem.201584143546410.1146/annurev‑biochem‑060614‑033955 25784053
    [Google Scholar]
  47. LionakiE. GkikasI. DaskalakiI. IoannidiM.K. KlapaM.I. TavernarakisN. Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis.Nat. Commun.202213165110.1038/s41467‑022‑28272‑1 35115503
    [Google Scholar]
  48. ImanikiaS. ÖzbeyN.P. KruegerC. CasanuevaM.O. TaylorR.C. Neuronal XBP-1 Activates Intestinal Lysosomes to Improve Proteostasis in C. elegans.Curr. Biol.2019291423222338.e710.1016/j.cub.2019.06.031 31303493
    [Google Scholar]
  49. RuzC. AlcantudJ.L. Vives MonteroF. DuranR. Bandres-CigaS. Proteotoxicity and neurodegenerative diseases.Int. J. Mol. Sci.20202116564610.3390/ijms21165646 32781742
    [Google Scholar]
  50. RieckherM. GarinisG.A. SchumacherB. Molecular pathology of rare progeroid diseases.Trends Mol. Med.202127990792210.1016/j.molmed.2021.06.011 34272172
    [Google Scholar]
  51. VermezovicJ. StergiouL. HengartnerM.O. d’Adda di FagagnaF. Differential regulation of DNA damage response activation between somatic and germline cells in Caenorhabditis elegans.Cell Death Differ.201219111847185510.1038/cdd.2012.69 22705849
    [Google Scholar]
  52. McKinnonP.J. DNA repair deficiency and neurological disease.Nat. Rev. Neurosci.200910210011210.1038/nrn2559 19145234
    [Google Scholar]
  53. SkjeldamH.K. KassahunH. FensgårdØ. SenGuptaT. BabaieE. LindvallJ.M. ArczewskaK. NilsenH. Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.DNA Repair 20109886187010.1016/j.dnarep.2010.04.009 20493785
    [Google Scholar]
  54. MorinagaH. YonekuraS.I. NakamuraN. SugiyamaH. YoneiS. Zhang-AkiyamaQ.M. Purification and characterization of Caenorhabditis elegans NTH, a homolog of human endonuclease III: Essential role of N-terminal region.DNA Repair 20098784485110.1016/j.dnarep.2009.04.020 19481506
    [Google Scholar]
  55. PapalucaA. WagnerJ.R. SaragoviH.U. RamotarD. UNG-1 and APN-1 are the major enzymes to efficiently repair 5-hydroxymethyluracil DNA lesions in C. elegans.Sci. Rep.201881686010.1038/s41598‑018‑25124‑1 29717169
    [Google Scholar]
  56. BelanO. AnandR. BoultonS.J. Mechanism of mitotic recombination: Insights from C. elegans.Curr. Opin. Genet. Dev.202171101810.1016/j.gde.2021.06.005 34186335
    [Google Scholar]
  57. GoldmanS.M. QuinlanP.J. RossG.W. MarrasC. MengC. BhudhikanokG.S. ComynsK. KorellM. ChadeA.R. KastenM. PriestleyB. ChouK.L. FernandezH.H. CambiF. LangstonJ.W. TannerC.M. Solvent exposures and parkinson disease risk in twins.Ann. Neurol.201271677678410.1002/ana.22629 22083847
    [Google Scholar]
  58. WalA. WalP. VigH. SamadA. KhandaiM. TyagiS. A systematic review of various In-vivo screening models as well as the mechanisms involved in parkinson’s disease screening procedures.Curr. Rev. Clin. Exp. Pharmacol.202419212413610.2174/2772432817666220707101550 35796452
    [Google Scholar]
  59. BraungartE. GerlachM. RiedererP. BaumeisterR. HoenerM.C. Caenorhabditis elegans MPP+ model of Parkinson’s disease for high-throughput drug screenings.Neurodegener. Dis.200414-517518310.1159/000080983 16908987
    [Google Scholar]
  60. van HamT.J. ThijssenK.L. BreitlingR. HofstraR.M.W. PlasterkR.H.A. NollenE.A.A.C. elegans model identifies genetic modifiers of alpha-synuclein inclusion formation during aging.PLoS Genet.200843e100002710.1371/journal.pgen.1000027 18369446
    [Google Scholar]
  61. van der GootA.T. ZhuW. Vázquez-ManriqueR.P. SeinstraR.I. DettmerK. MichelsH. FarinaF. KrijnenJ. MelkiR. BuijsmanR.C. Ruiz SilvaM. ThijssenK.L. KemaI.P. NeriC. OefnerP.J. NollenE.A.A. Delaying aging and the aging-associated decline in protein homeostasis by inhibition of tryptophan degradation.Proc. Natl. Acad. Sci. USA201210937149121491710.1073/pnas.1203083109 22927396
    [Google Scholar]
  62. BüttnerS. HabernigL. BroeskampF. RuliD. VögtleF.N. VlachosM. MacchiF. KüttnerV. Carmona-GutierrezD. EisenbergT. RingJ. MarkakiM. TaskinA.A. BenkeS. RuckenstuhlC. BraunR. Van den HauteC. BammensT. van der PerrenA. FröhlichK.U. WinderickxJ. KroemerG. BaekelandtV. TavernarakisN. KovacsG.G. DengjelJ. MeisingerC. SigristS.J. MadeoF. Endonuclease G mediates α-synuclein cytotoxicity during Parkinson’s disease.EMBO J.201332233041305410.1038/emboj.2013.228 24129513
    [Google Scholar]
  63. FanningS. HaqueA. ImberdisT. BaruV. BarrasaM.I. NuberS. TermineD. RamalingamN. HoG.P.H. NobleT. SandoeJ. LouY. LandgrafD. FreyzonY. NewbyG. SoldnerF. Terry-KantorE. KimT.E. HofbauerH.F. BecuweM. JaenischR. PincusD. ClishC.B. WaltherT.C. FareseR.V.Jr SrinivasanS. WelteM.A. KohlweinS.D. DettmerU. LindquistS. SelkoeD. Lipidomic analysis of α-synuclein neurotoxicity identifies stearoyl CoA desaturase as a target for parkinson treatment.Mol. Cell201973510011014.e810.1016/j.molcel.2018.11.028 30527540
    [Google Scholar]
  64. MartinezB.A. CaldwellK.A. CaldwellG.A.C. elegans as a model system to accelerate discovery for Parkinson disease.Curr. Opin. Genet. Dev.20174410210910.1016/j.gde.2017.02.011 28242493
    [Google Scholar]
  65. CooperJ.F. Van RaamsdonkJ.M. Modeling Parkinson’s disease in C. elegans.J. Parkinsons Dis.201881173210.3233/JPD‑171258 29480229
    [Google Scholar]
  66. BettensK. SleegersK. Van BroeckhovenC. Genetic insights in Alzheimer’s disease.Lancet Neurol.20131219210410.1016/S1474‑4422(12)70259‑4 23237904
    [Google Scholar]
  67. ScheunerD. EckmanC. JensenM. SongX. CitronM. SuzukiN. BirdT.D. HardyJ. HuttonM. KukullW. LarsonE. Levy-LahadL. ViitanenM. PeskindE. PoorkajP. SchellenbergG. TanziR. WascoW. LannfeltL. SelkoeD. YounkinS. Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer’s disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer’s disease.Nat. Med.19962886487010.1038/nm0896‑864 8705854
    [Google Scholar]
  68. McCollG. RobertsB.R. GunnA.P. PerezK.A. TewD.J. MastersC.L. BarnhamK.J. ChernyR.A. BushA.I. The Caenorhabditis elegans A beta 1-42 model of Alzheimer disease predominantly expresses A beta 3-42.J. Biol. Chem.200928434226972270210.1074/jbc.C109.028514 19574211
    [Google Scholar]
  69. TreuschS. HamamichiS. GoodmanJ.L. MatlackK.E.S. ChungC.Y. BaruV. ShulmanJ.M. ParradoA. BevisB.J. ValastyanJ.S. HanH. Lindhagen-PerssonM. ReimanE.M. EvansD.A. BennettD.A. OlofssonA. DeJagerP.L. TanziR.E. CaldwellK.A. CaldwellG.A. LindquistS. Functional links between Aβ toxicity, endocytic trafficking, and Alzheimer’s disease risk factors in yeast.Science201133460601241124510.1126/science.1213210 22033521
    [Google Scholar]
  70. FangE.F. HouY. PalikarasK. AdriaanseB.A. KerrJ.S. YangB. LautrupS. Hasan-OliveM.M. CaponioD. DanX. RocktäschelP. CroteauD.L. AkbariM. GreigN.H. FladbyT. NilsenH. CaderM.Z. MattsonM.P. TavernarakisN. BohrV.A. Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease.Nat. Neurosci.201922340141210.1038/s41593‑018‑0332‑9 30742114
    [Google Scholar]
  71. XieC. ZhuangX.X. NiuZ. AiR. LautrupS. ZhengS. JiangY. HanR. GuptaT.S. CaoS. Lagartos-DonateM.J. CaiC.Z. XieL.M. CaponioD. WangW.W. Schmauck-MedinaT. ZhangJ. WangH. LouG. XiaoX. ZhengW. PalikarasK. YangG. CaldwellK.A. CaldwellG.A. ShenH.M. NilsenH. LuJ.H. FangE.F. Amelioration of Alzheimer’s disease pathology by mitophagy inducers identified via machine learning and a cross-species workflow.Nat. Biomed. Eng.202261769310.1038/s41551‑021‑00819‑5 34992270
    [Google Scholar]
  72. TabriziS.J. FlowerM.D. RossC.A. WildE.J. Huntington disease: New insights into molecular pathogenesis and therapeutic opportunities.Nat. Rev. Neurol.2020161052954610.1038/s41582‑020‑0389‑4 32796930
    [Google Scholar]
  73. MorleyJ.F. BrignullH.R. WeyersJ.J. MorimotoR.I. The threshold for polyglutamine-expansion protein aggregation and cellular toxicity is dynamic and influenced by aging in Caenorhabditis elegans.Proc. Natl. Acad. Sci. USA20029916104171042210.1073/pnas.152161099 12122205
    [Google Scholar]
  74. VoisineC. VarmaH. WalkerN. BatesE.A. StockwellB.R. HartA.C. Identification of potential therapeutic drugs for huntington’s disease using Caenorhabditis elegans.PLoS One200726e50410.1371/journal.pone.0000504 17551584
    [Google Scholar]
  75. Muñoz-LobatoF. Rodríguez-PaleroM.J. Naranjo-GalindoF.J. ShephardF. GaffneyC.J. SzewczykN.J. HamamichiS. CaldwellK.A. CaldwellG.A. LinkC.D. Miranda-VizueteA. Protective role of DNJ-27/ERdj5 in Caenorhabditis elegans models of human neurodegenerative diseases.Antioxid. Redox Signal.201420221723510.1089/ars.2012.5051 23641861
    [Google Scholar]
  76. KimD.K. ChoK.W. AhnW.J. AcuñaD. JeongH. LeeH.J. LeeS.J. Cell-to-cell transmission of polyglutamine aggregates in C. elegans.Exp. Neurobiol.201726632132810.5607/en.2017.26.6.321 29302199
    [Google Scholar]
  77. RagagninA.M.G. ShadfarS. VidalM. JamaliM.S. AtkinJ.D. Motor neuron susceptibility in ALS/FTD.Front. Neurosci.20191353210.3389/fnins.2019.00532 31316328
    [Google Scholar]
  78. ZareiS. CarrK. ReileyL. DiazK. GuerraO. AltamiranoP. PaganiW. LodinD. OrozcoG. ChineaA. A comprehensive review of amyotrophic lateral sclerosis.Surg. Neurol. Int.20156117110.4103/2152‑7806.169561 26629397
    [Google Scholar]
  79. WangJ. FarrG.W. HallD.H. LiF. FurtakK. DreierL. HorwichA.L. An ALS-linked mutant SOD1 produces a locomotor defect associated with aggregation and synaptic dysfunction when expressed in neurons of Caenorhabditis elegans.PLoS Genet.200951e100035010.1371/journal.pgen.1000350 19165329
    [Google Scholar]
  80. TherrienM. RouleauG.A. DionP.A. ParkerJ.A. Deletion of C9ORF72 results in motor neuron degeneration and stress sensitivity in C. elegans.PLoS One2013812e8345010.1371/journal.pone.0083450 24349511
    [Google Scholar]
  81. RentonA.E. MajounieE. WaiteA. Simón-SánchezJ. RollinsonS. GibbsJ.R. SchymickJ.C. LaaksovirtaH. van SwietenJ.C. MyllykangasL. KalimoH. PaetauA. AbramzonY. RemesA.M. KaganovichA. ScholzS.W. DuckworthJ. DingJ. HarmerD.W. HernandezD.G. JohnsonJ.O. MokK. RytenM. TrabzuniD. GuerreiroR.J. OrrellR.W. NealJ. MurrayA. PearsonJ. JansenI.E. SondervanD. SeelaarH. BlakeD. YoungK. HalliwellN. CallisterJ.B. ToulsonG. RichardsonA. GerhardA. SnowdenJ. MannD. NearyD. NallsM.A. PeuralinnaT. JanssonL. IsoviitaV.M. KaivorinneA.L. Hölttä-VuoriM. IkonenE. SulkavaR. BenatarM. WuuJ. ChiòA. RestagnoG. BorgheroG. SabatelliM. HeckermanD. RogaevaE. ZinmanL. RothsteinJ.D. SendtnerM. DrepperC. EichlerE.E. AlkanC. AbdullaevZ. PackS.D. DutraA. PakE. HardyJ. SingletonA. WilliamsN.M. HeutinkP. Pickering-BrownS. MorrisH.R. TienariP.J. TraynorB.J. A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.Neuron201172225726810.1016/j.neuron.2011.09.010 21944779
    [Google Scholar]
  82. RudichP. SnoznikC. WatkinsS.C. MonaghanJ. PandeyU.B. LamitinaS.T. Nuclear localized C9orf72-associated arginine-containing dipeptides exhibit age-dependent toxicity in C. elegans.Hum. Mol. Genet.201726244916492810.1093/hmg/ddx372 29036691
    [Google Scholar]
  83. MitraJ. GuerreroE.N. HegdeP.M. LiachkoN.F. WangH. VasquezV. GaoJ. PandeyA. TaylorJ.P. KraemerB.C. WuP. BoldoghI. GarrutoR.M. MitraS. RaoK.S. HegdeM.L. Motor neuron disease-associated loss of nuclear TDP-43 is linked to DNA double-strand break repair defects.Proc. Natl. Acad. Sci. USA2019116104696470510.1073/pnas.1818415116 30770445
    [Google Scholar]
  84. CaoD. An autoregulation loop in fust-1 for circular RNA regulation in Caenorhabditis elegans.Genetics20212193iyab14510.1093/genetics/iyab145 34740247
    [Google Scholar]
  85. MarkertS.M. SkoruppaM. YuB. MulcahyB. ZhenM. GaoS. SendtnerM. StigloherC. Overexpression of an ALSassociated FUS mutation in C. elegans disrupts NMJ morphology and leads to defective neuromuscular transmission. Biol. Open,2020912bio.05512910.1242/bio.05512933148607
    [Google Scholar]
  86. JablonskiA.M. LamitinaT. LiachkoN.F. SabatellaM. LuJ. ZhangL. OstrowL.W. GuptaP. WuC.Y. DoshiS. Mojsilovic-PetrovicJ. LansH. WangJ. KraemerB. KalbR.G. Loss of RAD-23 protects against models of motor neuron disease by enhancing mutant protein clearance.J. Neurosci.20153542142861430610.1523/JNEUROSCI.0642‑15.2015 26490867
    [Google Scholar]
  87. WangX. HaoL. SaurT. JoyalK. ZhaoY. ZhaiD. LiJ. PribadiM. CoppolaG. CohenB.M. ButtnerE.A. Forward genetic screen in Caenorhabditis elegans Suggests F57A10.2 and acp-4 As suppressors of C9ORF72 related phenotypes.Front. Mol. Neurosci.2016911310.3389/fnmol.2016.00113 27877110
    [Google Scholar]
  88. WheelerJ.M. McMillanP. StrovasT.J. LiachkoN.F. Amlie-WolfA. KowR.L. KleinR.L. SzotP. RobinsonL. GuthrieC. SaxtonA. KanaanN.M. RaskindM. PeskindE. TrojanowskiJ.Q. LeeV.M.Y. WangL.S. KeeneC.D. BirdT. SchellenbergG.D. KraemerB. Activity of the poly(A) binding protein MSUT2 determines susceptibility to pathological tau in the mammalian brain.Sci. Transl. Med.201911523eaao654510.1126/scitranslmed.aao6545 31852801
    [Google Scholar]
  89. KraemerB.C. BurgessJ.K. ChenJ.H. ThomasJ.H. SchellenbergG.D. Molecular pathways that influence human tau-induced pathology in Caenorhabditis elegans.Hum. Mol. Genet.20061591483149610.1093/hmg/ddl067 16600994
    [Google Scholar]
  90. GriffinE.F. ScopelS.E. StephenC.A. HolzhauerA.C. VajiM.A. TuckeyR.A. BerkowitzL.A. CaldwellK.A. CaldwellG.A. ApoE-associated modulation of neuroprotection from Aβ-mediated neurodegeneration in transgenic Caenorhabditis elegans.Dis. Model. Mech.2019122dmm.03721810.1242/dmm.03721830683808
    [Google Scholar]
  91. SarasijaS. LaboyJ.T. AshkavandZ. BonnerJ. TangY. NormanK.R. Presenilin mutations deregulate mitochondrial Ca2+ homeostasis and metabolic activity causing neurodegeneration in Caenorhabditis elegans.eLife20187e3305210.7554/eLife.33052 29989545
    [Google Scholar]
  92. LuT. AronL. ZulloJ. PanY. KimH. ChenY. YangT.H. KimH.M. DrakeD. LiuX.S. BennettD.A. ColaiácovoM.P. YanknerB.A. REST and stress resistance in ageing and Alzheimer’s disease.Nature2014507749344845410.1038/nature13163 24670762
    [Google Scholar]
  93. ChatterjeeN. González-DurruthyM. CostaM.D. RibeiroA.R. Vilas-BoasV. Vilasboas-CamposD. MacielP. Alfaro-MorenoE. Differential impact of diesel exhaust particles on glutamatergic and dopaminergic neurons in Caenorhabditis elegans: A neurodegenerative perspective.Environ. Int.202418610859710.1016/j.envint.2024.108597 38579453
    [Google Scholar]
  94. Van PeltK.M. TruttmannM.C. Caenorhabditis elegans as a model system for studying aging-associated neurodegenerative diseases.Transl. Med. Aging20204607210.1016/j.tma.2020.05.001 34327290
    [Google Scholar]
  95. CooperJ.F. MachielaE. DuesD.J. SpielbauerK.K. SenchukM.M. Van RaamsdonkJ.M. Activation of the mitochondrial unfolded protein response promotes longevity and dopamine neuron survival in Parkinson’s disease models.Sci. Rep.2017711644110.1038/s41598‑017‑16637‑2 29180793
    [Google Scholar]
  96. KnightA.L. YanX. HamamichiS. AjjuriR.R. MazzulliJ.R. ZhangM.W. DaigleJ.G. ZhangS. BoromA.R. RobertsL.R. LeeS.K. DeLeonS.M. Viollet-DjelassiC. KraincD. O’DonnellJ.M. CaldwellK.A. CaldwellG.A. The glycolytic enzyme, GPI, is a functionally conserved modifier of dopaminergic neurodegeneration in Parkinson’s models.Cell Metab.201420114515710.1016/j.cmet.2014.04.017 24882066
    [Google Scholar]
  97. HarringtonA.J. YacoubianT.A. SloneS.R. CaldwellK.A. CaldwellG.A. Functional analysis of VPS41-mediated neuroprotection in Caenorhabditis elegans and mammalian models of Parkinson’s disease.J. Neurosci.20123262142215310.1523/JNEUROSCI.2606‑11.2012 22323726
    [Google Scholar]
  98. GriffinE.F. YanX. CaldwellK.A. CaldwellG.A. Distinct functional roles of Vps41-mediated neuroprotection in Alzheimer’s and Parkinson’s disease models of neurodegeneration.Hum. Mol. Genet.201827244176419310.1093/hmg/ddy308 30508205
    [Google Scholar]
  99. RegitzC. FitzenbergerE. MahnF.L. DußlingL.M. WenzelU. Resveratrol reduces amyloid-beta (Aβ1–42)-induced paralysis through targeting proteostasis in an Alzheimer model of Caenorhabditis elegans.Eur. J. Nutr.201655274174710.1007/s00394‑015‑0894‑1 25851110
    [Google Scholar]
  100. PalikarasK. LionakiE. TavernarakisN. Coordination of mitophagy and mitochondrial biogenesis during ageing in C. elegans.Nature2015521755352552810.1038/nature14300 25896323
    [Google Scholar]
  101. MartinezB.A. PetersenD.A. GaetaA.L. StanleyS.P. CaldwellG.A. CaldwellK.A. Dysregulation of the mitochondrial unfolded protein response induces non-Apoptotic dopaminergic neurodegeneration in C. elegans models of parkinson’s Disease.J. Neurosci.20173746110851110010.1523/JNEUROSCI.1294‑17.2017 29030433
    [Google Scholar]
  102. SammiS.R. FoguthR.M. NievesC.S. De PerreC. WipfP. McMurrayC.T. LeeL.S. CannonJ.R. Perfluorooctane sulfonate (PFOS) produces dopaminergic neuropathology in caenorhabditis elegans.Toxicol. Sci.2019172241743410.1093/toxsci/kfz191 31428778
    [Google Scholar]
  103. MulcahyB. IbbettP. Holden-DyeL. O’ConnorV. The C. elegans cysteine-string protein homologue, DNJ-14, is dispensable for neuromuscular junction maintenance across ageing. J. Exp. Biol.2019222Pt 22jeb.20545010.1242/jeb.20545031624097
    [Google Scholar]
  104. VaccaroA. TauffenbergerA. AshP.E.A. CarlomagnoY. PetrucelliL. ParkerJ.A. TDP-1/TDP-43 regulates stress signaling and age-dependent proteotoxicity in Caenorhabditis elegans.PLoS Genet.201287e100280610.1371/journal.pgen.1002806 22792076
    [Google Scholar]
  105. AkinyemiA.J. MiahM.R. IjomoneO.M. TsatsakisA. SoaresF.A.A. TinkovA.A. SkalnyA.V. VenkataramaniV. AschnerM. Lead (Pb) exposure induces dopaminergic neurotoxicity in Caenorhabditis elegans: Involvement of the dopamine transporter.Toxicol. Rep.2019683384010.1016/j.toxrep.2019.08.001 31463204
    [Google Scholar]
  106. PeresT.V. ArantesL.P. MiahM.R. BornhorstJ. SchwerdtleT. BowmanA.B. LealR.B. AschnerM. Role of caenorhabditis elegans AKT-1/2 and SGK-1 in manganese Toxicity.Neurotox. Res.201834358459610.1007/s12640‑018‑9915‑1 29882004
    [Google Scholar]
  107. GaetaA.L. CaldwellK.A. CaldwellG.A. Found in translation: The utility of C. elegans alpha-synuclein models of parkinson’s disease.Brain Sci.2019947310.3390/brainsci9040073 30925741
    [Google Scholar]
  108. GoodmanM.B. SenguptaP. How Caenorhabditis elegans senses mechanical stress, temperature, and other physical stimuli.Genetics20192121255110.1534/genetics.118.300241 31053616
    [Google Scholar]
  109. BaskoyluS.N. YersakJ. O’HernP. GrosserS. SimonJ. KimS. SchuchK. DimitriadiM. YanagiK.S. LinsJ. HartA.C. Single copy/knock-in models of ALS SOD1 in C. elegans suggest loss and gain of function have different contributions to cholinergic and glutamatergic neurodegeneration.PLoS Genet.20181410e100768210.1371/journal.pgen.1007682 30296255
    [Google Scholar]
  110. LeeY. ChoiS. KimK.W. Dithianon exposure induces dopaminergic neurotoxicity in Caenorhabditis elegans.Ecotoxicol. Environ. Saf.202325511475210.1016/j.ecoenv.2023.114752 36924561
    [Google Scholar]
  111. IkenakaK. TsukadaY. GilesA.C. AraiT. NakaderaY. NakanoS. KawaiK. MochizukiH. KatsunoM. SobueG. MoriI. A behavior-based drug screening system using a Caenorhabditis elegans model of motor neuron disease.Sci. Rep.2019911010410.1038/s41598‑019‑46642‑6 31300701
    [Google Scholar]
  112. SalamS. AnsariA. AmonS. RezaiP. SelvaganapathyP.R. MishraR.K. GuptaB.P. A microfluidic phenotype analysis system reveals function of sensory and dopaminergic neuron signaling in C. elegans electrotactic swimming behavior.Worm201322e2455810.4161/worm.24558 24058875
    [Google Scholar]
  113. HobertO. Behavioral plasticity in C. elegans: Paradigms, circuits, genes.J. Neurobiol.200354120322310.1002/neu.10168 12486705
    [Google Scholar]
  114. LengertE. ParakhonskiyB. KhalenkowD. ZečićA. VangheelM. Monje MorenoJ.M. BraeckmanB.P. SkirtachA.G. Laser-induced remote release in vivo in C. elegans from novel silver nanoparticles-alginate hydrogel shells.Nanoscale20181036172491725610.1039/C8NR00893K 30191939
    [Google Scholar]
  115. FredensJ. Engholm-KellerK. GiessingA. PultzD. LarsenM.R. HøjrupP. Møller-JensenJ. FærgemanN.J. Quantitative proteomics by amino acid labeling in C. elegans.Nat. Methods201181084584710.1038/nmeth.1675 21874006
    [Google Scholar]
  116. HameedS. IkegamiK. SugiyamaE. MatsushitaS. KimuraY. HayasakaT. SugiuraY. MasakiN. WakiM. OhtaI. HossenM.A. SetouM. Direct profiling of the phospholipid composition of adult Caenorhabditis elegans using whole-body imaging mass spectrometry.Anal. Bioanal. Chem.2015407257589760210.1007/s00216‑015‑8932‑7 26310845
    [Google Scholar]
  117. TorinoS. CorradoB. IodiceM. CoppolaG. Pdms-based microfluidic devices for cell culture.Inventions 2018336510.3390/inventions3030065
    [Google Scholar]
  118. HaN.M. TranS.H. ShimY.H. KangK. Caenorhabditis elegans as a powerful tool in natural product bioactivity research.Appl. Biol. Chem.20226511810.1186/s13765‑022‑00685‑y
    [Google Scholar]
  119. CornagliaM. LehnertT. GijsM.A.M. Microfluidic systems for high-throughput and high-content screening using the nematode Caenorhabditis elegans.Lab Chip201717223736375910.1039/C7LC00509A 28840220
    [Google Scholar]
  120. BlaiseB.J. GiacomottoJ. TribaM.N. ToulhoatP. PiottoM. EmsleyL. SégalatL. DumasM.E. ElenaB. Metabolic profiling strategy of Caenorhabditis elegans by whole-organism nuclear magnetic resonance.J. Proteome Res.2009852542255010.1021/pr900012d 19267476
    [Google Scholar]
  121. CorsiA.K. WightmanB. ChalfieM. A Transparent Window into Biology: A Primer on Caenorhabditis elegans.Genetics2015200238740710.1534/genetics.115.176099 26088431
    [Google Scholar]
  122. AnJ.H. BlackwellT.K. SKN-1 links C. elegans mesendodermal specification to a conserved oxidative stress response.Genes Dev.200317151882189310.1101/gad.1107803 12869585
    [Google Scholar]
  123. TulletJ.M.A. GreenJ.W. AuC. BenedettoA. ThompsonM.A. ClarkE. GilliatA.F. YoungA. SchmeisserK. GemsD. The SKN ‐1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms.Aging Cell20171651191119410.1111/acel.12627 28612944
    [Google Scholar]
  124. MurphyC.T. McCarrollS.A. BargmannC.I. FraserA. KamathR.S. AhringerJ. LiH. KenyonC. Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans.Nature2003424694627728310.1038/nature01789 12845331
    [Google Scholar]
  125. TangX. LiuB. WangX. YuQ. FangR. Epidermal growth factor, through alleviating oxidative stress, protect IPEC-J2 Cells from Lipopolysaccharides-Induced Apoptosis.Int. J. Mol. Sci.201819384810.3390/ijms19030848 29538305
    [Google Scholar]
  126. MuddN. LiceagaA.M. Caenorhabditis elegans as an in vivo model for food bioactives: A review.Curr. Res. Food Sci.2022584585610.1016/j.crfs.2022.05.001 35619588
    [Google Scholar]
  127. ZhaoS. ChengQ. PengQ. Antioxidant peptides derived from the hydrolyzate of purple sea urchin (Strongylocentrotus nudus) gonad alleviate oxidative stress in Caenorhabditis elegans.J. Funct. Foods201848594604
    [Google Scholar]
  128. HeX. MaQ. NRF2 cysteine residues are critical for oxidant/electrophile-sensing, Kelch-like ECH-associated protein-1-dependent ubiquitination-proteasomal degradation, and transcription activation.Mol. Pharmacol.20097661265127810.1124/mol.109.058453 19786557
    [Google Scholar]
  129. MartorellP. BatallerE. LlopisS. GonzalezN. ÁlvarezB. MontónF. OrtizP. RamónD. GenovésS. A cocoa peptide protects Caenorhabditis elegans from oxidative stress and β-amyloid peptide toxicity.PLoS One201385e6328310.1371/journal.pone.0063283 23675471
    [Google Scholar]
  130. ZhangZ. MaH. WangX. ZhaoZ. ZhangY. ZhaoB. GuoY. XuL. A tetrapeptide from maize protects a transgenic Caenorhabditis elegans Aβ 1-42 model from Aβ-induced toxicity.RSC Advances2016662568515685810.1039/C6RA06130C
    [Google Scholar]
  131. FayD.S. Classical genetic methods.WormBook2013158 24395816
    [Google Scholar]
  132. SutphinG.L. KaeberleinM. Measuring Caenorhabditis elegans life span on solid media.J. Vis. Exp.2009271152 19488025
    [Google Scholar]
  133. RomussiS. GiuntiS. AndersenN. De RosaM.J.C. elegans: A prominent platform for modeling and drug screening in neurological disorders.Expert Opin. Drug Discov.202419556558510.1080/17460441.2024.2329103 38509691
    [Google Scholar]
  134. MontañoK.J. CuéllarC. SotilloJ. Rodent models for the study of soil-transmitted helminths: A proteomics approach.Front. Cell. Infect. Microbiol.20211163957310.3389/fcimb.2021.639573 33968800
    [Google Scholar]
  135. GruberJ. ChenC.B. FongS. NgL.F. TeoE. HalliwellB. Caenorhabditis elegans: What we can and cannot learn from aging worms.Antioxid. Redox Signal.201523325627910.1089/ars.2014.6210 25544992
    [Google Scholar]
  136. WangC. ZhengC. Using Caenorhabditis elegans to model therapeutic interventions of neurodegenerative diseases targeting microbe-Host interactions.Front. Pharmacol.20221387534910.3389/fphar.2022.875349 35571084
    [Google Scholar]
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