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ABSTRACT
Introduction
Human neurodevelopmental and neurodegenerative diseases (NDevDs and NDegDs, respectively) encompass a broad spectrum of disorders affecting the nervous system with an increasing incidence. In this context, the nematode C. elegans, has emerged as a benchmark model for biological research, especially in the field of neuroscience.
Areas covered
The authors highlight the numerous advantages of this tiny worm as a model for exploring nervous system pathologies and as a platform for drug discovery. There is a particular focus given to describing the existing models of C. elegans for the study of NDevDs and NDegDs. Specifically, the authors underscore their strong applicability in preclinical drug development. Furthermore, they place particular emphasis on detailing the common techniques employed to explore the nervous system in both healthy and diseased states.
Expert opinion
Drug discovery constitutes a long and expensive process. The incorporation of invertebrate models, such as C. elegans, stands as an exemplary strategy for mitigating costs and expediting timelines. The utilization of C. elegans as a platform to replicate nervous system pathologies and conduct high-throughput automated assays in the initial phases of drug discovery is pivotal for rendering therapeutic options more attainable and cost-effective.
Graphical abstract
Article highlights
Due to its simplicity, genetic tractability, thoroughly studied nervous system and its high degree of conservation with mammals, C. elegans has become an essential tool for neuroscience research.
C. elegans models for human neurodevelopmental and neurodegenerative diseases (NDevDs and NDegDs) profoundly contribute to the study of disease mechanisms and potential therapeutic interventions.
Robust methodologies have been developed to examine the nematode’s nervous system in both healthy and diseased states.
The adaptation of this animal to implement large-scale and automated pharmacological assays enables cost-effective and efficient drug screening processes.
C. elegans serves as a pivotal platform for studying neurological diseases and conducting drug screenings.
Abbreviations
| AD | = | Alzheimer’s disease |
| ALS | = | Amyotrophic Lateral Sclerosis (ALS) |
| ASD | = | Autism Spectrum Disorder |
| Aβ | = | β-amyloid |
| BSR | = | basal slowing response |
| C. elegans | = | Caenorhabditis elegans |
| C9ORF72 | = | Chromosome 9 open reading frame 72 |
| DNC | = | dorsal nerve cord |
| E/I | = | excitation/inhibition |
| FUS | = | Fused in Sarcoma |
| GECIs | = | Genetically encoded calcium indicators |
| GEVIs | = | Genetically encoded voltage indicators |
| HD | = | Huntington’s disease |
| HTS | = | High-Throughput Screening |
| HTT | = | huntingtin |
| MRNs | = | mechanoreceptor neurons |
| NDegD | = | neurodegenerative disease |
| NDevD | = | neurodevelopmental disease |
| NMJ | = | neuromuscular junction |
| NS | = | nervous system |
| PD | = | Parkinson’s disease |
| polyQ | = | polyglutamine |
| PTZ | = | pentylenetetrazole |
| RNAi | = | RNA interference |
| SOD-1 | = | superoxide dismutase 1 |
| TDP-43 | = | TAR DNA-binding protein |
| TRNs | = | touch receptor neurons |
| VNC | = | ventral nerve cord |
| α-syn | = | alpha synuclein protein |
Acknowledgments
The authors thank D Rayes, G Blanco and I Berge for helpful discussions.
Declaration of interest
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/17460441.2024.2329103