Caenorhabditis elegans models
Caenorhabditis elegans (nematode) is a transparent invertebrate with 1mm in length and has a short lifespan and well characterized neuroanatomy. This model has became a good tool for studying the mechanisms of AD. Furthermore, it has been estimated that several AD-related genes and signal transductions are conserved in Caenorhabditis elegans, including apl-1, sel-12, hop-1, ptl-1 and some pathways. Recently, the Aβ-expressing nematode models and nematode tauopathy models have been well established. Creative Bioarray specializes in providing customized pharmacodynamic research services to help customers assess the efficacy of drug candidates and study the associated pathological mechanisms through Caenorhabditis elegans models.
Figure. 1. Caenorhabditis elegans
Our Capabilities
- We use Caenorhabditis elegans models to screen for drugs targeting AD.
- We provide Life span assay to to screen for drugs that could prolong the lifespan of nematodes.
- We evaluate various biomarkers through WB, IHC, sequencing, etc.
Assays available
- Memory test
- Life span assay
- Pharyngeal pumping and chemotaxis
- Fecundity Assay
- Aβ-Induced Paralysis Assay
- Stress Resistance Assays
- RT-PCR
- RNAi
- Oxidative stress
- Neuroinflammation
- Phosphorylated tau
- Neurofilament Light Chain levels
- Amyloid β-protein level
- Plaque load
Creative Bioarray has years of experience in establishing Caenorhabditis elegans models. We also provide adjacent services to meet your specific needs. We are confident to help you to overcome possible upcoming challenges in your research. With our help, we wish to facilitate your study with high efficiency.
Study examples
Figure. 2. MICA reduces paralysis due to Aβ expression in muscles of C. elegans. A) L1 nematodes of strain CL4176 Temperature inducible Aβ expressing worms were cultured on medium containing MICA at concentrations ranging from 2.5 to 50 mM. Protection against paralysis was assessed relative to protection due to RNAi of the dld-1 gene [(+) dld-1] or the untreated strain [CL4176]. T = 0 refers to the time of induction of Aβ expression by temperature up-shift to 25 °C. B) The effect of co-treatment with 5 mM MICA and dld-1 suppression by RNAi after 24 h of temperature induction. Bars = mean ± SD. Graphs show the average percentage values of active worms between treatments from three independent trials of 60–80 worms. Statistical analysis employed the log-rank survival test.
Figure. 3. MICA alleviates impaired chemotaxis, hypersensitivity to serotonin and reduced fecundity caused by neuronal expression of Aβ. L1 stage nematodes of strains CL2355 (neuronal Aβ) and their matched control CL2122 were cultured with or without 5 mM MICA for 36 h at 16 °C plus 25 °C for an additional 36 h to induce transgene expression. A) Impairment of chemotaxis due to Aβ expression is significantly alleviated by exposure to 5 mM MICA. B) Hypersensitivity toward serotonin resulting from neuronal expression of Aβ is substantially reduced by exposure to 5 mM MICA. C) Egg production that is reduced due to Aβ expression is partially restored by MICA. D) Egg hatching is delayed by neuronal expression of Aβ, but this effect is alleviated by MICA treatment. 30-50 worms were used for each treatment in each of three independent trials, except for fecundity and egg hatching assays where 10 worms were used in each of three independent trials. Bars = Mean ± SD.
Quotation and ordering
If you have any special needs or questions regarding our services, please feel free to contact us. We look forward to cooperating with you in the future.
Reference
- Ahmad W et al. 5-Methoxyindole-2-carboxylic acid (MICA) suppresses Aβ-mediated pathology in, C. elegans[J]. Experimental Gerontology, 2018, 108:215-225.
