Neurodegeneration

Strong phenotypic models in a naturally ageing organism

Neurodegenerative diseases are chronic and debilitating conditions linked with age, with few therapeutic interventions. The incidence of Alzheimer’s, Parkinson’s, and related diseases are set to double every 20 years as the population ages globally¹.

C. elegans provides effective models of neurodegenerative disease through overexpression of human proteins implicated in their pathophysiology. These loss of function models age in weeks, with characteristic neurodegenerative phenotypes that can be scored rapidly and used to test diverse interventions with our WormGazer™ technology.

Our strong phenotype model and advantage

We provide you with a strong phenotypic model system for neurodegenerative diseases, including muscular changes that result in variable paralysis and neurological changes that affect mobility and cognitive behaviours. This is combined with the ability to continuously track and quantify these complex changes, in real time, using our automated WormGazer™ technology.

Contact us for more information and data examples from our in-house C. elegans models of Huntington’s Disease, Alzheimer’s Disease, Parkinson’s Disease. See our Transgenics page to discover how we can make a custom model designed for your specific needs.

Natural age-related neurodegeneration and the C. elegans model

Ageing is a major risk factor for neurodegeneration and associated diseases. As such, we also offer assays for neuronal functional decline using naturally ageing, wild type populations. These models are free from the overexpression of proteins or pathway induction.

Neurotransmission in C. elegans uses several identical receptors and signalling pathways to mammals, allowing its successful use to model neuronal function². These include acetylcholine (ACh), g-aminobutyric acid (GABA), dopamine, serotonin and glutamate. Excitatory neurotransmission at the neuromuscular junction is elicited through ACh and inhibited by GABA.

Age-related mobility decline in C. elegans Alzheimer’s amyloid beta 1-42 model vs. control strain

In this video, we demonstrate the use of our unique WormGazer^™ technology to measure mobility decline in a C. elegans strain modified to express the human amyloid peptide (Aβ_1-42) as a model for Alzheimer’s disease vs. a wild-type control model.

Continuous monitoring for key signs of neurodegeneration (decline in mobility, preceding paralysis)

Test your compound or product in a naturally ageing organism

Consultancy from leading experts for study design input

Automated WormGazer™ technology with high throughput and data reproducibility

Multi-faceted healthspan approach, to monitor disease-relevant changes, including neuronal function throughout the ageing process

Reliable data compared to artificial degeneration induced in rodents

Acute and chronic testing for therapeutic compound effects on health and longevity

Key insights into targets and modes of action using genetic and molecular tools

Large populations with consistent and time efficient experiments with predictive power for mammals

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