Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by significant degeneration of upper motor neurons (UMNs) and lower motor neurons (LMNs). Specifically, UMN degeneration causes excessive neuroexcitatory responses and spasticity, while LMN degeneration can directly lead to weakened muscle strength, fasciculations, and progressive atrophy. As the disease progresses, patients experience widespread muscle size loss, irreversible paralysis, and eventual mortality. The exact cause of ALS is not completely clear, and no effective cure exists.

C. elegans for ALS research

C. elegans serves as a powerful model for ALS research due to its simplicity and genetic similarity to humans. Currently, approximately 20 ALS-related genes have been identified, such as SOD1, TARDBP, FUS, and C9orf72, which are commonly mutated in typical ALS cases.

Our Services

The ALS models we can provide include but are not limited to:

ØSOD1 Mutation Model

Display ALS-like features, such as motor neuron degeneration, protein aggregation, and impaired motor ability.

ØTDP-43 Mutation Model

Abnormal aggregation of TDP-43 leads to motor neuron degeneration, behavioral changes, and shortened lifespan.

ØFUS Mutation Model

Aggregation of FUS proteins leads to neuronal degeneration, manifested by movement disorders, cell death and behavioral abnormalities.

Related Services

Customized experimental plans for other ALS models are available upon request. Contact us for more details.