Pharmacological inhibition of acetylcholinesterase improves the locomotion defective phenotype of a SCA3 C. elegans model.

Franziska Pohl, Victoria Lindsay-McGee, Paul Kong Thoo Lin, Patricia Maciel, Andreia Teixeira-Castro

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Inhibition of acetylcholinesterase (AChE) is a common used treatment option for Alzheimer’s disease. However, there has been limited research on the potential use of AChE inhibitors for the treatment of Machado-Joseph disease (MJD)/Spinocerebellar Ataxia 3 (SCA3), in spite of the positive results using AChE inhibitors in patients with other inherited ataxias. MJD/SCA3, the most common form of dominant Spinocerebellar Ataxia worldwide, is caused by an expansion of the polyglutamine tract within the ataxin-3 protein, and is characterized by motor impairments. Our study shows that administration of the AChE inhibitor neostigmine is beneficial in treating the locomotion defective phenotype of a SCA3/MJD model of C. elegans and highlights the potential contribution of AChE enzymes to mutant ataxin-3-mediated toxicity.
Original languageEnglish
Pages (from-to)1-7
Number of pages7
JournalmicroPublication Biology
Early online date6 Feb 2024
DOIs
Publication statusE-pub ahead of print - 6 Feb 2024

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