Low-frequency magnetic fields can improve behavioral abnormalities and suppress Aβ accumulation detected by thioflavin T in Caenorhabditis elegans models of Alzheimer's disease.

Amyloid β (Aβ) accumulation and Aβ-related senile plaques, the pathological hallmarks of Alzheimer's disease (AD), damage neurons and impair cognitive functions in patients. Previous studies have shown that low‑field magnetic stimulation attenuates Aβ and enhances cognitive performance. In this study, AD models of Caenorhabditis elegans expressing Aβ in the nerves were placed in a low-frequency magnetic field (LFMF) and then subjected to a chemotaxis assay to evaluate attractive behavior. In control C. elegans (CL2122), which do not express Aβ but carried only the vector, the chemotactic behavior was normal and unaffected by LFMF. In contrast, in the AD model expressing Aβ within the nervous system, abnormalities in chemotactic behavior were observed; however, these were improved in a manner dependent on LFMF strength. In addition, the AD model expressing Aβ in the muscle exhibited paralysis, which was significantly attenuated by LFMF. Thioflavin T staining revealed that, in the AD model expressing in muscles, Aβ accumulation declined in the LFMF-treated group compared to that of the non-LFMF group. These results suggest that LFMF can improve abnormal chemotactic behavior and attenuate Aβ-induced paralysis by suppressing the accumulation and aggregation of Aβ in a C. elegans model of AD.