High homocysteine (Hcy) levels, mainly caused by vitamin B deficiency, have been reported to induce amyloid-β (Aβ) formation and tau hyperphosphorylation in mouse models of Alzheimer's disease. However, the relationship between B deficiency and Aβ aggregation is poorly understood, as is the associated mechanism. In the current study, we used the transgenic strain GMC101, which expresses human Aβ peptides in muscle cells, to investigate the effects of B deficiency on Aβ aggregation-associated paralysis.
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