Bombycis excrementum reduces amyloid-β oligomer-induced memory impairments, neurodegeneration, and neuroinflammation in mice.

Alzheimer's disease (AD) is the most common cause of progressive dementia and is characterized by memory impairments, neuronal death, and neuroinflammation. AD-related pathophysiology is caused primarily by the presence of amyloid-β oligomers (AβO). Recently, an increased focus has been directed toward natural compounds or medicinal extracts for the treatment of AD. Extracts from Bombycis excrementum (BE), which is composed of various bioactive constituents and mulberry leaves (the preferred food of silkworms), have been shown to possess anti-inflammatory, anti-diabetic, and anti-oxidative effects. Additionally, mulberry leaves exert anti-amyloidogenic action and neuroprotective effects against Aβ peptides but it is unknown whether BE has a therapeutic effect on AD-related pathologies. Therefore, the present study examined whether BE inhibits AβO-induced memory loss, neuronal death, and inflammation. Behavioral tests revealed that BE significantly ameliorated AβO-induced memory impairments and inhibited AβO-induced neuronal loss in cultured cells and the brains of mice. BE also significantly inhibited microgliosis and astrogliosis following intra-hippocampal AβO injections in mice. Furthermore, BE significantly attenuated the release of nitric oxide from microglia and reduced AβO-induced S100-β cytokine release from activated astrocytes. These results suggest that BE may be a candidate agent for the treatment of AD.