Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease, which is accompanied by memory loss and cognitive dysfunction. Although a number of trials to treat AD are in progress, there are no drugs available that inhibit the progression of AD. As the aggregation of amyloid-β (Aβ) peptides in the brain is considered to be the major pathology of AD, inhibition of Aβ aggregation could be an effective strategy for AD treatment. Jowiseungchungtang (JWS) is a traditional oriental herbal formulation that has been shown to improve cognitive function in patients or animal models with dementia. However, there are no reports examining the effects of JWS on Aβ aggregation. Thus, we investigated whether JWS could protect against both Aβ aggregates and Aβ-mediated pathology such as neuroinflammation, neurodegeneration, and impaired adult neurogenesis in 5 five familial Alzheimer’s disease mutations (5XFAD) mice, an animal model for AD. In an in vitro thioflavin T assay, JWS showed a remarkable anti-Aβ aggregation effect. Histochemical analysis indicated that JWS had inhibitory effects on Aβ aggregation, Aβ-induced pathologies, and improved adult hippocampal neurogenesis in vivo. Taken together, these results suggest the therapeutic possibility of JWS for AD targeting Aβ aggregation, Aβ-mediated neurodegeneration, and impaired adult hippocampal neurogenesis.
Highlights
Alzheimer’s disease (AD) is the most common aging-associated neurodegenerative diseases
These results suggest that JWS effectively enhances adult hippocampal neurogenesis in 5XFAD mice
We demonstrated that JWS inhibits Aβ aggregation and accumulation, attenuates neuroinflammation and neuronal death, and restores adult hippocampal neurogenesis
Summary
Alzheimer’s disease (AD) is the most common aging-associated neurodegenerative diseases. Mutations in the APP gene can change the sequence of amino acids at the cleavage sites of the β-secretase and presenilin 1 (PSEN1)/PSEN2 mutation alters γ-secretase-dependent functions [6]. These abnormal cleavage processes result in the production of insoluble Aβ peptides and formation of oligomer aggregates [7]. Unless the aggregated Aβ peptides are cleared, Aβ accumulates in the brain [8] These neurotoxic Aβ aggregates lead to hallmark symptoms of AD such as synapse loss, neuroinflammation, memory impairment, and cognitive dysfunction [9,10]. Inhibiting Aβ aggregation might still be considered as the most promising treatment strategy for AD
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