Jowiseungchungtang Inhibits Amyloid-β Aggregation and Amyloid-β-Mediated Pathology in 5XFAD Mice

Area of Science:

• Neuroscience
• Pharmacology
• Herbal Medicine

Background:

• Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and cognitive decline.
• Current treatments for AD do not halt disease progression, highlighting the need for novel therapeutic strategies.
• Amyloid-beta (Aβ) peptide aggregation in the brain is a primary pathological hallmark of AD.

Purpose of the Study:

• To investigate the effects of Jowiseungchungtang (JWS) on Aβ aggregation and related pathologies in a mouse model of Alzheimer's disease.
• To evaluate JWS's potential to mitigate neuroinflammation, neurodegeneration, and impaired adult neurogenesis associated with Aβ.
• To explore JWS as a therapeutic agent targeting the core pathologies of AD.

Main Methods:

• In vitro thioflavin T assay to assess JWS's anti-Aβ aggregation activity.
• Utilized 5 familial Alzheimer's disease mutations (5XFAD) mice, a relevant animal model for AD.
• In vivo histochemical analysis to evaluate Aβ aggregation, neuropathology, and hippocampal neurogenesis.

Main Results:

• JWS demonstrated significant inhibition of Aβ aggregation in vitro.
• Histochemical analysis confirmed JWS's ability to inhibit Aβ aggregation and Aβ-induced pathologies in vivo.
• JWS treatment improved adult hippocampal neurogenesis in the 5XFAD mouse model.

Conclusions:

• JWS exhibits potent anti-amyloid-beta aggregation properties.
• JWS shows therapeutic potential for Alzheimer's disease by targeting Aβ aggregation, neurodegeneration, and neurogenesis deficits.
• This study suggests JWS as a promising candidate for AD treatment development.