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Rubrofusarin inhibits Aβ aggregation and ameliorates memory loss in an Aβ-induced Alzheimer's disease-like mouse
Eunbi Cho1, Mudan Cai2, Huiyoung Kwon1
1Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, Busan, 49315, Republic of Korea.
Abstract:
The misfolding and aggregation of amyloid β (Aβ) peptide is a common histopathologic characteristic in patients with Alzheimer's disease, so is considered to play an critical role. In the present study, we examined the effect of rubrofusarin, an ingredient of Cassiae semen, on Aβ aggregation and memory loss in an AD mouse model. Rubrofusarin inhibited Aβ aggregation in a concentration-dependent manner. Moreover, rubrofusarin dis-aggregated preformed Aβ fibrils in a concentration-dependent manner. Although aggregated Aβ induced memory loss, Aβ pre-incubated with rubrofusarin failed to induce memory loss. Moreover, rubrofusarin administration ameliorated Aβ aggregates-induced memory loss. Finally, rubrofusarin reduced glial fibrillary acidic protein or Iba-1-positive area, markers of neuroinflammation, in the hippocampus of Aβ-treated mice. These results suggest that rubrofusarin can decrease Aβ fibril formation and ameliorate memory loss in the AD mouse model.
Insights
Rubrofusarin, from Cassiae semen, effectively inhibits amyloid-beta (Aβ) aggregation and improves memory in Alzheimer
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) peptide misfolding and aggregation.
- Aβ aggregation is a critical factor in the pathogenesis of Alzheimer's disease.
Purpose of the Study:
- To investigate the therapeutic potential of rubrofusarin, a Cassiae semen component, against Aβ aggregation and memory deficits in an AD mouse model.
- To evaluate rubrofusarin's effects on Aβ fibril formation, disaggregation, and neuroinflammation.
Main Methods:
- In vitro assessment of rubrofusarin's effect on Aβ aggregation and preformed Aβ fibril disaggregation.
- In vivo evaluation of rubrofusarin's impact on Aβ-induced memory loss and neuroinflammation in a mouse model.
- Quantification of neuroinflammation markers (GFAP, Iba-1) in the hippocampus.
Main Results:
- Rubrofusarin demonstrated a concentration-dependent inhibition of Aβ aggregation and disaggregation of preformed Aβ fibrils.
- Rubrofusarin administration prevented Aβ-induced memory loss and ameliorated existing memory deficits.
- Rubrofusarin treatment significantly reduced neuroinflammation markers in the hippocampus of Aβ-treated mice.
Conclusions:
- Rubrofusarin exhibits potent anti-amyloidogenic and neuroprotective properties.
- Rubrofusarin shows promise as a therapeutic agent for Alzheimer's disease by targeting Aβ pathology and neuroinflammation.
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