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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Bulbocodin D ameliorate cognitive impairment in APP/PS1 transgenic mice by modulating amyloid-beta burden, oxidative
1Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, 110122, Liaoning, China.
Rationale:
Amyloid β peptide (Aβ) triggers a series of pathological events including microglial activation, oxidative stress, and inflammation-causing neuronal death and typical pathological changes in Alzheimer's disease (AD).
Objectives:
This study aimed to investigate the therapeutic effects and mechanism of bulbocodin D for AD in vivo.
Methods:
In this study, Morris water maze (MWM) analysis was used to detect the cognitive ability of APP/PS1 mice after gavage with bulbocodin D for 2 months. Levels of Aβ40, Aβ42, IL-1β, and TNF-α were evaluated by ELISA. Aβ plaques and biomarkers of neuroinflammation were also investigated through histological analysis.
Results:
We established that bulbocodin D significantly improved cognitive deficits in APP/PS1 transgenic mice and reduced the levels of amyloid plaque, Aβ40, and Aβ42. Bulbocodin D also reduced levels of microglial markers IbA1, GFAP, and antioxidant enzymes and reduced the products of lipid peroxidation and proinflammatory cytokines.
Conclusion:
In summary, the present study provides preclinical evidence that oral bulbocodin D can reduce AD pathology.
Insights
Bulbocodin D shows promise in treating Alzheimer's disease (AD). This study found it improved cognitive function and reduced key AD pathologies in mice, suggesting a potential new therapy.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is characterized by amyloid-beta peptide (Aβ) triggering microglial activation, oxidative stress, and inflammation.
- These pathological events lead to neuronal death and characteristic brain changes in AD.
Purpose of the Study:
- To investigate the therapeutic potential and underlying mechanisms of bulbocodin D in an in vivo model of Alzheimer's disease.
- To evaluate the efficacy of bulbocodin D in mitigating AD-related pathology.
Main Methods:
- Morris water maze (MWM) analysis was employed to assess cognitive function in APP/PS1 transgenic mice treated with bulbocodin D.
- Enzyme-linked immunosorbent assay (ELISA) was used to quantify levels of Aβ40, Aβ42, IL-1β, and TNF-α.
- Histological analysis examined Aβ plaques and neuroinflammation markers.
Main Results:
- Bulbocodin D significantly ameliorated cognitive deficits in APP/PS1 mice.
- Treatment with bulbocodin D led to a reduction in amyloid plaque burden, including Aβ40 and Aβ42 levels.
- Bulbocodin D decreased microglial activation markers (Iba1, GFAP), oxidative stress indicators, and pro-inflammatory cytokines.
Conclusions:
- The study provides preclinical evidence supporting the oral administration of bulbocodin D as a potential therapeutic agent for Alzheimer's disease.
- Bulbocodin D demonstrates efficacy in reducing core AD pathologies, including amyloid deposition and neuroinflammation.
