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Milrinone Ameliorates the Neuroinflammation and Memory Function of Alzheimer's Disease in an APP/PS1 Mouse Model
Qingyou Chen1, Yue Yin2, Li Li1
1Department of Neurology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar City, Heilongjiang Province, 161000, People's Republic of China.
Purpose:
Alzheimer's disease (AD) is a complex neurodegenerative disorder, which is characterized by memory loss and cognitive deficits. The neuroprotective role of milrinone on the injury of spinal cord or cerebral ischemia-reperfusion has been confirmed. However, the accurate function of milrinone on AD pathogeny is still unclear.
Methods:
APP/PS1 transgenic mouse was used to explore the role of milrinone in behaviour tests, and the effects on histopathologic features of AD such as the formation of neuronal amyloid-β (Aβ) plaque, microglial activation, tau protein hyperphosphorylation, oxidative stress, and neuroinflammation. Lipopolysaccharide (LPS)/Aβ-treated BV-2 cells were used to understand the anti-inflammation mechanism of milrinone on AD in vitro.
Results:
Our in vivo results showed that milrinone ameliorates the memory functions of AD mice. Meanwhile, milrinone reduced Aβ deposits, repressed microglial activation and tau protein hyperphosphorylation, attenuated the oxidative stress, and decreased the levels of inflammatory cytokines. The in vitro results demonstrated that milrinone could inhibit the secretion of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α via regulation of NLRP3 inflammasomes and TLR4/MyD88/NF-κB signalling pathway.
Conclusion:
Overall, milrinone could ameliorate the memory loss and cognitive deficits through repressing the multiple pathological processes of AD, suggesting that milrinone may be an underlying and effective drug for treating AD clinically.
Insights
Milrinone improves memory in Alzheimer
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder causing memory loss and cognitive deficits.
- Milrinone's neuroprotective effects are known for spinal cord injury and ischemia-reperfusion.
- Milrinone's specific role in Alzheimer's disease pathogenesis remains unclear.
Purpose of the Study:
- To investigate the therapeutic potential of milrinone in Alzheimer's disease.
- To elucidate the mechanisms underlying milrinone's effects on AD pathology.
Main Methods:
- Utilized APP/PS1 transgenic mice for in vivo behavioral and histopathological assessments.
- Examined effects on amyloid-beta (Aβ) plaque formation, microglial activation, and tau hyperphosphorylation.
- Employed LPS/Aβ-treated BV-2 cells for in vitro mechanistic studies on anti-inflammation.
Main Results:
- Milrinone significantly ameliorated memory deficits in AD mouse models.
- Reduced Aβ deposition, microglial activation, tau hyperphosphorylation, oxidative stress, and inflammatory cytokines.
- In vitro, milrinone inhibited IL-1β, IL-6, and TNF-α secretion via NLRP3 inflammasomes and TLR4/MyD88/NF-κB pathway.
Conclusions:
- Milrinone alleviates cognitive decline in AD by targeting multiple pathological pathways.
- Demonstrates potential as an effective therapeutic agent for clinical treatment of Alzheimer's disease.
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