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Neuroprotective Effects of Leptin on the APP/PS1 Alzheimer's Disease Mouse Model: Role of Microglial and
Jing Ma1, Yi-Hui Hou2, Zhe-Yan Liao2
1Department of Neurology, Chengde Medical University Affiliated Hospital, Chengde Medical University, Chengde, People's Republic of China.
Background:
Microglia are closely linked to Alzheimer's disease (AD) many years ago; however, the pathological mechanisms of AD remain unclear. The purpose of this study was to determine whether leptin affected microglia in the hippocampus of young and aged male APP/PS1 mice.
Objective:
In a transgenic model of AD, we investigated the association between intraperitoneal injection of leptin and microglia.
Methods:
We intraperitoneal injection of leptin (1mg/kg) every day for one week and analyzed inflammatory markers in microglia in the hippocampus of adult (6 months) and aged (12 months) APP/PS1 mice.
Results:
In all leptin treatment group, the brain Aβ levels were decrease. We found increased levels of IL-1β, IL-6 and microglial activation in the hippocampus of adult mice. Using aged mice as an experimental model for chronic neuroinflammation and leptin resistance, the number of Iba-1+ microglia and the levels of IL-1β/IL-6 in the hippocampus were greatly increased as compared to the adult. But between the leptin treatment and un-treatment, there were no difference.
Conclusion:
Leptin signaling would regulate the activation of microglia and the release of inflammatory factors, but it is not the only underlying mechanism in the neuroprotective effects of AD pathogenesis.
Insights
Leptin affects microglia and inflammatory markers in Alzheimer
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia are implicated in Alzheimer's disease (AD) pathogenesis.
- The precise pathological mechanisms involving microglia in AD remain unclear.
- Leptin's role in modulating microglial activity in AD is under investigation.
Purpose of the Study:
- To investigate the effect of leptin on microglia in the hippocampus of young and aged male APP/PS1 mice.
- To determine if leptin administration influences inflammatory markers and microglial activation in a transgenic mouse model of AD.
Main Methods:
- Administration of leptin (1mg/kg) via intraperitoneal injection daily for one week.
- Analysis of inflammatory markers (IL-1β, IL-6) and microglial activation (Iba-1) in the hippocampus.
- Study conducted on adult (6 months) and aged (12 months) APP/PS1 mice.
Main Results:
- Leptin treatment decreased brain amyloid-beta (Aβ) levels in all groups.
- In adult mice, leptin increased IL-1β, IL-6, and microglial activation.
- Aged mice exhibited higher baseline Iba-1+ microglia and IL-1β/IL-6 levels, with no significant difference observed after leptin treatment compared to untreated aged mice.
Conclusions:
- Leptin signaling influences microglial activation and inflammatory factor release.
- Leptin's neuroprotective effects in AD pathogenesis involve mechanisms beyond its direct impact on microglia.
- Age-related leptin resistance may affect leptin's efficacy in modulating neuroinflammation.
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