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Inhibiting microRNA-142-5p improves learning and memory in Alzheimer's disease rats via targeted regulation of the
Weiwei Liang1, Zhuojun Xie2, Dong Liao3
1Department of General Practice, The First People's Hospital of Yunnan Province, Kunming, Yunnan, China.
Objective:
MicroRNAs (miRNAs) have been recognized as possible biomarkers for Alzheimer's disease (AD). MiR-142-5p has been reported to be abnormally expressed in brain tissues. However, the role of miR-142-5p in AD pathogenesis keeps unclear. This study aimed to investigate the effect of miR-142-5p on the learning and memory of AD rats via regulation of protein tyrosine phosphatase nonreceptor type 1 (PTPN1)-mediated protein kinase B (Akt) pathway.
Methods:
The AD model was established by injection of Aβ1-42 oligomer once into the lateral ventricle of rats, and the spatial learning and memory ability of rats was measured. AD rats were injected with miR-142-5p or PTPN1 vectors to explore their functions in inflammation, Aβ, p-tau protein, apoptosis in brain tissues, and the effects on Akt pathway. The targeting relationship between miR-142-5p and PTPN1 was detected.
Results:
Overexpressed miR-142-5p, down-regulated PTPN1 and inactivated Akt pathway were exhibited in AD. MiR-142-5p targeted PTPN1 to mediate Akt pathway. Reduced miR-142-5p and elevated PTPN1 improved the behavior of AD rats. MiR-142-5p targeted PTPN1 to effectively inhibit Aβ formation and abnormal phosphorylation of p-tau protein, suppress the inflammation in the brain tissues of AD rat, and improve the survival rate of brain tissue cells. MiR-142-5p regulated PTPN1 to activate the Akt pathway, further inhibiting the apoptosis of brain neurons in AD rats.
Conclusion:
Down-regulating miR-142-5p targets PTPN1 to activate Akt pathway, thus improving the learning and memory of AD rats and playing an anti-AD role.
Insights
Down-regulating microRNA-142-5p (miR-142-5p) in Alzheimer\
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are emerging as potential biomarkers for Alzheimer\'s disease (AD).
- MiR-142-5p expression is altered in brain tissues, but its specific role in AD pathogenesis remains unclear.
- Understanding the molecular mechanisms underlying AD is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the impact of miR-142-5p on learning and memory in a rat model of Alzheimer\'s disease.
- To elucidate the regulatory role of miR-142-5p in the protein tyrosine phosphatase nonreceptor type 1 (PTPN1)-mediated protein kinase B (Akt) pathway.
- To determine the therapeutic potential of modulating miR-142-5p in AD.
Main Methods:
- An Alzheimer\'s disease rat model was established using Aβ1-42 oligomer injection.
- Spatial learning and memory were assessed in AD rats.
- miR-142-5p and PTPN1 vectors were administered to evaluate their effects on AD pathology, inflammation, and the Akt pathway.
Main Results:
- Overexpression of miR-142-5p led to down-regulated PTPN1 and inactivated Akt pathway in AD rats.
- MiR-142-5p directly targeted PTPN1, inhibiting Aβ formation, p-tau phosphorylation, and neuroinflammation.
- Modulating miR-142-5p improved cognitive function and neuronal survival by activating the Akt pathway.
Conclusions:
- Down-regulation of miR-142-5p targets PTPN1 to activate the Akt pathway, thereby enhancing learning and memory in AD rats.
- MiR-142-5p plays a protective role against Alzheimer\'s disease progression.
- Targeting the miR-142-5p/PTPN1/Akt axis represents a promising therapeutic strategy for Alzheimer\'s disease.
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