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Published on: June 10, 2013
Pterosin B improves cognitive dysfunction by promoting microglia M1/M2 polarization through inhibiting Klf5/Parp14
Yan Zhang1, Ji-Cong Chen2, Jia-Hao Zheng3
1Department of Neurology, Fujian Institute of Geriatrics, Center for Cognitive Neurology, Fujian Medical University Union Hospital, 29 Xinquan Road, Fuzhou 350001, China; Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, 88 Jiaotong Road, Fuzhou 350001, China; Institute of Clinical Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou 350001, China.
Pterosin B (PB) improves cognitive function and reduces Alzheimer's disease (AD) pathology by modulating microglia polarization through the Klf5/Parp14 pathway.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Pterosin B (PB) shows in vitro neuroprotection, but its efficacy and mechanism in Alzheimer's disease (AD) are unclear.
- Investigating novel therapeutic strategies for AD is crucial due to its increasing prevalence.
Purpose of the Study:
- To elucidate the anti-AD effects of Pterosin B (PB).
- To determine the underlying molecular mechanisms of PB in Alzheimer's disease models.
Main Methods:
- PB's therapeutic effects were assessed in APP/PS1 mice and LPS-induced BV-2 cells.
- Cognitive function, pathological damage, microglia polarization, metabolic reprogramming, and key molecular pathways (Klf5/Parp14) were analyzed.
Main Results:
- PB treatment improved cognitive function and reduced neuropathology in AD mice.
- PB modulated microglia from M1 to M2 phenotype by regulating metabolic reprogramming via the Klf5/Parp14 pathway.
- Klf5 expression in AD patients correlated with cognitive decline and AD biomarkers.
Conclusions:
- Pterosin B (PB) demonstrates therapeutic potential for Alzheimer's disease (AD).
- PB ameliorates cognitive dysfunction by inhibiting the Klf5/Parp14 pathway, thereby modulating microglia M1/M2 polarization.
