ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2021
Levistolide A Attenuates Alzheimer's Pathology Through Activation of the PPARγ Pathway.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Levistolide A Alleviates Myocardial Ischemia-Reperfusion Injury Partly by Improving Calcium Homeostasis via the ADORA2B/cAMP/PKA/PLB/SERCA2α Signaling Axis.Current issues in molecular biology · 2026Article
- Article
- Empagliflozin Attenuates Pulmonary Arterial Remodeling Through Peroxisome Proliferator-Activated Receptor Gamma Activation.ACS pharmacology & translational science · 2024Article
- Levistilide A Exerts a Neuroprotective Effect by Suppressing Glucose Metabolism Reprogramming and Preventing Microglia Polarization Shift: Implications for Parkinson's Disease.Molecules (Basel, Switzerland) · 2024Article
- Chuanxiong Renshen Decoction Inhibits Alzheimer's Disease Neuroinflammation by Regulating PPARγ/NF-κB Pathway.Drug design, development and therapy · 2024Article
- MiRNA-338-3p Inhibits Neuroinflammation in the Corpus Callosum of LCV-LPS Rats Via STAT1 Signal Pathway.Cellular and molecular neurobiology · 2023Article
- Research progress of PPARγ regulation of cholesterol and inflammation in Alzheimer's disease.Metabolic brain disease · 2023Review
- Patchouli alcohol as a selective estrogen receptor β agonist ameliorates AD-like pathology of APP/PS1 model mice.Acta pharmacologica Sinica · 2022Article
- Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Article
- A Tau Pathogenesis-Based Network Pharmacology Approach for Exploring the Protections ofFrontiers in pharmacology · 2022Article
- Conditional deletion of MAD2B in forebrain neurons enhances hippocampus-dependent learning and memory in mice.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by β-amyloid (Aβ) protein deposition, neurofibrillary tangle (NFT) formation, and neuronal loss in the brain. The current study was designed to investigate the potential mechanisms by which levistolide A affects the pathogenesis of AD in an amyloid precursor protein/presenilin 1 (APP/PS1) transgenic (Tg) mouse model of AD and N2a/APP695swe cells. Specifically, behavioral changes in levistolide A-treated APP/PS1 Tg mice were assessed by the nest-building and Morris water maze (MWM) tests. Levistolide A treatment clearly ameliorated memory deficits and cognitive decline in APP/PS1 Tg mice. Aβ generation and the inflammatory response in APP/PS1 Tg mouse brains were clearly reduced after long-term levistolide A application. Mechanistically, levistolide A concurrently stimulated the expression of α-secretase and decreased the generation of β- and γ-secretases. In addition, levistolide A inhibited the phosphorylation of tau in the brains of the Tg mice. Furthermore, in vitro and in vivo experiments suggested that peroxisome proliferator-activated receptor γ (PPARγ) is the key transcription factor that mediates the regulatory effects of levistolide A on the expression of α-, β-, and γ-secretases and phosphorylation of tau. Collectively, these findings show that levistolide A may be a candidate for the treatment of AD.
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Registered trials
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