ArticleNeural plasticity2026
Berberine Alleviates Lipopolysaccharide-Induced Impairments in Neuroplasticity and Spatial Memory by Modulating Microglial Polarization via MAPK Signaling Inhibition.
Article in Neural plasticity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Review
- Metabolic and Anti-Inflammatory Effects of Berberine-Rationale for Its Therapeutic Potential in Polycystic Ovary Syndrome.International journal of molecular sciences · 2026Review
- Targeting mitochondrial dysfunction and neuroprotection in neurodegenerative disorders: emerging therapeutic potential of berberine and polymeric nanoparticle-based delivery systems.Inflammopharmacology · 2026Review
- Berberine Alleviates Lipopolysaccharide-Induced Impairments in Neuroplasticity and Spatial Memory by Modulating Microglial Polarization via MAPK Signaling Inhibition.Neural plasticity · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Neuroinflammation-induced cognitive impairment is characterized by a continued decline in memory, executive functioning, and information-processing abilities. Although berberine (BBR) exhibits anti-inflammatory and neuroprotective properties, its ability to mitigate cognitive deficits by regulating microglial-mediated neuroinflammation remains incompletely understood. To investigate the potential of BBR in mitigating microglial-mediated neuroinflammation and its detrimental effects on neuroplasticity and spatial memory, a mouse model was established through intrahippocampal microinjection of lipopolysaccharide (LPS). The results showed that BBR pretreatment significantly improved cognitive performance, suppressed microglial activation, reduced hippocampal neuronal damage, and increased the density of functional dendritic spines. Mechanistic analysis revealed that BBR treatment inhibited the phosphorylation of key proteins in the MAPK signaling pathway within microglia. These findings suggest that BBR is a promising therapeutic agent for mitigating neuroinflammation-induced cognitive impairment and provide significant evidence for its potential application in treating inflammation-related cognitive deficits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.