ArticleBehavioural brain research2016
The flavonoid baicalein rescues synaptic plasticity and memory deficits in a mouse model of Alzheimer's disease.
Article in Behavioural brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 110 citations in OpenAlex.
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- Protective Effects of Pomiferin on Aluminum Chloride-induced Memory Impairment: Evidence from Behavioral, Biochemical, and Insilico Studies.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Multi-target intervention mechanisms and prospects of the traditional Chinese medicine Scutellaria baicalensis georgi in Alzheimer's disease.Frontiers in pharmacology · 2026Review
- Effects of plant-derived dietary antioxidants on Alzheimer's disease: Focus on ferroptosis.Asia Pacific journal of clinical nutrition · 2025Review
- Destabilisation of Alzheimer's amyloid-β protofibrils by Baicalein: mechanistic insights from all-atom molecular dynamics simulations.Molecular diversity · 2025Article
- Brain Glycogen-Its Metabolic Role in Neuronal Health and Neurological Disorders-An Extensive Narrative Review.Metabolites · 2025Review
- Natural products against tau hyperphosphorylation-induced aggregates: Potential therapies for Alzheimer's disease.Archiv der Pharmazie · 2025Review
- Neuroprotective Effect of Naturally Occurring Flavonoids.Central nervous system agents in medicinal chemistry · 2025Review
- Flavonoids and Alzheimer's disease: reviewing the evidence for neuroprotective potential.Molecular and cellular biochemistry · 2025Review
- Baicalin and baicalein from Scutellaria baicalensis Georgi alleviate aberrant neuronal suppression mediated by GABA from reactive astrocytes.CNS neuroscience & therapeutics · 2024Article
- What Threshold of Amyloid Reduction Is Necessary to Meaningfully Improve Cognitive Function in Transgenic Alzheimer's Disease Mice?Journal of Alzheimer's disease reports · 2024Article
- Comprehensive Insights into Pathophysiology of Alzheimer's Disease: Herbal Approaches for Mitigating Neurodegeneration.Current Alzheimer research · 2024Review
- Broadening horizons: ferroptosis as a new target for traumatic brain injury.Burns & trauma · 2024Review
- Baicalein Attenuates Neuroinflammation in LPS-Treated BV-2 Cells by Inhibiting Glycolysis via STAT3/c-Myc Pathway.Neurochemical research · 2023Article
- Article
- Anti-inflammatory potential of baicalein combined with silk fibroin protein in a zebrafish model (Danio rerio).Biotechnology letters · 2023Article
- Baicalein-corrected gut microbiota may underlie the amelioration of memory and cognitive deficits in APP/PS1 mice.Frontiers in pharmacology · 2023Article
- Natural product-based bioactive agents in combination attenuate neuroinflammation in a tri-culture model.Frontiers in pharmacology · 2023Article
- Omics-based biomarkers discovery for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2022Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that disruptions of synaptic functions correlate with the severity of cognitive deficit in Alzheimer's disease (AD). Our previous study demonstrated that baicalein enhances long-term potentiation (LTP) in acute rat hippocampal slices and improves hippocampus-dependent contextual fear conditioning in rats. Given that baicalein possess various biological activities, especially its effects on synaptic plasticity and cognitive function, we examined the effect of baicalein on synaptic function both in vitro and in vivo in AD model. The effect of baicalein on Aβ42 oligomer impaired LTP was investigated by electrophysiological methods. Baicalein was administered orally via drinking water to the APP/PS1 mice and sex- and age-matched wild-type mice. Treatment started at 5 months of age and mice were assessed for cognition and AD-like pathology at 7-month-old. Cognition was analyzed by Morris water maze test, fear conditioning test, and novel object recognition test. Changes in hippocampal 12/15 Lipoxygenase (12/15LO) and glycogen synthase kinase 3β (GSK3β) activity, Aβ production, tau phosphorylation, synaptic plasticity, and dendritic spine density were evaluated. Baicalein prevented Aβ-induced impairments in hippocampal LTP through activation of serine threonine Kinase (Akt) phosphorylation. Long-term oral administration of baicalein inhibited 12/15LO and GSK3β activity, reduced β-secretase enzyme (BACE1), decreased the concentration of total Aβ, and prevented phosphorylation of tau in APP/PS1 mice. Meanwhile, baicalein restored spine number, synaptic plasticity, and memory deficits. Our results strengthen the potential of the flavonoid baicalein as a novel and promising oral bioactive therapeutic agent that prevents memory deficits in AD.
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