ArticleFrontiers in pharmacology2024
Xixin Decoction's novel mechanism for alleviating Alzheimer's disease cognitive dysfunction by modulating amyloid-β transport across the blood-brain barrier to reduce neuroinflammation.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- MFSD2A in health and disease: lysolipid transport, barrier physiology, and translational boundaries.Molecular biomedicine · 2026Review
- 10,11-Dehydrocurvularin attenuates LPS-induced neuroinflammation in BV2 cells by inhibiting the TLR2/MyD88/NLRP3 signaling pathway.Biochemistry and biophysics reports · 2026Article
- Cinnamaldehyde Attenuates Hyperuricemia-Associated Renal Injury by Modulating Urate Transporters and AIF1- and CMPK2/NLRP3-Related Inflammatory Signaling.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- Biological functions and clinical implications of the CMPK2 across multisystemic diseases.Cell & bioscience · 2025Review
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10 authors.
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Abstract
Purpose: Xixin Decoction (XXD) is a classical formula that has been used to effectively treat dementia for over 300 years. Modern clinical studies have demonstrated its significant therapeutic effects in treating Alzheimer's disease (AD) without notable adverse reactions. Nevertheless, the specific mechanisms underlying its efficacy remain to be elucidated. This investigation sought to elucidate XXD's impact on various aspects of AD pathology, including blood-brain barrier (BBB) impairment, neuroinflammatory processes, and amyloid-β (Aβ) deposition, as well as the molecular pathways involved in these effects. Methods: Results: Conclusion: XXD may exert its effects by regulating the P-gp/ECS axis, the RAGE/LRP1 receptor system, and the expression of MRP2 and Mfsd2a proteins, thereby modulating the transport function of the BBB to expedite the clearance of Aβ, reduce cerebral Aβ accumulation, and consequently inhibit the activation of microglia induced by Aβ aggregation. This process may suppress the activation of the CMPK2/NLRP3 and TLRs/NF-κB pathways, diminish the production of inflammatory cytokines and chemokines, alleviate neuroinflammation associated with microglia in the brain of AD, and ultimately improve AD pathology.
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