Icariin Attenuates Synaptic and Cognitive Deficits in an A β <subscript>1-42</subscript> -Induced Rat Model of Alzheimer's Disease.
In: BioMed research international, Jg. 2017 (2017), S. 7464872
Online
academicJournal
Zugriff:
Icariin (ICA), a prenylated flavanol glycoside present in abundant quantities in Epimedium sagittatum , has shown promise in the treatment and prevention of Alzheimer's disease. Damage to synaptic plasticity induced by amyloid-beta-mediated neurotoxicity is considered a main pathological mechanism driving the learning and memory deficits present in patients with Alzheimer's disease. This study investigated the neuroprotective effects of icariin in an A β 1-42 -induced rat model of Alzheimer's disease. Our results showed that A β 1-42 injection induced loss of learning and memory behaviour in the Morris water maze, which could be reversed with intragastric administration of ICA. Furthermore, ICA reversed decreases in PSD-95, BDNF, pTrkB, pAkt, and pCREB expressions and prevented deterioration of synaptic interface structure. These findings indicate that ICA may improve synaptic plasticity through the BDNF/TrkB/Akt pathway and provide further evidence for its clinical application to improve learning and memory in patients with Alzheimer's disease.
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Icariin Attenuates Synaptic and Cognitive Deficits in an A β <subscript>1-42</subscript> -Induced Rat Model of Alzheimer's Disease.
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Autor/in / Beteiligte Person: | Sheng, C ; Xu, P ; Zhou, K ; Deng, D ; Zhang, C ; Wang, Z |
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Zeitschrift: | BioMed research international, Jg. 2017 (2017), S. 7464872 |
Veröffentlichung: | New York, NY : Hindawi Pub. Co., 2017 |
Medientyp: | academicJournal |
ISSN: | 2314-6141 (electronic) |
DOI: | 10.1155/2017/7464872 |
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