ArticleMetabolic brain disease2016
Safflower yellow ameliorates cognition deficits and reduces tau phosphorylation in APP/PS1 transgenic mice.
Article in Metabolic brain disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Apicidin attenuates memory deficits by reducing the Aβ load in APP/PS1 mice.CNS neuroscience & therapeutics · 2023Article
- Article
- Safflower Yellow Improves Synaptic Plasticity in APP/PS1 Mice by Regulating Microglia Activation Phenotypes and BDNF/TrkB/ERK Signaling Pathway.Neuromolecular medicine · 2020Article
- Safflower Yellow Improves the Synaptic Structural Plasticity by Ameliorating the Disorder of Glutamate Circulation in AβNeurochemical research · 2020Article
- Safflower yellow attenuates learning and memory deficits in amyloid β-induced Alzheimer's disease rats by inhibiting neuroglia cell activation and inflammatory signaling pathways.Metabolic brain disease · 2019Article
- Ellagic acid ameliorates learning and memory impairment in APP/PS1 transgenic mice via inhibition of β-amyloid production and tau hyperphosphorylation.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), the most common cause of dementia worldwide, is mainly characterized by the aggregated β-amyloid (Aβ) and hyperphosphorylated tau. Safflower yellow (SY) is a novel water extract of natural safflower and has been suggested to ameliorate memory deficits in several animal models of dementia. In this study, we aimed to investigate the effect and mechanism of SY on deficits of learning and memory and hyperphosphorylation of tau in APP/PS1 double transgenic mice. APP/PS1 mice were administered with SY (10, 30, 100 mg/kg) by oral gavage for three months at the age of six months. The ability of learning and memory was investigated using the step-down test and Morris water maze test, and protein level in the brain was evaluated using western blot. Here, we found that SY treatment can improve spatial learning and memory ability, and reduce tau hyperphosphorylation at Ser199, Thr205, Ser396, Ser404 sites in APP/PS1 mice. In addition, the activity the of cyclin-dependent kinase 5 (CDK-5) and glycogen synthase kinase 3β (GSK-3β), major kinases involved in tau phosphorylation, was siginificantly decreased in APP/PS1 mice by SY treatment. These results support SY can serve as a promising multitarget neuronal therapeutic agent for the treatment of AD.
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