RGD Reference Report - Flavonoid-rich ethanol extract from the leaves of Diospyros kaki attenuates cognitive deficits, amyloid-beta production, oxidative stress, and neuroinflammation in APP/PS1 transgenic mice. - Rat Genome Database

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Flavonoid-rich ethanol extract from the leaves of Diospyros kaki attenuates cognitive deficits, amyloid-beta production, oxidative stress, and neuroinflammation in APP/PS1 transgenic mice.

Authors: Ma, Yingjuan  Ma, Bin  Shang, Yuying  Yin, Qingqing  Hong, Yan  Xu, Song  Shen, Chao  Hou, Xunyao  Liu, Xueping 
Citation: Ma Y, etal., Brain Res. 2018 Jan 1;1678:85-93. doi: 10.1016/j.brainres.2017.10.001. Epub 2017 Oct 14.
RGD ID: 13782077
Pubmed: PMID:29038004   (View Abstract at PubMed)
DOI: DOI:10.1016/j.brainres.2017.10.001   (Journal Full-text)

Amyloid-ß peptide (Aß) initiates a cascade of pathological events, including activation of microglial cells, oxidative stress, and inflammation, leading to neuronal death and the typical pathological changes in Alzheimer's disease (AD). Flavonoids have been reported to exert neuroprotective activities, not only through their generally accepted antioxidant effects, but also through their ability to protect against neurotoxin-induced injury. Flavonoids reduce Aß production, inhibit neuroinflammation, increase cerebrovascular function, and improve cognitive performance. Here, we analyzed the effects of a flavonoid-rich ethanol extract from the leaves of Diospyros kaki (FLDK) in APP/PS1 transgenic mice. We found that oral treatment with FLDK reversed learning and memory impairment, reduced Aß burden and expression of ß-site amyloid precursor protein cleavage enzyme 1 (BACE1), and decreased microglial activation in senile plaques. FLDK restored antioxidant enzyme activities, as well as reduced the lipid peroxidation product, malondialdehyde, and inflammatory mediators. These results demonstrate that FLDK alleviates cognitive decline and reduces Aß burden, microglial activation, oxidative stress, and inflammation responses. Thus, FLDK treatment may be a potential therapeutic strategy for preventing and treating AD, at least in part via its anti-oxidant and anti-inflammatory biological activities and its effect on the Aß producing enzyme BACE1.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Alzheimer's disease treatmentISOBace1 (Mus musculus)13782077; 13782077 RGD 
Alzheimer's disease treatmentIEP 13782077 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bace1  (beta-secretase 1)

Genes (Mus musculus)
Bace1  (beta-site APP cleaving enzyme 1)

Genes (Homo sapiens)
BACE1  (beta-secretase 1)


Additional Information