Protective Effect of Caffeic Acid against Alzheimer’s Disease Pathogenesis via Modulating Cerebral Insulin Signaling, β‑Amyloid Accumulation, and Synaptic Plasticity in Hyperinsulinemic Rats

Protective Effect of Caffeic Acid against Alzheimer’s Disease Pathogenesis via Modulating Cerebral Insulin Signaling, β‑Amyloid Accumulation, and Synaptic Plasticity in Hyperinsulinemic Rats

This study investigated the alleviative effect of caffeic acid (CA) on Alzheimer’s disease (AD) pathogenesis and associated mechanisms in high-fat (HF) diet-induced hyperinsulinemic rats. The results of a Morris water maze indicated that, by administrating CA (30 mg/kg b.w./day) for 30 weeks, the me...

Full description

Saved in:
Bibliographic Details
Published in:Journal of agricultural and food chemistry Vol. 67; no. 27; pp. 7684 - 7693
Main Authors: Chang, Wenchang, Huang, Dawei, Lo, Y. Martin, Tee, Qinqiao, Kuo, Poling, Wu, James Swibea, Huang, Wenchung, Shen, Szuchuan
Format: Journal Article
Language:English
Published: United States American Chemical Society 10-07-2019
Subjects:
cerebral carbohydrate metabolism
caffeic acid
hyperinsulinemic
Alzheimer’s disease
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:This study investigated the alleviative effect of caffeic acid (CA) on Alzheimer’s disease (AD) pathogenesis and associated mechanisms in high-fat (HF) diet-induced hyperinsulinemic rats. The results of a Morris water maze indicated that, by administrating CA (30 mg/kg b.w./day) for 30 weeks, the memory and learning impairments in HF-induced hyperinsulinemic rats were significantly ameliorated. CA also enhanced superoxide dismutase and glutathione free radical scavenger activity in hyperinsulinemic rats. The Western blot data further confirmed that protein expressions of phosphorylated-glycogen synthase kinase 3β (GSK3β) were significantly increased, whereas the expression of phosphorylated-tau protein decreased in the hippocampus of rats administered with CA in comparison with the HF group. Moreover, the expression of amyloid precursor protein (APP) and β-site APP cleaving enzyme were attenuated, subsequently lowering the level of β-amyloid 1–42 (Aβ 1–42) in the hippocampus of CA-treated hyperinsulinemic rats. CA also significantly increased the expression of synaptic proteins in HF rats.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0021-8561
1520-5118
DOI:10.1021/acs.jafc.9b02078