Abstract
To examine the effect of consuming polyphenol-rich Oriental plum (Prunus salicina Lindl) on the cognitive performance and the expressions of cerebral neurodegeneration-related proteins in diabetic rats, Wistar rats were assigned into 4 groups: control (C, n = 14), nicotinamide/streptozotocin-induced DM rats (DM, n = 13), DM rats fed metformin (0.05% w/w in the diet, MT, n = 18), and DM rats fed freeze-dried oriental plum powder (2% w/w in the diet, OP, n = 16) for 2 months. The cognitive performance was evaluated by testing in a Morris water maze. The insulin resistance, serum lipid peroxidation, expressions of pathological proteins of AD, beta-amyloid (Aβ) and phosphorylated tau protein were also measured. Consumption of plums significantly improved the spatial learning ability, reduced the insulin resistance, lipid peroxidation, Aβ and phosphorylated tau protein expressions in the cerebral cortex (all P β deposition in the hippocampus of diabetic rats. In conclusion, polyphenol-rich Oriental plums ameliorated the cognitive decline and reduced the expressions of pathological proteins of AD by possibly reducing hyperglycemia, insulin resistance, and oxidative stress in diabetic rats.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia among older people and the most-prevalent neurodegenerative disease, a disease with progressive impairment of the structures and functions of neurons [1,2,3]
The most prevailing hypothesis proposes that insulin resistance and impaired glucose metabolism in the brain play important roles in diabetes-caused AD [8]
There were no significant differences in body weight (BW) between the control and diabetic rats on the day (−1 month) diabetes was initially confirmed
Summary
Alzheimer’s disease (AD) is the most common form of dementia among older people and the most-prevalent neurodegenerative disease, a disease with progressive impairment of the structures and functions of neurons [1,2,3]. The major features of AD are progressive memory loss, cognitive impairment, and abnormal expressions of proteins in the brain, such as accumulation of β-amyloid (Aβ) and hyperphosphorylation of tau proteins [3]. Evidence demonstrated that type 2 diabetes is one of the main risk factors for sAD [2]. One study suggested that over 80% of cases of AD had either type 2 diabetes or impaired fasting glucose [6]. Review studies suggested that systemic insulin resistance is accompanied by central insulin resistance, and such impaired insulin signaling results in abnormal protein expressions in the brain and cognitive decline [2,9]. A few studies were reported in a review using animal models with type 2 diabetes to investigate the possible pathogenesis of AD [1]
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