Green Tea Extracts Attenuate Brain Dysfunction in High-Fat-Diet-Fed SAMP8 Mice.

Onishi Onishi,Ishino Ishino,Kitazawa Kitazawa,Mochizuki Mochizuki,Unno Unno,Shimba Shimba,Yoto Yoto,Meguro Meguro,Tokimitsu Tokimitsu,Pervin Pervin,Miura Miura

doi:10.3390/nu11040821

Onishi Onishi, Ishino Ishino + Show 9 more

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https://doi.org/10.3390/nu11040821

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Abstract

Unhealthy diet promotes progression of metabolic disorders and brain dysfunction with aging. Green tea extracts (GTEs) have various beneficial effects and alleviate metabolic disorders. GTEs have neuroprotective effects in rodent models, but their effects against brain dysfunction in models of aging fed unhealthy diets are still unclear. Here, we showed that GTEs attenuate high-fat (HF) diet-induced brain dysfunction in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, HF diet, or HF diet with 0.5% GTEs (HFGT) for four months. The HF diet reduced memory retention and induced amyloid β1–42 accumulation, whereas GTEs attenuated these changes. In HF diet-fed mice, lipid oxidative stress, assessed by malondialdehyde levels, was increased. The levels of proteins that promote synaptic plasticity, such as brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95), were reduced. These alterations related to brain dysfunction were not observed in HFGT diet-fed mice. Overall, our data suggest that GTEs intake might attenuate brain dysfunction in HF diet-fed SAMP8 mice by protecting synaptic plasticity as well as via anti-oxidative effects. In conclusion, GTEs might ameliorate unhealthy diet-induced brain dysfunction that develops with aging.

Highlights

Alzheimer’s Disease International reported that dementia has become a worldwide health problem with global increases in population sizes and life expectancy [1]
Aβ1–42 accumulation and MDA elevation, and NEP decline (Figure S3; NEP levels tend to be decreased) in the HF group suggest that lipid oxidative stress under excessive fat intake was related to Aβ1–42 accumulation caused by a decline in the Aβ1–42 degradation enzyme NEP
Our findings show that four-month Green tea extracts (GTEs) intake attenuates brain dysfunction in HF diet-fed senescence-accelerated mouse prone-8 (SAMP8) mice; this effect is accompanied by a decrease in oxidative stress and Aβ1–42 accumulation, which are considered important causative factors in AD pathogenesis and progression [35,63]

Summary

Introduction

Alzheimer’s Disease International reported that dementia has become a worldwide health problem with global increases in population sizes and life expectancy [1]. According to their new report, 50 million people live with dementia, and the global social cost reached US$1 trillion in. Unhealthy diet including excessive fats can lead to type 2 diabetes, insulin resistance, hypertension, and other conditions linked to obesity [5,6]. Type 2 diabetes is a risk factor for cognitive impairment [7,8], and insulin resistance is associated with brain atrophy and poor cognitive function in late middle-aged adults [9]. Senescence-resistant inbred strain 1 (SAMR1) and senescence-accelerated mouse (SAM)

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