Green Tea Extracts Attenuate Brain Dysfunction in High-Fat-Diet-Fed SAMP8 Mice
Shintaro Onishi1, Shinichi Meguro2, Monira Pervin3
1Biological Science Research, Kao Corporation, Akabane, Ichikai-machi, Haga-gun, Tochigi 321-3497, Japan. oonishi.shintarou@kao.com.
Nutrients
|April 14, 2019
Summary
Green tea extracts (GTEs) can protect against brain dysfunction and memory loss caused by unhealthy diets in aging mice. GTEs help maintain synaptic plasticity and reduce oxidative stress, suggesting a potential benefit for cognitive aging.
Area of Science:
- Neuroscience
- Nutritional Science
- Gerontology
Background:
- Unhealthy diets accelerate metabolic disorders and cognitive decline during aging.
- Green tea extracts (GTEs) exhibit metabolic and neuroprotective benefits, but their impact on aging-related brain dysfunction from poor diets is not fully understood.
- Senescence-accelerated mouse prone-8 (SAMP8) mice serve as a model for studying aging and age-related diseases.
Purpose of the Study:
- To investigate the neuroprotective effects of GTEs in SAMP8 mice fed a high-fat (HF) diet.
- To determine if GTEs can mitigate HF diet-induced cognitive impairment and brain dysfunction in aging mice.
Main Methods:
- SAMP8 mice were assigned to three groups: control diet, HF diet, or HF diet supplemented with 0.5% GTEs (HFGT) for four months.
- Cognitive function was assessed by memory retention tests.
- Brain tissue analysis included measuring amyloid-beta (Aβ₁₋₄₂), malondialdehyde (MDA) levels, and the expression of synaptic plasticity proteins like brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95).
Main Results:
- HF diet consumption led to reduced memory retention and increased Aβ₁₋₄₂ accumulation in SAMP8 mice.
- HF diet-fed mice showed elevated lipid oxidative stress (increased MDA levels) and reduced levels of synaptic plasticity proteins (BDNF, PSD95).
- GTE supplementation in the HFGT group attenuated these negative effects, preserving memory function and synaptic integrity.
Conclusions:
- GTEs may counteract high-fat diet-induced brain dysfunction in aging mice (SAMP8 model).
- The neuroprotective mechanisms of GTEs involve preserving synaptic plasticity and exerting anti-oxidative effects.
- GTEs show potential for ameliorating diet-induced cognitive aging and brain dysfunction.
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