کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5630668 | 1580621 | 2017 | 12 صفحه PDF | دانلود رایگان |
- High fat diet-induced cognitive deficits were reversible by low fat diet treatment.
- High fat diet-induced inflammatory response was reversible by low fat diet treatment.
- High fat diet-induced acceleration of β-amyloid accumulation was partially reversible.
- APP/PSEN1 mice on high fat diet showed greater glucose intolerance than wild-type mice.
This study assessed the extent to which high fat diet (HFD)-induced β-amyloid accumulation and cognitive decline in APP/PSEN1 mice are reversible through control of fat intake. Ten months of HFD (60% calories from fat) led to significant deficits in a 2-trial Y maze task, and nest building assay, and decreased voluntary locomotor activity. The HFD induced an inflammatory response, indicated by increased expression of several inflammatory markers. Substituting a low fat diet led to pronounced weight loss and correction of glucose intolerance, decreases in the inflammatory response, and improved performance on behavioral tasks in both wild-type and APP/PSEN1 transgenic mice. Insoluble β-amyloid levels, and extent of tau phosphorylation were also lower following dietary reversal in APP/PSEN1 mice compared to high fat-fed animals, indicating that the inflammatory response may have contributed to key pathogenic pathways in the Alzheimer's disease model. The data suggest that weight loss can be a vital strategy for cognitive protection, but also highlight potential mechanisms for intervention when sustained weight loss is not possible.
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Journal: Neurobiology of Disease - Volume 100, April 2017, Pages 87-98