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Reversal of high fat diet-induced obesity improves glucose tolerance,
inflammatory response, ß-amyloid accumulation and cognitive decline in the
APP/PSEN1 mouse model of Alzheimer's disease.

Authors	Walker JM, Dixit S, Saulsberry AC, May JM, Harrison FE
Submitted By	Submitted Externally on 2/1/2017
Status	Published
Journal	Neurobiology of disease
Year	2017
Date Published	1/1/2017
Volume : Pages	100 : 87 - 98
PubMed Reference	28108292
Abstract	This study assessed the extent to which high fat diet (HFD)-induced ß-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 ß-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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