Journal
NEUROBIOLOGY OF DISEASE
Volume 100, Issue -, Pages 87-98Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2017.01.004
Keywords
Obesity; Cognition; Behavior; Inflammatory response, beta-amyloid, high fat diet
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Funding
- National Institute on Aging [ROl AG038739]
- T32 Training [DK7061, DK050435]
- Vanderbilt Kennedy Center through National Institute for Child Health and Human Development [U54HD083211]
- Vanderbilt Diabetes Research Training Center and grants [DK059637, DK020593]
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This study assessed the extent to which high fat diet (HFD)-induced beta-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 beta-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. (C) 2017 Elsevier Inc. All rights reserved.
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