Journal
NEUROBIOLOGY OF AGING
Volume 80, Issue -, Pages 154-172Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2019.03.018
Keywords
Aging; Brain Health; Obesity; Neuroinflammation; Cerebrovascular Health; Exercise
Categories
Funding
- The Jane B. Cook Foundation
- The Jackson Laboratory Nathan Shock Center of Excellence in the Basic Biology of Aging, National Institute on Aging [K01 AG049050, P30 AG10133, R01 AG19771]
- Alzheimer's Association
- Indiana University HealtheIndiana University School of Medicine Strategic Research Initiative
- Indiana Clinical and Translational Science Institute (CTSI)
- Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant) [U01 AG024904]
- DOD ADNI (Department of Defense) [W81XWH-12-2-0012]
- National Institute on Aging
- AbbVie
- Alzheimer's Drug Discovery Foundation
- Araclon Biotech
- BioClinica, Inc
- Biogen
- Bristol-Myers Squibb Company
- CereSpir, Inc
- Cogstate
- Eisai Inc
- Elan Pharmaceuticals, Inc
- Eli Lilly and Company
- Euroimmun
- F. Hoffmann-La Roche Ltd
- Genentech, Inc
- Fujirebio
- GE Healthcare
- IXICO Ltd
- Janssen Alzheimer Immunotherapy Research & Development, LLC.
- Johnson & Johnson Pharmaceutical Research & Development LLC.
- Lumosity
- Lundbeck
- Merck Co, Inc
- Meso Scale Diagnostics, LLC.
- NeuroRx Research
- Neurotrack Technologies
- Novartis Pharmaceuticals Corporation
- Pfizer Inc
- Piramal Imaging
- Servier
- Takeda Pharmaceutical Company
- Transition Therapeutics
- Canadian Institutes of Health Research
- National Institute of Biomedical Imaging and Bioengineering
- Northern California Institute for Research and Education
- [RF1AG051496]
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Obesity in the western world has reached epidemic proportions, and yet the long-term effects on brain health are not well understood. To address this, we performed transcriptional profiling of brain regions from a mouse model of western diet (WD)-induced obesity. Both the cortex and hippocampus from C57BL/6J (B6) mice fed either a WD or a control diet from 2 months of age to 12 months of age (equivalent to midlife in a human population) were profiled. Gene set enrichment analyses predicted that genes involved in myelin generation, inflammation, and cerebrovascular health were differentially expressed in brains from WD-fed compared to control diet-fed mice. White matter damage and cerebrovascular decline were evident in brains from WD-fed mice using immunofluorescence and electron microscopy. At the cellular level, the WD caused an increase in the numbers of oligodendrocytes and myeloid cells suggesting that a WD is perturbing myelin turnover. Encouragingly, cerebrovascular damage and white matter damage were prevented by exercising WD-fed mice despite mice still gaining a significant amount of weight. Collectively, these data show that chronic consumption of a WD in B6 mice causes obesity, neuroinflammation, and cerebrovascular and white matter damage, but these potentially damaging effects can be prevented by modifiable risk factors such as exercise. (C) 2019 The Authors. Published by Elsevier Inc.
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