High-fat diet increases gliosis and immediate early gene expression in APOE3 mice, but not APOE4 mice.
Open accessAbstract
Background: APOE4 is the strongest genetic risk factor for Alzheimer’s disease (AD), and obesity is a strong environmental risk factor for AD. These factors result in multiple central nervous system (CNS) disturbances and significantly increase chances of AD. Since over 20% of the US population carry the APOE4 allele and over 40% are obese, it is important to understand how these risk factors interact to affect neurons and glia in the CNS. Methods: We fed male and female APOE3 and APOE4 knock-in mice a high-fat diet (HFD-45% kcal fat) or a "control" diet (CD-10% kcal fat) for 12 weeks beginning at 6 months of age. At the end of the 12 weeks, brains were collected and analyzed for gliosis, neuroinflammatory genes, and neuronal integrity. Results: APOE3 mice on HFD, but not APOE4 mice, experienced increases in gliosis as measured by GFAP and Iba1 immunostaining. APOE4 mice on HFD showed a stronger increase in the expression of Adora2a than APOE3 mice. Finally, APOE 3 mice on HFD, but not APOE4 mice, also showed increased neuronal expression of immediate early genes cFos and Arc. Conclusions: These findings demonstrate that APOE genotype and obesity interact in their effects on important processes particularly related to inflammation and neuronal plasticity in the CNS. During the early stages of obesity, the APOE3 genotype modulates a response to HFD while the APOE4 genotype does not. This supports a model where early dysregulation of inflammation in APOE4 brains could predispose to CNS damages from various insults and later result in the increased CNS damage normally associated with the APOE4 genotype.
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Early dysregulation of inflammation in APOE4 brains could predispose to CNS damage from various insults, including diet, and later results in increased CNS damage normally associated with the APOE4 genotype.
“A second study concluded that early dysregulation of inflammation in APOE4 brains could predispose to CNS damage from various insults, including diet, and later results in the increased CNS damage normally associated with the APOE4 genotype (Jones et al., 2021).”
From Plcg2M28L Interacts With High Fat/High Sugar Diet to Accelerate Alzheimer’s Disease-Relevant Phenotypes in Mice (2022) · cites this paper as Jones et al., 2021
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- Authors
- Jones, N. S., Watson, K. Q., & Rebeck, G. W.
- Affiliations
- Georgetown University (US)
- Corresponding author
- Rebeck, G. William
- Venue
- Journal of Neuroinflammation
- Published
- 2021-09-18
- Volume
- 18
- Issue
- 1
- Pages
- 214-214
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC8449905
- OpenAlex
- W3200511728
- Cited by
- 26
- References
- 59
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 5 · 2023: 11 · 2022: 5
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (R21 AG074139, R01 NS100704, F99 NS119746-01)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- APOE ε4, APOE3, high-fat diet, obesity, Alzheimer's disease risk, gliosis, neuroinflammation, immediate early genes, c-fos, Arc, adenosine A2A receptor, glial fibrillary acidic protein, Iba1, neuroplasticity, gene-diet interaction
- MeSH terms
- Animals, Brain, Female, Gliosis, Male, Mice, Inbred C57BL, Mice, Transgenic, Gene Expression, Genes, Immediate-Early, Mice, Apolipoprotein E3, Apolipoprotein E4, Gene Knock-In Techniques, Diet, High-Fat
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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