Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function
Open accessAbstract
Obesity is a major public health problem affecting overall physical and emotional well-being. Despite compelling data suggesting an association between obesity and cognitive dysfunction, this phenomenon has received relatively little attention. Neuroimaging studies in obese humans report reduced size of brain regions involved in cognition, but few studies have investigated the cellular processes underlying cognitive decline in obesity or the influence of obesity on cognition in the absence of obesity-related illnesses. Here, a rat model of diet-induced obesity was used to explore changes in brain regions important for cognition. Obese rats showed deficits on cognitive tasks requiring the prefrontal and perirhinal cortex. Cognitive deficits were accompanied by decreased dendritic spine density and synaptic marker expression in both brain regions. Microglial morphology was also changed in the prefrontal cortex. Detrimental changes in the prefrontal cortex and perirhinal cortex occurred before metabolic syndrome or diabetes, suggesting that these brain regions may be particularly vulnerable to early stage obesity.
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Chronic HFD exposure in rodents, leading to obesity, gives rise to impairments in prefrontal cortex-dependent functions accompanied by changes in dendritic spine density and synaptic remodeling.
“chronic HFD exposure in rodents, leading to obesity, gives rise to impairments in prefrontal cortex-dependent functions that are accompanied by changes in dendritic spine density and synaptic remodeling [105].”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [105]
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- Authors
- Bocarsly, M. E., Fasolino, M., Kane, G. A., LaMarca, E. A., Kirschen, G. W., Karatsoreos, I. N., McEwen, B. S., & Gould, E.
- Affiliations
- Princeton University (US)
- Washington State University (US)
- Rockefeller University (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2015-12-07
- Volume
- 112
- Issue
- 51
- Pages
- 15731-15736
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC4697408
- OpenAlex
- W2191806457
- Cited by
- 250
- References
- 54
- Citations by year
- 2026: 8 · 2025: 21 · 2024: 30 · 2023: 27 · 2022: 27 · 2021: 35 · 2020: 22 · 2019: 27 · 2018: 24 · 2017: 18 · 2016: 9
- FWCI
- 9.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- HHS | NIH | National Institute of Neurological Disorders and Stroke (1R21NS087460)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- obesity, cognitive impairment, diet-induced obesity, prefrontal cortex, perirhinal cortex, dendritic spine density, synaptic markers, microglial morphology, synaptic plasticity, rat model
- MeSH terms
- Animals, Anxiety, Cognition Disorders, Dendrites, Disease Models, Animal, Male, Obesity, Synapses, Rats, Sprague-Dawley, Prefrontal Cortex, Microglia, Cell Shape, Rats
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