High-fat Diet-Induced Deregulation of Hippocampal Insulin Signaling and Mitochondrial Homeostasis Deficiences Contribute to Alzheimer Disease Pathology in Rodents
Open accessAbstract
Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide. The situation is compounded by the fact that apart from the direct costs associated with overweight pathology, obesity presents itself with a number of comorbidities, including an increased risk for the development of neurodegenerative disorders. Alzheimer disease (AD), the main cause of senile dementia, is no exception. Spectacular failure of the pharmaceutical industry to come up with effective AD treatment strategies is forcing the broader scientific community to rethink the underlying molecular mechanisms leading to cognitive decline. To this end, the emphasis is once again placed on the experimental animal models of the disease. In the current study, we have focused on the effects of a high-fat diet (HFD) on hippocampal-dependent memory in C57/Bl6 Wild-type (WT) and APPswe/PS1dE9 (APP/PS1) mice, a well-established mouse model of familial AD. Our results indicate that the continuous HFD administration starting at the time of weaning is sufficient to produce β-amyloid-independent, hippocampal-dependent memory deficits measured by a 2-object novel-object recognition test (NOR) in mice as early as 6months of age. Furthermore, the resulting metabolic syndrome appears to have direct effects on brain insulin regulation and mitochondrial function. We have observed pathological changes related to both the proximal and distal insulin signaling pathway in the brains of HFD-fed WT and APP/PS1 mice. These changes are accompanied by a significantly reduced OXPHOS metabolism, suggesting that mitochondria play an important role in hippocampus-dependent memory formation and retention in both the HFD-treated and AD-like rodents at a relatively young age.
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Insulin resistance leads to reduced Aβ degradation by insulin-degrading enzyme, promoting Aβ accumulation.
“It is also worth noting that insulin resistance leads to a reduced Aβ degradation by IDE, hence promoting the Aβ accumulation (Ho et al., 2004; Zhao et al., 2004; Petrov et al., 2015).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Petrov et al., 2015
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- Authors
- Petrov, D., Pedrós, I., Artiach, G., Sureda, F. X., Barroso, E., Pallàs, M., Casadesús, G., Beas-Zarate, C., Carro, E., Ferrer, I., Vazquez-Carrera, M., Folch, J., & Camins, A.
- Affiliations
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (ES)
- Kent State University (US)
- Research Institute Hospital 12 de Octubre (ES)
- Corresponding author
- Camins, Antoni
- ORCID
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2015-09
- Volume
- 1852
- Issue
- 9
- Pages
- 1687-1699
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W256530927
- Cited by
- 163
- References
- 78
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 15 · 2023: 14 · 2022: 14 · 2021: 19 · 2020: 17 · 2019: 14 · 2018: 24 · 2017: 10 · 2016: 22 · 2015: 3
- FWCI
- 14.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Generalitat de Catalunya (2009/SGR00853)
- Spanish Ministerio de Ciencia e Innovación (SAF2011-23631, SAF2012-39852-C02-01, SAF2012-30708)
- CONACYT (Mexico) (0177594)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- high-fat diet, Alzheimer's disease, hippocampus, insulin signaling, mitochondrial homeostasis, metabolic syndrome, obesity, APP/PS1 mice, novel object recognition, hippocampal-dependent memory, oxidative phosphorylation, neurodegeneration
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