ArticlePhysiological reports2018
Evaluation of neuropathological effects of a high-fat high-sucrose diet in middle-aged male C57BL6/J mice.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 29 citations in OpenAlex.
- Murine Non-Transgenic Models of Alzheimer's Disease Pathology: Focus on Risk Factors.Brain sciences · 2025Review
- Nutrigenomic influence of a curcumin-supplemented high glycemic diet on hippocampal microvasculature in male C57BL/6J mice.Frontiers in nutrition · 2025Article
- APOE4 rat model of Alzheimer's disease: sex differences, genetic risk and diet.BMC neuroscience · 2024Article
- COMPARATIVE EFFECT OF A HIGH FAT WITH OR WITHOUT HIGH LEVELS OF SUCROSE DIETS ON PERIPHERAL NEUROPATHY IN C57BL/6J MICE.Journal of diabetic complications & therapy · 2022Article
- Resveratrol, Metabolic Dysregulation, and Alzheimer's Disease: Considerations for Neurogenerative Disease.International journal of molecular sciences · 2021Review
- Examination of BDNF Treatment on BACE1 Activity and Acute Exercise on Brain BDNF Signaling.Frontiers in cellular neuroscience · 2021Article
- Understanding the Link Between Maternal Overnutrition, Cardio-Metabolic Dysfunction and Cognitive Aging.Frontiers in neuroscience · 2021Review
- High-Fat and High-Sucrose Diets Impair Time-of-Day Differences in Spatial Working Memory of Male Mice.Obesity (Silver Spring, Md.) · 2020Article
- Adenosine Metabolism in the Cerebral Cortex from Several Mice Models during Aging.International journal of molecular sciences · 2020Article
- Dysregulation of protein degradation in the hippocampus is associated with impaired spatial memory during the development of obesity.Behavioural brain research · 2020Article
- Role of Insulin Resistance in the Alzheimer's Disease Progression.Neurochemical research · 2020Review
- Resolvin D1 Prevents the Impairment in the Retention Memory and Hippocampal Damage in Rats Fed a Corn Oil-Based High Fat Diet by Upregulation of Nrf2 and Downregulation and Inactivation of pNeurochemical research · 2020Article
- Detection of presymptomatic Alzheimer's disease through breath biomarkers.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Evaluation of neuropathological effects of a high-fat high-sucrose diet in middle-aged male C57BL6/J mice.Physiological reports · 2018Article
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction related to diet-induced obesity has recently been linked to the pathogenesis of sporadic Alzheimer's disease (AD). However, the underlying mechanisms linking obesity and AD remain unclear. The purpose of this study was to examine early alterations in brain insulin signaling, inflammatory/stress markers, and energetic stress in a model of diet-induced obesity during middle age. Male C57BL/6J mice were randomized to either a control diet (AGE n = 12) or high-fat and sucrose diet (AGE-HFS n = 12) for 13-weeks from 20-weeks of age. Prefrontal cortex and hippocampal samples were collected at 20-weeks of age (BSL n = 11) and at 33-weeks of age (AGE and AGE-HFS). The HFS diet resulted in increased body weight (30%; P = 0.0001), increased %fat mass (28%; P = 0.0001), and decreased %lean mass (33%; P = 0.0001) compared to aged controls. In the prefrontal cortex, AGE-HFS resulted in increased 5' adenosine monophosphate - activated protein kinase (AMPK) phosphorylation (P = 0.045). In the hippocampus, AGE-HFS resulted in increased extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) phosphorylation and protein kinase B (Akt) serine473 and glycogen synthase kinase (GSK) phosphorylation (P < 0.05). Results from this study demonstrate that aging combined with a HFS diet results in increased inflammation (pERK and pJNK) and energetic stress (pAMPK) in the hippocampus and prefrontal cortex, respectively. Together these novel results provide important information for future targets in early AD pathogenesis.
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