ArticleScientific reports2020
Chia seeds as a potential cognitive booster in the APP23 Alzheimer's disease model.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Nutritional and Health Potential of Edible Seeds: Micronutrient Bioavailability and Mechanistic Insights.Food science & nutrition · 2026Review
- Sex-specific changes in energy demand during the preplaque stage in a transgenic Alzheimer's mouse model.Biology of sex differences · 2025Article
- Chia (Salvia hispanica L.), a functional 'superfood': new insights into its botanical, genetic and nutraceutical characteristics.Annals of botany · 2024Review
- Isolation ofMicroorganisms · 2024Article
- Harmony in Motion: Unraveling the Nexus of Sports, Plant-Based Nutrition, and Antioxidants for Peak Performance.Antioxidants (Basel, Switzerland) · 2024Review
- Enriching the Mediterranean diet could nourish the brain more effectively.Frontiers in nutrition · 2024Review
- Chia seeds oil ameliorate chronic immobilization stress-induced neurodisturbance in rat brains via activation of the antioxidant/anti-inflammatory/antiapoptotic signaling pathways.Scientific reports · 2023Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose hypometabolism potentially contributes to Alzheimer's disease (AD) and might even represent an underlying mechanism. Here, we investigate the relationship of diet-induced metabolic stress and AD as well as the therapeutic potential of chia seeds as a modulator of glucose metabolism in the APP23 mouse model. 4-6 (pre-plaque stage, PRE) and 28-32 (advanced-plaque stage, ADV) weeks old APP23 and wild type mice received pretreatment for 12 weeks with either sucrose-rich (SRD) or control diet, followed by 8 weeks of chia seed supplementation. Although ADV APP23 mice generally showed functioning glucose homeostasis, they were more prone to SRD-induced glucose intolerance. This was accompanied by elevated corticosterone levels and mild insulin insensitivity. Chia seeds improved spatial learning deficits but not impaired cognitive flexibility, potentially mediated by amelioration of glucose tolerance, attenuation of corticosterone levels and reversal of SRD-induced elevation of pro-inflammatory cytokine levels. Since cognitive symptoms and plaque load were not aggravated by SRD-induced metabolic stress, despite enhanced neuroinflammation in the PRE group, we conclude that impairments of glucose metabolism do not represent an underlying mechanism of AD in this mouse model. Nevertheless, chia seeds might provide therapeutic potential in AD as shown by the amelioration of cognitive symptoms.
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Registered trials
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