Chia seeds as a potential cognitive booster in the APP23 Alzheimer’s disease model

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

Additional file 1: of Indomethacin promotes survival of new neurons in the adult murine hippocampus accompanied by anti-inflammatory effects following MPTP-induced dopamine depletion

Figure S1. Effects of dopamine depletion and indomethacin treatment on the stages of adult hippocampal neurogenesis. Neuronal development originates from a Nestin-positive, triangular-shaped stem cell (type 1). Then, neurogenesis progresses over the stages of the putative progenitor cells (type 2a, type 2b, and type 3) and ends in the NeuN-positive mature granule cell. Neurotoxic treatment leads to a decreased number of newly generated (type 2a cells) and mature neurons, whereas indomethacin treatment afterwards promotes the development towards mature neurons. MPTP: 1-methyl-4-(2′-methylphenyl)-1,2,3,6-tetrahydropyridine hydrochloride; NeuN: neuronal nuclei. (TIF 624 kb