Chia Seed Does Not Improve Cognitive Impairment in SAMP8 Mice Fed with High Fat Diet.

BACKGROUND

Chia seed is an ancient seed with the richest plant source of α-linolenic acid, which has been demonstrated to improve metabolic syndrome associated risk factors. Under high fat diet (HFD) condition, the senescence-accelerated mouse-prone 8 (SAMP8) mice demonstrated worsen Alzheimer's disease (AD) related pathology compared to low fat diet fed SAMP8 mice.

OBJECTIVE

To explore whether chia seed supplementation might improve cognitive impairment under aging and metabolic stress via high fat diet (HFD) fed SAMP8 mice as a model.

DESIGN

SAMP8 mice and senescence-accelerated mouse-resistant 1 (SAMR1) were randomized into 4 groups, i.e., SAMR1 low fat diet group (SAMR1-LFD), SAMP8-HFD and SAMP8-HFD group supplemented with 10% chia seed (SAMP8-HFD+Chia). At the end of the intervention, cognitive function was measured via Morris water maze (MWM) test. Hippocampus and parietal cortex were dissected for further analysis to measure key markers involved AD pathology including Aβ, tau and neuro-inflammation.

RESULTS

During navigation trials of MWM test, mice in SAMP8-LFD group demonstrated impaired learning ability compared to SAMR1-LFD group, and chia seed had no effect on learning and memory ability for HFD fed SAMP8 mice. As for Alzheimer's disease (AD) related pathology, chia seed not only increased α-secretase such as ADAM10 and insulin degrading enzyme (IDE), but also increased β-secretase including beta-secretase 1 (BACE1) and cathepsin B, with an overall effects of elevation in the hippocampal Aβ level; chia seed slightly reduced p-Tauser404 in the hippocampus; while an elevation in neuro-inflammation with the activation of glial fibrillary acidic protein (GFAP) and Ibα-1 were observed post chia seed supplementation.

CONCLUSIONS

Chia seed supplementation did not improve cognitive impairment via MWM in HFD fed SAMP8 mice. This might be associated with that chia seed increased key enzymes involved both in non-amyloidogenic and amyloidogenic pathways, and neuro-inflammation. Future studies are necessary to confirm our present study.