Impact of Krill Oil Supplementation on Neuroinflammation and Spatial Memory in Aged Rats

Objective Investigate the potential of dietary krill oil (KO), a marine‐based, long chain, omega‐3 ( n ‐3) polyunsaturated fatty acid (PUFA), to negate the deleterious effects of high fat diets and aging on neuroinflammation and spatial learning in a rat model. Background/Hypothesis KO exhibits anti‐inflammatory properties comparable to other sources of n ‐3 PUFA, but with several biochemical advantages. Phospholipid‐bound fatty acids in KO exhibit improved bioavailability when compared to triacylglyceride bound n ‐3 PUFA such as fish oil. Moreover, KO contains astaxanthin, a powerful antioxidant that counters harmful oxidative stress in the brain, as well as choline which is an essential neurotransmitter precursor with neuroprotective properties. Hence, we hypothesized that KO supplementation would improve deficiencies in spatial learning and elevated neuroinflammatory protein levels induced by high fat diet and normal aging in rats. Methods Thirty‐two male, Sprague Dawley rats, aged 15 months were divided into four dietary groups consisting of varying amounts of saturated fats, with and without krill oil supplementation: Control (CON), Control with krill oil (CONKO), High fat (HF), High fat with krill oil (HFKO). HF and CON experimental diets consisted of 60% and 23% calories from saturated fats, respectively. Food intake and body weight were assessed weekly. After 12‐weeks of dietary supplementation, Morris Water Maze (MWM) testing was conducted to compare spatial learning abilities between groups. Moreover, inflammatory cytokine concentrations, including interleukin (IL)‐1β, IL‐4, IL‐6, IL‐10 and tumor necrosing factor‐α (TNF‐α), were analyzed using multiplex bead‐based protein assays. Results Despite evidence of learning by each group over the course of MWM testing, no significant difference between dietary groups in reaching the platform was identified. Furthermore, no statistically significant difference in inflammatory cytokines was identified. Total food consumption was significantly less in the HF group when compared to CON (p=.047) and CONKO (p=.030), whereas body weight was significantly higher in the HFKO group when compared to CON (p=.024) and CONKO (p=.030). Otherwise, no significant difference in food consumption or body weight was identified. Conclusions KO supplementation did not significantly improve the effects of aging and high fat diet consumption on spatial memory or neuroinflammatory signaling proteins. Some evidence suggests that the unique properties of KO, a more novel source n ‐3 PUFA, have the potential to decrease neuroinflammation and improve cognition. Indeed, considering an aging population, the proliferation of western‐style diets, and the associated increase in neurodegenerative diseases such as Alzheimer’s disease, there is a need for preventive interventions. Further investigations are still needed to weigh the potential benefits of n ‐3 dietary supplementation, aging, obesity, and neurodegenerative disease.