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. 2019 Feb;41(1):77-87.
doi: 10.1007/s11357-019-00051-9. Epub 2019 Feb 9.

Astaxanthin Supplementation Modulates Cognitive Function and Synaptic Plasticity in Young and Aged Mice

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Free PMC article

Astaxanthin Supplementation Modulates Cognitive Function and Synaptic Plasticity in Young and Aged Mice

Bethany Grimmig et al. Geroscience. .
Free PMC article

Abstract

The incidence of neurodegenerative disorders and cognitive impairment is increasing. Rising prevalence of age-related medical conditions is associated with a dramatic economic burden; therefore, developing strategies to manage these health concerns is of great public health interest. Nutritionally based interventions have shown promise in treatment of these age-associated conditions. Astaxanthin is a carotenoid with reputed neuroprotective properties in the context of disease and injury, while emerging evidence suggests that astaxanthin may also have additional biological activities relating to neurogenesis and synaptic plasticity. Here, we investigate the potential for astaxanthin to modulate cognitive function and neural plasticity in young and aged mice. We show that feeding astaxanthin to aged mice for 1 month improves performance on several hippocampal-dependent cognitive tasks and increases long-term potentiation. However, we did not observe an alteration in neurogenesis, nor did we observe a change in microglial-associated IBA1 immunostaining. This demonstrates the potential for astaxanthin to modulate neural plasticity and cognitive function in aging.

Keywords: Aging; Cognitive decline; Inflammation; Neuroplasticity; Nutraceutical.

Conflict of interest statement

Disclaimer

The contents of this presentation do not represent the views of the Department of Veterans Affairs or the United States Government.

Conflict of interest

PCB is the co-Founder of Natura Therapeutics, Inc., and has served on the scientific advisory board for Nutrex Hawaii.

Figures

Fig. 1
Fig. 1
One month of dietary supplementation of AXT was able to enhance early-phase LTP at the CA1-CA3 synapse in the hippocampus. Both age groups that consumed an AXT-enriched diet demonstrate an increased slope of the fEPSPs after theta-burst stimulation compared to their age-matched controls. Aged animals treated with AXT (A AXT) show enhanced LTP compared to the aged control mice (A CTL). Young ATX-supplemented animals (Y AXT) also show enhanced LTP compared to the young mice on the CTL diet (Y CTL) (a), and this trend remains significantly different during the last 10 min of the experiment (b). One-way ANOVA; F 24.72; **p < 0.01, ***p < 0.001. The observed trends in enhanced early-phase LTP were not due to direct dietary-induced alterations of synaptic transmission, indicated by similar relationships between stimulus intensity and synaptic response (c) or by short-term plasticity mediated at the presynaptic site (data not shown)
Fig. 2
Fig. 2
One month of dietary supplementation of AXT does not significantly alter neurogenesis in the dentate gyrus. AXT treatment does not significantly stimulate the proliferation of neural progenitor cells in the subgranular zone of the hippocampus (a) or increase the differentiation to neuronal lineage in the same region (b). Two-way ANOVA n.s.
Fig. 3
Fig. 3
Consuming a diet enriched with AXT does not significantly alter the expression of IBA 1 in the hippocampus (a), cortex (b), or striatum (c). Two-way ANOVA n.s.
Fig. 4
Fig. 4
One month of consuming a diet supplemented with AXT increased time of interaction with the novel object (a). One-way ANOVA, p < 0.001; F 4.436. Two-tailed T tests, *p < 0.0.5. The exploration of the familiar object was similar across all experimental conditions (b). One-way ANOVA n.s. This dietary effect on increased recognition of the novel object is apparent in both young and aged animals, although not due to alterations in locomotor activity around the test chamber (data not shown)
Fig. 5
Fig. 5
One month of dietary supplementation of AXT improves the memory retention of aged mice in the 24-h fear-conditioning paradigm, indicated by increased freezing behavior in response to the environment where they previously experienced aversive events (a). Two-way ANOVA, dietary effect, *p < 0.05; F 1, 89. Two-tailed T test, **p < 0.01. Both young and aged mice treated with AXT show an improved performance in the altered context paradigm, demonstrating an increase in freezing behavior to the presentation of the conditioned stimulus compared to the freezing behavior in the first phase of the test before exposure to the tone associated with the foot shock. However, the effect is only significant in the aged animals (b). Repeated measure ANOVA, *p < 0.05. Aged animals show more freezing behavior compared to the young during training. However, by the end of the training, mice show a comparable freezing response and there is no discernable influence of AXT on the learning curve (c). One-way ANOVA of the percent freezing during the last minute of training indicates no significant interaction

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