astaxanthine and Cognitive-Dysfunction

Dementia and its first or transitional stage, mild cognitive impairment (MCI), is a major concern for the aging Japanese society. Thus, the use of dietary supplements to improve or maintain cognitive function has become a topic of public interest.. In this study, we evaluated the effects of a composite supplement containing food-derived antioxidants, specifically astaxanthin and sesamin (AS), on cognitive function in people with MCI.. Twenty-one healthy participants with MCI were recruited in our double-blind placebo-controlled pilot study. They were assigned to either an AS group, who received ingestible capsules containing AS, or a placebo group, who received identical placebo capsules. To assess cognitive functions, we performed the Japanese version of the Central Nervous System Vital Signs (CNSVS) test and the Alzheimer's Disease Assessment Scale-Cog test at baseline, after 6 weeks, and after 12 weeks of dietary supplementation.. The CNSVS test revealed significant improvements in psychomotor speed and processing speed in the AS group compared with the placebo group, suggesting that the daily supplementation of AS improved cognitive functions related to the ability to comprehend, and perform complex tasks quickly and accurately.. Our results provide support for the use of AS as a dietary supplementation for improving cognitive functions.

Topics: Aged; Cognitive Dysfunction; Dietary Supplements; Dioxoles; Double-Blind Method; Female; Humans; Lignans; Male; Middle Aged; Neuropsychological Tests; Pilot Projects; Treatment Outcome; Xanthophylls

Cognitive alterations are a common feature associated with many neurodegenerative diseases and are considered a major health concern worldwide. Cognitive alterations are triggered by microglia activation and oxidative/inflammatory processes in specific areas of the central nervous system. Consumption of bioactive compounds with antioxidative and anti-inflammatory effects, such as astaxanthin and spirulina, can help in preventing the development of these pathologies. In this study, we have investigated the potential beneficial neuroprotective effects of a low dose of astaxanthin (ASX) microencapsulated within spirulina (ASXSP) in female rats to prevent the cognitive deficits associated with the administration of LPS. Alterations in memory processing were evaluated in the Y-Maze and Morris Water Maze (MWM) paradigms. Changes in microglia activation and in gut microbiota content were also investigated. Our results demonstrate that LPS modified long-term memory in the MWM and increased microglia activation in the hippocampus and prefrontal cortex. Preventive treatment with ASXSP ameliorated LPS-cognitive alterations and microglia activation in both brain regions. Moreover, ASXSP was able to partially revert LPS-induced gut dysbiosis. Our results demonstrate the neuroprotective benefits of ASX when microencapsulated with spirulina acting through different mechanisms, including antioxidant, anti-inflammatory and, probably, prebiotic actions.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cognitive Dysfunction; Female; Humans; Lipopolysaccharides; Memory Disorders; Powders; Rats; Spirulina

We first explore whether aircraft noise (AN) induces cognitive deficit via inducing oxidative damage in multiple vital organs including intestines, hearts and hippocampus tissues. Second, we explore whether the AN-induced cognitive deficits and inflammatory and oxidative damage to multiple organs can be alleviated by Astaxanthin (AX) pretreatment.. Cognitive deficits were induced by subjecting the mice to AN 2 h daily for 7 consecutive days. An intragastrical dose of AX emulsifier (at the dose of daily feed intake [6 g] of a mouse three times weekly) was given to mice for consecutive 8 weeks prior to the start of AN. Cognitive functions were evaluated by using passive avoidance apparatus, Y-maze, Morris water maze and novel recognition test. Intestinal permeability was determined by measuring the intestinal clearance of fluorescein-isothiocyante. Evans Blue extravasation assay was used to measure the permeability of blood-brain-barrier. Inflammatory and oxidative damage to multiple organs were determined by measuring several pro-inflammatory cytokines and oxidative stress indicators in intestines; hearts and hippocampus.. Mice treated with AN displayed exacerbated stress reactions, cognitive deficits, gut barrier hyperpermeability, increased upload of lipopolysaccharide translocation, systemic pro-inflammatory cytokines overproduction, blood-brain-barrier hyperpermeability, hippocampal neuroinflammation and increased levels of oxidative stress indicators in intestine, heart and hippocampus. All of the above-mentioned disorders caused by AN were significantly (P < 0.05) reversed by AX.. Our data indicate that AX pretreatment alleviates cognitive deficits in aircraft noised mice by attenuating inflammatory and oxidative damage to intestines, hearts and hippocampal tissues.

Topics: Aircraft; Animals; Cognitive Dysfunction; Heart; Hippocampus; Inflammation; Intestinal Absorption; Intestines; Male; Mice; Mice, Inbred C57BL; Noise, Transportation; Oxidative Stress; Xanthophylls

Neuroprotective effect of astaxanthin-s-allyl cysteine diester (AST-SAC) against high glucose (HG)-induced oxidative stress in in vitro and cognitive decline under diabetes conditions in in vivo has been explored. Pretreatment of AST-SAC (5, 10 and 15 μM) dose-dependently preserved the neuronal cells (SH-SY5Y) viability against HG toxicity through i) decreasing oxidative stress (decreasing reactive oxygen species generation and increasing endogenous antioxidants level); ii) protecting mitochondrial function [oxidative phosphorylation (OXPHOS) complexes activity and mitochondrial membrane potential (MMP)]; and iii) decreasing p53 level thereby subsequently decreasing the level of apoptotic marker proteins. Male Spraque-Dawley rats were orally administered AST-SAC (1 mg/kg/day) for 45 days in streptozotocin-induced diabetes mellitus (DM) rats. AST-SAC administration prevented the loss of spatial memory in DM rats as determined using the novel object location test. AST-SAC administration alleviated the DM-induced injury in brain such as increased cholinesterases activity, elevated oxidative stress and mitochondrial dysfunction. Altogether, the results from the present study demonstrated that AST-SAC averted the neuronal apoptosis and preserved the cognitive function against HG toxicity under DM conditions.

Topics: Animals; Cell Line, Tumor; Cell Survival; Cognitive Dysfunction; Cysteine; Diabetes Mellitus, Experimental; Dose-Response Relationship, Drug; Glucose; Humans; Male; Mitochondria; Neurons; Oxidative Stress; Rats; Rats, Sprague-Dawley; Tumor Suppressor Protein p53; Xanthophylls

Topics: Administration, Oral; Alzheimer Disease; Amyloid beta-Peptides; Animal Shells; Animals; Cognitive Dysfunction; Disease Models, Animal; Lipid Peroxidation; Male; Maze Learning; Memory Disorders; Oxidative Stress; Penaeidae; Rats; Rats, Wistar; Vitamin E; Xanthophylls

Alzheimer's disease is characterized by progressive disruption of cholinergic neurotransmission and impaired cognitive functions. In rodents, scopolamine has been used to induce cholinergic dysfunction resulting in cognitive impairments and an increment of oxidative stress in the brain. Here we tested whether oxidative stress can be attenuated via an antioxidant (astaxanthin) to rescue scopolamine-induced spatial memory. For this purpose, we administered either 0.9% saline (control), or scopolamine (SCP), or scopolamine plus astaxanthin (SCP + AST) to Swiss albino mice (ten weeks old; n = 20) for 28 consecutive days and subsequently examined animals' locomotor activity, spatial learning, and memory performance. The mice were then euthanized and prefrontal cortex (PFC), striatum (ST), hippocampus (HP), and liver tissues were assayed for antioxidant enzymes, glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and nitric oxide (NO). The SCP group exhibited impaired spatial learning and significantly altered levels of antioxidant enzymes and NO in the PFC, ST, and HP. In contrast, SCP + AST treatment did not cause spatial learning deficits. Furthermore, this condition also showed unaltered levels of SOD and NO in the ST and HP. Taken together, our results show that scopolamine may interrupt the striatal-hippocampal cholinergic activity resulting in impaired spatial memory. At the same time, these impairments are extinguished with astaxanthin by preventing oxidative damage in the striatal-hippocampal cholinergic neurons. Therefore, we suggest astaxanthin as a potential treatment to slow the onset or progression of cognitive dysfunctions that are elicited by abnormal cholinergic neurotransmission in Alzheimer's disease.

Topics: Acetylcholine; Alzheimer Disease; Animals; Antioxidants; Brain; Catalase; Cognition; Cognitive Dysfunction; Disease Models, Animal; Glutathione; Hippocampus; Lipid Peroxidation; Male; Maze Learning; Memory Disorders; Mice; Oxidative Stress; Scopolamine; Spatial Memory; Superoxide Dismutase; Xanthophylls

Increasing evidence indicates that environmental tobacco smoke (ETS) impairs cognitive function and induces oxidative stress in the brain. Recently, astaxanthin (ATX), a marine bioactive compound, has been reported to ameliorate cognitive deficits. However, the underlying pathogenesis remains unclear. In this study, ATX administration (40 mg/kg and 80 mg/kg, oral gavage) and cigarette smoking were carried out once a day for 10 weeks to investigate whether the p38 MAPK is involved in cognitive function in response to ATX treatment in the cortex and hippocampus of ETS mice. Results indicated that ATX administration improved spatial learning and memory of ETS mice (

Topics: Animals; Catalase; Cerebral Cortex; Cognition; Cognitive Dysfunction; Cytokines; Glutathione; Hippocampus; Interleukin-6; Male; Malondialdehyde; Mice; NF-kappa B; Nicotiana; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Smoke; Tumor Necrosis Factor-alpha; Xanthophylls

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.

Topics: Aging; Animals; Behavior, Animal; Cognition; Cognitive Dysfunction; Dietary Supplements; Hippocampus; Inflammation; Long-Term Potentiation; Male; Mice; Mice, Inbred C57BL; Microglia; Neurodegenerative Diseases; Neurogenesis; Neuronal Plasticity; Neuroprotective Agents; Xanthophylls

Chemobrain refers to a common sequelae experienced by 15-80% of cancer patients exposed to chemotherapeutics. The antineoplastic agent doxorubicin (DOX) has been implicated in a strenuous neurotoxicity manifested as decline in cognitive functions, most probably via cytokine-induced oxidative and nitrosative damage to brain tissues. Astaxanthin (AST), a naturally occurring carotenoid, is reputable for its outstanding antioxidant, anti-inflammatory, and antiapoptotic activities. Therefore, the aim of the current study was to investigate the potential neuroprotective and memory-enhancing effects of AST against DOX-induced behavioral and neurobiological abnormalities. Briefly, AST treatment (25 mg/kg) significantly protected against DOX-induced memory impairment. Furthermore, AST restored hippocampal histopathological architecture, halted DOX-induced oxidative and inflammatory insults, mitigated the increase in acetylcholinesterase activity, and consistently downregulated the overactive apoptotic machineries. In conclusion, these findings suggest that AST offers neuroprotection against DOX-induced cognitive impairment which could be explained at least partly by its antioxidant, anti-inflammatory, and antiapoptotic effects.

Topics: Acetylcholinesterase; Animals; Anti-Inflammatory Agents; Antioxidants; Apoptosis; Behavior, Animal; Biomarkers; Cognitive Dysfunction; Disease Models, Animal; Doxorubicin; Glial Fibrillary Acidic Protein; Hippocampus; Inflammation; Male; Models, Biological; Motor Activity; Nerve Degeneration; Neuroprotective Agents; Oxidative Stress; Rats; Xanthophylls