astaxanthine and Memory-Disorders

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

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

Astaxanthin (AXT), a xanthophyll carotenoid compound, has potent antioxidant, anti-inflammatory and neuroprotective properties. Neuroinflammation and oxidative stress are significant in the pathogenesis and development of Alzheimer's disease (AD). Here, we studied whether AXT could alleviate neuroinflammation, oxidative stress and memory loss in lipopolysaccharide (LPS) administered mice model. Additionally, we investigated the anti-oxidant activity and the anti-neuroinflammatory response of AXT in LPS-treated BV-2 microglial cells. The AXT administration ameliorated LPS-induced memory loss. This effect was associated with the reduction of LPS-induced expression of inflammatory proteins, as well as the production of reactive oxygen species (ROS), nitric oxide (NO), cytokines and chemokines both in vivo and in vitro. AXT also reduced LPS-induced β-secretase and Aβ

Topics: Amyloid beta-Protein Precursor; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Avoidance Learning; Cell Line; Inflammation; Lipopolysaccharides; Maze Learning; Memory Disorders; Mental Recall; Mice; Mice, Inbred ICR; Microglia; Oxidative Stress; Signal Transduction; STAT3 Transcription Factor; Xanthophylls

Oxidative stress has been implicated in the pathogenesis of neurodegenerative disorders, such as vascular cognitive impairment (VCI). The present study was performed to investigate the potential neuroprotective effect of the antioxidant astaxanthin (ATX) in a mouse model of VCI. VCI was induced in male ICR mice by repeated occlusion of the bilateral common carotid artery, leading to repeated cerebral ischemia/reperfusion (IR) injury. After surgery, the mice received ATX or an equal volume of vehicle by daily intragastric administration for 28days. The results showed that ATX treatment ameliorated learning and memory deficits after repeated cerebral IR. ATX administration rescued the number of surviving pyramidal neurons in the CA1 and CA3 regions. The concentration of malondialdehyde was decreased, and the levels of reduced glutathione and superoxide dismutase in the hippocampus were increased. Electron microphotography revealed that damage to the ultrastructure of neurons was also reduced by ATX administration. In addition, the expression levels of Cytochrome C (Cyt C), cleaved Caspase-3 and Bax were lower and the expression of Bcl-2 was higher compared to control IR mice. Our findings demonstrate that ATX is able to suppresse learning and memory impairment caused by repeated cerebral IR and that this effect is associated with attenuation of oxidative stress.

Topics: Animals; Antioxidants; Apoptosis; Brain Ischemia; Cytochromes c; Dementia, Vascular; Disease Models, Animal; Glutathione; Hippocampus; Learning; Male; Malondialdehyde; Maze Learning; Memory Disorders; Mice; Mice, Inbred ICR; Neurons; Neuroprotective Agents; Oxidative Stress; Reperfusion; Reperfusion Injury; Superoxide Dismutase; Xanthophylls

Cognitive function is impaired by imbalanced diet consumption. High-fat diet (HFD) induces oxidative stress and metabolic disorders, which results in neuronal damage and interferes with synaptic transmission and neurogenesis; hence, a decline in learning and memory. Antioxidants are believed to have positive effects on cognitive function. The objective of this study was to determine the relation between the chronic consumption of a HFD and antioxidants on passive avoidance learning (PAL) in male rats. Wistar rats were randomly assigned into the following five groups (N=6-8): Control group-consumed an ordinary diet; HFD group-received high-fat diets only; ANO group-received HFD plus antioxidants (vitamins C and E and astaxanthin (ASX)); RHFD group-received the restricted HFD (30% less than the HFD group); and RANO group-received restricted HFD plus antioxidants (30% less than the ANO group). Following 6months of controlled dietary condition as mentioned above, in each experimental group, the PAL was assessed using shuttle box apparatus. Our results showed that HFD caused a decrease in step through latency in the retention test (STLr) and increased the time spent in the dark compartment in the retention test (TDC) when compared to the control group. Antioxidant supplementation caused an increase in STLr and decrease in TDC when compared to the control group. Furthermore, RHFD and RANO had no significant effect on STLr and TDC compared with the control group. According to our results, HFD impairs PAL and the combination of vitamins C and E and astaxanthin improves PAL deficits in the HFD group.

Topics: Animals; Antioxidants; Ascorbic Acid; Avoidance Learning; Cholesterol; Diet, High-Fat; Drug Therapy, Combination; Male; Memory Disorders; Rats; Rats, Wistar; Triglycerides; Vitamin E; Xanthophylls