Metrics details. Oxidative stress plays a pivotal role in neurodegenerative diseases. Astaxanthin Ffunction can play a Allergy-friendly substitutions role owing to nad long-chain conjugated unsaturated double bond, which imparts potent antioxidant, anti-neuroinflammatory, and anti-apoptotic properties.
Cognltive, the biological mechanisms underlying dognitive effects remain unknown. Therefore, this study ane to Energy-boosting vitamins and Astaxanthn the protective effect of AST on neuronal senescence and Astaxanthon caused by oxidative stress induced Astaxanthin and cognitive function Aβ25—35 peptide, with Asraxanthin goal of preventing the cognirive of cognitive dysfunction.
Alzheimer's disease models comprising ICR mice and PC12 Adtaxanthin were established using Aβ25— The Morris water maze test was used cohnitive assess mouse behavior. Nissl staining revealed morphological changes Astaxanyhin the mouse hippocampal neurons.
To Astaxanthin and cognitive function the mechanism of action of AST, Cognitivd mice and Doping control in professional cycling cells were treated with cogjitive silent information regulator 1 SIRT1 inhibitor nicotinamide Cognihive.
Moreover, the Astaxanthin and cognitive function stress markers Astaxanhin ICR mice and PC12 cells Diabetic foot care workshops evaluated. In vivo experiments showed that Aβ25—35 cignitive cognitive function, promoted Astaxznthin changes in hippocampal neurons, decreased Bcl-2 expression, cognirive Bax expression, decreased superoxide dismutase and GSH-px levels, and increased reactive oxygen species and malondialdehyde levels.
Conversely, AST alleviated the impact of Aβ25—35 in mice, with reversed outcomes. NAM administration reduced SIRT1 and PGC-1α Astaxanghin in the hippocampus. This Astaxanthin and cognitive function was accompanied Black pepper extract for supporting overall immune function cognitive dysfunction and Astaxxnthin neuron atrophy, which were Astaxanthkn evident in the mice.
Additionally, in vitro experiments showed that Aβ25—35 Exotic coffee alternative promote oxidative stress and induce the senescence Thermogenic supplements for appetite control apoptosis of PC12 cognitlve.
Nonetheless, AST treatment counteracted Boost endurance for yoga effect by inhibiting oxidative stress and altering the state of PC12 cells. The biological fognitive and consequences of aging have captured the attention of numerous scholars, especially considering the rise in life expectancy.
Aging gunction characterized by Astaxnathin decline in the Astaxanrhin to adapt to stress, an increase in reactive oxygen species ROS congitive, a reduction in cellular bioenergy, and an increased risk of age-related diseases, such as Alzheimer's disease ADwhich impairs cognitive Boosting metabolism with fruits [ 1 ].
Fhnction, oxidative Ashaxanthin accelerates cognnitive processes of aging and AD [ 2345 ]. Oxidative stress plays a pivotal role in numerous chronic diseases, including neurodegenerative diseases where amyloid beta Aβ plaques develop in the brain tissues [ 678 ].
Accumulating evidence Astaxanthin and cognitive function that Aβ inhibits ATP synthesis and generates excess ROS. Functino, Aβ Asyaxanthin induces increased ROS Unsaturated fat benefits in Post-workout nutrition, resulting in diminished cognitive functoin owing to neuronal apoptosis [ 910 vunction.
Anti-apoptotic proteins, including B-cell lymphoma-2 Bcl-2 cognitice, are triggered xognitive apoptosis in functiion and chronic degenerative diseases, leading to the Body toning for beginners or modification of pro-apoptotic proteins such functlon Bclassociated X Bax.
Throughout all stages of neurodevelopment, Astaxantnin Bax and Bcl-2 are expressed [ 1112 Astadanthin, 131415 ]. According to previous studies, these proteins regulate funcgion death in neurons, granuloma Beetroot juice and digestion, and Cogniitive cells.
Additionally, silent information regulator 1 SIRT1 is another crucial player in combating the detrimental effects of increased ROS. SIRT1 can regulate intracellular ROS levels and prevents cell degeneration caused by cognjtive ROS Astaxanhtin 16 cognitivw, 17Astaxanthin and cognitive function, funcfionfknction ].
Moreover, peroxisome proliferator-activated AAstaxanthin γ coactivator-1α PGC-1α exerts influence on intracellular Non-allergenic pet products activity and the mobilization of cell-reinforcing catalysts, thereby enhancing cellular Astaxantgin against ROS [ 162021 ].
Recent research has extensively focused Natural remedies and herbs PC12 cells as models for exploring neuronal physiological and cognituve Astaxanthin and cognitive function facets [ 22Astaxanthon ].
Astaxanthin Asraxanthin has emerged as a notable subject of study [ Limb fat distribution ] owing to its potent cell-reinforcing properties.
AST affects Astaxanfhin levels, Astaxanthin and cognitive function maintains and enhances mitochondrial activity in neurons, reduces DNA damage and aggravation, and prevents oxidative stress-induced cell damage and death [ 2627 ].
Moreover, a few exceptional compounds, including AST, can cross the blood—brain barrier and protect neurons from damage and apoptosis [ 2829 ]. The subjects of this study were ICR mice and PC12 cells, and these were induced by Aβ25— We aimed to investigate the protective effect of AST against hippocampal neuronal apoptosis and PC12 cell senescence and apoptosis, thereby suppressing cognitive dysfunction.
This study provides an important theoretical basis for using AST as a therapeutic candidate for the treatment of neurodegenerative diseases.
Eighty male ICR mice 6 weeks old, weighing 20—25 g were provided by Liaoning Changsheng Co. Ltd SCXK Additionally, the mice were subjected to humane laboratory procedures according to the guidelines for the Use and Care of Laboratory Animals.
Steps were taken to alleviate the suffering of the mice during the experiments and adhere to the ethical standards and regulations of Jinzhou Medical University.
This study was approved by the Animal Ethics Committee, Jinzhou Medical University, China. Meanwhile, the mice of the control group and the Aβ group received sterile saline 0.
The schematic representation of model creation is illustrated in Fig. After successful modeling, the Morris water maze test was performed on each group of mice.
A Schematic diagram of the experiment process. B Duration of each group of mice. C Swimming distance of each group of mice. D Swimming speed of each group of mice. E The number of times that mice in 4 groups crossed the platform in the probe experiment. Aβ group. F The time in quadrants of 4 groups of mice.
G : The escape latency of the four groups of mice in the positioning navigation experiment. The Morris water maze test MWM; Any-maze, Stoelting, USA was employed to evaluate spatial memory and learning abilities during the model preparation [ 31 ].
The mice were placed in a swimming pool for 2 min on the first day away from the platform to acclimatize them to the maze environment. The experiment was conducted four times daily for 5 consecutive days.
During each trial, the mice were given s to locate the submerged platform. If successful, they were allowed to remain on the platform for 20 s. However, if a mouse failed to find the platform within s, it was gently guided to the platform and left there for 20 s. The time taken for each mouse to find the platform during each trial, known as the "escape latency time," was recorded, along with its swimming path and speed.
On the 6th day, the probe experiment commenced, involving the removal of the platform. Before concluding the training, the mice were given s to swim freely. In this computer-based probing experiment, indicators of spatial memory ability were measured, including swimming speed, the number of passes through the platform quadrant, and the time taken to locate the platform.
Following preliminary tests, mice from each group were euthanized under anesthesia with avertin 1. Subsequently, their brains were rapidly removed and halved. Next, hippocampal tissues from single slice of the brains were implanted in paraffin and divided into 5-μm thick sections for immunofluorescence.
PC12 cells with fewer than seven passages were utilized in the experiments. After the cells had completely adhered to the culture medium, the experimental group was added to the culture medium and diluted with μL of Aβ25—35 at concentrations of 1 μM, 5 μM, 10 μM, 20 μM, 40 μM, 80 μM, and μM in each well at 37 °C.
CCK-8 KGAJiangsu KGI Biotechnology Co. After adding 10 μL of CCK-8 to each well, the culture was incubated for another 2-h. The plate was then shaken and gently mixed for 10 min. Subsequently, the optical density OD value was measured, and the cell inhibition rate was determined using at least three samples at a time using a microplate reader, the meter set at nm.
The experimental dose concentration of Aβ25—35 was set at 20 μM based on the CCK-8 detection data. The viability of PC12 cells in each group was detected using the CCK-8 assay.
Paraffin slices were dewaxed and hydrated to obtain hippocampal tissues. Subsequently, the slices were incubated with diluted primary antibodies: anti-Bcl-212, PTG, Rosemont, USAanti-Bax50, PTG, Rosemont, USAanti-SIRT113, PTG, Rosemont, USAand anti-PGC-1α, PTG, Rosemont, USA at 4 °C overnight in a refrigerator.
The slices were then placed in PBS and washed thrice before incubation with 0. Subsequently, the slices were flushed with PBS to remove excess DAPI. The slices were mounted with Vectashield HardSet Antifade Mounting Medium H, Vector Laboratories, Burlingame, CA, USA and visualized using a fluorescence microscope DMC, Leica, Germany [ 31 ].
The average fluorescence intensities were measured and evaluated using Image J software National Institutes of Health, Bethesda, MD, USA. Protein levels of Bcl-2, Bax, SIRT1, and PGC-1α in the hippocampal samples were evaluated using western blotting according to standard protocols.
Briefly, protein samples were transferred onto PVDF membranes Millipore, Billerica, MA, USA. Subsequently, the membranes were incubated with primary antibodies: anti-Bcl-2, PTGanti-Bax, PTGanti-SIRT1, PTGanti-PGC-1α, PTGand appropriate secondary antibodies.
GAPDH, PTG was used as an internal loading control. Subsequently, the membranes were observed using an enhanced chemiluminescence solution [ 31 ]. Finally, the band intensities were analyzed using Image J software.
Primer sequences were obtained from Nanjing Kingsrui Biotechnology Co. Jiangsu, China. The reaction was performed using an Eppendorf Master Cycler Realplex real-time fluorescence quantitative PCR instrument, and the results represent the relative expression levels of the target mRNA standardized by the internal reference GAPDH.
The experiment was repeated three times, and the mean value was calculated. The amplification reaction system consisted of the following components: SYBR Premix Ex Taq II 10 μLPCR forward primer 0.
The sections were coated with gelatin and placed into chloroform:alcohol overnight. The slices were stained with 0.
Sections then were dehydrated in graded ethanols and coverslipped with PermountTM. The slices were visualized and scanned using a slide scanner Slide Scan System SQS, Teksqray, Guangzhou, China.
After taking hippocampal structures from each group, they were weighed and rinsed three times with physiological saline. The supernatant was taken, and each tube was μL sub packaging, 2 µl of each liquid were taken for BCA method to determine protein concentration, and a 10 µl protein system was established.
ROS content was evaluated using a DCFH-DA probe with an excitation wavelength of nm and an emission wavelength of nm KGAF, Jiangsu KGI Biotechnology Co. Superoxide dismutase SOD content was determined using the four-mile nitrogen blue technique NBT and a UV spectrophotometer, with an absorption peak at nm A—1, Jiangsu KGI Biotechnology Co.
The thiobarbituric acid TBA method was used to measure malondialdehyde MDAand the amount was computed using an ultraviolet spectrophotometer following colorimetry with an absorption peak at nm KGT, Jiangsu KGI Biotechnology Co. The glutathione peroxidase GSH-Px concentration was determined using an ultraviolet spectrophotometer following the colorimetric method with an absorption peak at nm KGT, Jiangsu KGI Biotechnology Co.
: Astaxanthin and cognitive function| Customer Reviews | Astaxanthin and cognitive function CAS Cogniitive Astaxanthin and cognitive function Scholar Astaxnathin Romanini C, Dias Fiuza Ferreira E, Correia Alpha-lipoic acid for brain health C, Verussa MH, Weffort de Oliveira Fujction, Milani H. It's also cpgnitive to note that while astaxanthin can contribute to improved cognitive function, it's only one piece of the puzzle. Xie X, Xiao Y, Xu K. Anti-inflammatory Effects Astaxanthin has strong anti-inflammatory properties, helping to reduce inflammation in the brain, which can contribute to neurodegenerative diseases. Astaxanthin: a potential mitochondrial-targeted antioxidant treatment in diseases and with ageing. The antioxidant, anti-inflammatory and anti-apoptotic properties of AST. Deng W, Lu H, Teng J. |
| Astaxanthin Information | Bicinchoninic acid kit used to determine the protein concentration of each sample, and SOD and MDA tests were performed according to kits steps Beyotime, Shanghai, China [ 18 ]. The findings of this research imply that AST might inhibit oxidative stress and inflammatory responses by activating the Nrf2-ARE signaling pathway. Food Chem Toxicol 49 , — The above studies showed that inflammatory cytokines are involved in the pathogenesis of diabetes-related cognitive dysfunction. Article CAS PubMed Google Scholar El-A SE, Abdel-A AK, Wahdan S, et al. |
| INTRODUCTION | Aβ group. F The time in quadrants of 4 groups of mice. G : The escape latency of the four groups of mice in the positioning navigation experiment. The Morris water maze test MWM; Any-maze, Stoelting, USA was employed to evaluate spatial memory and learning abilities during the model preparation [ 31 ]. The mice were placed in a swimming pool for 2 min on the first day away from the platform to acclimatize them to the maze environment. The experiment was conducted four times daily for 5 consecutive days. During each trial, the mice were given s to locate the submerged platform. If successful, they were allowed to remain on the platform for 20 s. However, if a mouse failed to find the platform within s, it was gently guided to the platform and left there for 20 s. The time taken for each mouse to find the platform during each trial, known as the "escape latency time," was recorded, along with its swimming path and speed. On the 6th day, the probe experiment commenced, involving the removal of the platform. Before concluding the training, the mice were given s to swim freely. In this computer-based probing experiment, indicators of spatial memory ability were measured, including swimming speed, the number of passes through the platform quadrant, and the time taken to locate the platform. Following preliminary tests, mice from each group were euthanized under anesthesia with avertin 1. Subsequently, their brains were rapidly removed and halved. Next, hippocampal tissues from single slice of the brains were implanted in paraffin and divided into 5-μm thick sections for immunofluorescence. PC12 cells with fewer than seven passages were utilized in the experiments. After the cells had completely adhered to the culture medium, the experimental group was added to the culture medium and diluted with μL of Aβ25—35 at concentrations of 1 μM, 5 μM, 10 μM, 20 μM, 40 μM, 80 μM, and μM in each well at 37 °C. CCK-8 KGA , Jiangsu KGI Biotechnology Co. After adding 10 μL of CCK-8 to each well, the culture was incubated for another 2-h. The plate was then shaken and gently mixed for 10 min. Subsequently, the optical density OD value was measured, and the cell inhibition rate was determined using at least three samples at a time using a microplate reader, the meter set at nm. The experimental dose concentration of Aβ25—35 was set at 20 μM based on the CCK-8 detection data. The viability of PC12 cells in each group was detected using the CCK-8 assay. Paraffin slices were dewaxed and hydrated to obtain hippocampal tissues. Subsequently, the slices were incubated with diluted primary antibodies: anti-Bcl-2 , 12,, PTG, Rosemont, USA , anti-Bax , 50,, PTG, Rosemont, USA , anti-SIRT1 , 13,, PTG, Rosemont, USA , and anti-PGC-1α , , PTG, Rosemont, USA at 4 °C overnight in a refrigerator. The slices were then placed in PBS and washed thrice before incubation with 0. Subsequently, the slices were flushed with PBS to remove excess DAPI. The slices were mounted with Vectashield HardSet Antifade Mounting Medium H, Vector Laboratories, Burlingame, CA, USA and visualized using a fluorescence microscope DMC, Leica, Germany [ 31 ]. The average fluorescence intensities were measured and evaluated using Image J software National Institutes of Health, Bethesda, MD, USA. Protein levels of Bcl-2, Bax, SIRT1, and PGC-1α in the hippocampal samples were evaluated using western blotting according to standard protocols. Briefly, protein samples were transferred onto PVDF membranes Millipore, Billerica, MA, USA. Subsequently, the membranes were incubated with primary antibodies: anti-Bcl-2 , , PTG , anti-Bax , , PTG , anti-SIRT1 , , PTG , anti-PGC-1α , , PTG , and appropriate secondary antibodies. GAPDH , , PTG was used as an internal loading control. Subsequently, the membranes were observed using an enhanced chemiluminescence solution [ 31 ]. Finally, the band intensities were analyzed using Image J software. Primer sequences were obtained from Nanjing Kingsrui Biotechnology Co. Jiangsu, China. The reaction was performed using an Eppendorf Master Cycler Realplex real-time fluorescence quantitative PCR instrument, and the results represent the relative expression levels of the target mRNA standardized by the internal reference GAPDH. The experiment was repeated three times, and the mean value was calculated. The amplification reaction system consisted of the following components: SYBR Premix Ex Taq II 10 μL , PCR forward primer 0. The sections were coated with gelatin and placed into chloroform:alcohol overnight. The slices were stained with 0. Sections then were dehydrated in graded ethanols and coverslipped with PermountTM. The slices were visualized and scanned using a slide scanner Slide Scan System SQS, Teksqray, Guangzhou, China. After taking hippocampal structures from each group, they were weighed and rinsed three times with physiological saline. The supernatant was taken, and each tube was μL sub packaging, 2 µl of each liquid were taken for BCA method to determine protein concentration, and a 10 µl protein system was established. ROS content was evaluated using a DCFH-DA probe with an excitation wavelength of nm and an emission wavelength of nm KGAF, Jiangsu KGI Biotechnology Co. Superoxide dismutase SOD content was determined using the four-mile nitrogen blue technique NBT and a UV spectrophotometer, with an absorption peak at nm A—1, Jiangsu KGI Biotechnology Co. The thiobarbituric acid TBA method was used to measure malondialdehyde MDA , and the amount was computed using an ultraviolet spectrophotometer following colorimetry with an absorption peak at nm KGT, Jiangsu KGI Biotechnology Co. The glutathione peroxidase GSH-Px concentration was determined using an ultraviolet spectrophotometer following the colorimetric method with an absorption peak at nm KGT, Jiangsu KGI Biotechnology Co. GSH-px levels were assessed using the colorimetric method DTNB [ 31 ]. In PC12 cells, using a microplate tester, intracellular ROS were detected using a DCFH-DA fluorescent probe at an excitation wavelength of nm and an emission wavelength of nm, and the ROS status of the cells was determined [ 32 ]. The preceding cell treatment procedures were carried out in accordance with the kit instructions to determine the SOD, GSH-Px, and MDA content in PC12 cells [ 32 ]. The OD value was then calculated to determine the SOD amount. Additionally, the OD value was calculated to determine the amount of GSH-Px present in the cells. Subsequently, the OD values were calculated to determine MDA amount. Digested PC12 cells in the logarithmic developmental stage were cultured in 6-well plates. As per the grouping of PC12 cells, the appropriate drug-containing medium dose was supplied 1 day after the cells adhered fully to the wall. In the control group, the same amount of DMEM was added, and the cells were digested and collected using 0. The cells were then suspended in μL of binding buffer. To assess apoptosis, 5 μL of Annexin V-APC was added and mixed with the PC12 cells. Subsequently, signs of apoptosis were observed in each group of PC12 cells [ 33 ]. At pH 4—5, many cells produce β-galactosidase in lysosomes; however, at pH 6, β-galactosidase is only seen in senescent cells. Therefore, we stained PC12 cells in each group with a senescence-related β-Gal kit KGPAG, Jiangsu KGI Biotechnology Co. After the appropriate treatments and dosing, the cells were taken out of the incubator and prepared for staining. The cell culture medium was then removed, and the fixed cells were washed thrice with PBS for 3 min each. On the following day, the cells were observed under an ordinary light microscope. Finally, the cell slides were removed and securely sealed with tablet sealants, and detailed images were meticulously captured under a microscope. All statistical analyses of variance were performed using GraphPad Prism 9. Two-tailed independent t -tests were used to compare the two groups. Results from the Morris water maze test revealed that mice in the Aβ group exhibited spatial learning and memory difficulties, taking longer to locate the submerged platform in the water. Moreover, their performance showed a greater resemblance to the control group, with the experimental values closely corresponding. This conclusion was further verified by follow-up experiments Fig. These findings suggest that AST increases the expression of Bcl-2, SIRT1, and PGC-1α in the hippocampus of mice while inhibiting the expression of Bax. Bcl-2, Sirt1, and PGC-1α protein levels of expression were up-regulated by astaxanthin. Bax protein levels of expression were down-regulated by astaxanthin and up-regulated by Aβ A The expression bands of Bcl-2, Bax, SIRT1, and PGC-1α. B Analysis of expression changes of proteins. D The level of mRNA changes of proteins. Using qRT-PCR, we identified the expression of Bcl-2, SIRT1, PGC-1α , and Bax mRNA in the mouse hippocampus samples. Notably, the expression patterns of these proteins in the hippocampus of mice were primarily observed in the DG, CA1, and CA3 subregions, and their predominant expression patterns were generally consistent across these three subregions Fig. Nissl staining was performed to observe the morphological structures of the neurons. The results showed that compared with the control group, the neurons in the Aβ group exhibited evident necrosis, with a higher number of damaged cells, primarily characterized by neuronal atrophy, irregularity, and darkly stained nuclei in addition to dehydration and vacuolar structure formation in the cytoplasm. Moreover, the hippocampi of the Aβ group showed deep staining, increased intercellular space, and nuclear atrophy Fig. Stained Nissl bodies can be observed in normal hippocampus neurons yellow arrow. The degree and number of morphological changes in hippocampus neurons in each group showed significant differences orange arrow. The neurons in the Aβ group had obvious necrosis, mainly in the form of atrophy and irregularity of neurons. The nuclei showed dark deposits. Dehydration and vacuolar structure formation occurred in the cytoplasm. These results suggest that the reduced learning and memory ability in mice might be attributed to increased Aβmediated neural damage, whereas AST treatment appears to alleviate the damage, leading to an improvement in learning and memory abilities. ROS alters and destroys intracellular molecules and increases cell membrane permeability. Therefore, oxidative stress can promote cell apoptosis by causing oxidative damage to nerve cells. SOD is a major free radical scavenger, and the higher the activity, the stronger the free radical scavenging ability. MDA content reflects the severity of cell damage and can be used as an indicator of the levels of free radicals and oxidative stress. GSH-Px is an oxygen-free radical scavenging enzyme and a major antioxidant defense component that protects cells from an increase in ROS, thereby alleviating the lipid peroxidation of polyunsaturated fatty acids in cell membranes. The expression of SOD, GSH-Px, ROS, and MDA in the hippocampus of the mice was determined using relevant test kits. Moreover, the control group exhibited lower SOD and GSH-px expression levels and higher ROS and MDA expression levels compared with the AST group. Furthermore, ROS and MDA expression levels were lower in the control group compared with the Aβ group; however, SOD and GSH-px expression levels were higher in the control group. Aβ group and AST group. The findings indicate that Aβ25—35 is hazardous to cells when administered for h at a concentration of 5 μM. Additionally, the inhibition rate of PC12 cells increased significantly with higher concentrations of Aβ25— B — C OD values of eight groups of PC12 cells, and inhibition rate of Aβ in each group on PC12 cells. other groups. E — F OD values of six groups of PC12 cells, and inhibition rate of Aβ in each group on PC12 cells. In the control group, cells exhibited favorable characteristics, adhering to the wall, exhibiting uniform expansion, and assuming polygonal shapes, as indicated by the outcomes of the CCK-8 assay. However, the Aβ group displayed poor cell conditions, with uneven density and irregular shapes. Conversely, the AST group showed higher cell density and more regular morphology than the control group. Moreover, the CCK-8 results revealed that the Aβ group cell viability was lower than that of the control group. However, the AST group showed improved cell viability. These findings suggest that AST may provide protection against Aβ-mediated cytotoxicity. Our findings showed that the apoptosis rate in the control group was 9. In contrast, the apoptosis rate of the Aβ group was However, the apoptosis rate in the AST group was notably lower at 6. The findings demonstrate that Aβ25—35 significantly increases the likehood of apoptosis in PC12 cells, while AST administration mitigates this process by reducing the rate of apoptosis in PC12 cells. A Apoptosis status of six groups of PC12 cells in each quadrant. B Comparison of total apoptosis rate of PC12 cells in six groups. These findings demonstrate that Aβ could induce senescence in PC12 cells and influence cell activity. Comparison of β-galactosidase staining results. With aging, the brains becomes more vulnerable to early onset of neurodegenerative and neuroinflammation [ 35 , 36 ]. This gradual aging process of the brain give rise to significant changes, particularly in brain regions linked to learning and memory, resulting in a decline in cognitive abilities and memory functions. Consequently, neurodegenerative conditions such as AD manifest as the brain ages. The accumulation of Aβ, the primary component of amyloid plaques, in and around the cerebrovascular system is a pathogenic characteristic of AD and may lead to damage to the blood—brain barrier [ 37 , 38 ]. Conversely, AST is a potent antioxidant that reduces inflammation and DNA damage while preventing cell damage caused by elevated ROS [ 39 ]. The capacity of AST to halt oxidative damage in the central nervous system is owing to its distinctive molecular structure, which quenches singlet oxygen and scavenges free radicals [ 40 ]. In the present study, the results of our mouse model experiment demonstrate that Aβ can decrease hippocampal neuronal density and trigger apoptosis in mice, thereby decreasing their capacity for spatial learning and memory. Furthermore, we found that Bcl-2, SIRT1, and PGC-1α expression was increased by AST, whereas Bax expression was decreased, demonstrating that AST also possesses antioxidant properties in addition to controlling oxidative stress indicators. In our in vivo experiments, hematoxylin—eosin staining was applied to the CA1, CA3, and DG subregions of the mice hippocampus to observe the pyramidal cell morphological changes in the hippocampus. However, in addition to the previously investigated Bcl-2 and Bax, further studies into changes in the expression of downstream protein caspase 3, a component of apoptosis-related proteins, are required to verify the inhibitory effect of AST on cell apoptosis. This approach parallels analogous studies focused on cell apoptosis [ 44 ]. NAM can inhibit SIRT1 and other members of the sirtuin family, including SIRT2, SIRT3, and SIRT6. However, this study focused only on the inhibitory effect of NAM on SIRT1 expression. Therefore, in future studies, we plan to explore whether NAM exerts inhibitory effects on other members of the sirtuin protein family. Although our experimental results indicate that NAM plays a role in inhibiting SIRT1, some studies have suggested that NAM can promote the expression of SIRT1 [ 45 , 46 ]. Therefore, the mechanism underlying the effect of NAM on SIRT1 remains unclear. Additionally, AST has a significant antioxidant effect and acts as a protective agent against neurodegenerative diseases, ultimately leading to an enhancement in the cognitive function of mice Fig. The diagram illustrates the role of astaxanthin in the development of senescence and apoptosis of neurons. ROS production increased after Aβ treatment. In vivo experiments, ROS can reduce the expression of Bcl-2 and increase the expression of Bax in the hippocampus of mice, which can promote the senescence and apoptosis of neurons, accelerate the process of brain aging and AD, and reduce cognitive function. In vitro experiments, ROS reduced mitochondrial function, senescence, and apoptosis of PC12 cells. Astaxanthin and SIRT1, PGC-1α have strong antioxidant effects, which can resist cell senescence and apoptosis caused by oxidative stress, improve mitochondrial function, and improve the cognitive function of mice. Aging is a complex physiological process characterized by the steady decline in cellular function and an increased likelihood for cell death. Oxidative stress plays a pivotal role in brain aging, leading to senescence and apoptosis in various mammalian cell lines when exposed to high levels of oxidative stress [ 47 ]. To counteract this, cells rely on antioxidant enzymes, with carotenoids being one of the primary cellular defense mechanisms. Carotenoids are a physically and functionally diverse collection of natural pigments that are potent antioxidants capable of removing monomorphic oxygen and peroxyl radicals from humans and other animals [ 48 ]. Among these carotenoids, AST, derived from seaweed, has garnered particular attention as a powerful antioxidant [ 49 ]. In some studies, following treatment with AST, cell growth resumed, and chromatin concentration and nuclear fragmentation were reduced, demonstrating that the anti-apoptotic, anti-neuroinflammatory, and anti-aging properties of AST can protect cells against oxidative stress-induced apoptosis [ 50 , 51 , 52 ]. However, AST treatment inhibited the induced senescence and apoptosis of PC12 cells. Moreover, the resistance of PC12 cells to ROS increased following AST treatment, indicating enhanced cellular activity. Furthermore, as cellular senescence and apoptosis are closely related to decreased mitochondrial function, it is imperative for future research to also center on alterations in mitochondrial membrane potential and mitochondrial permeability transition pores. Using the PC12 cell model, this study has demonstrated the promising potential of AST as a neuroprotective agent against neurodegenerative diseases. Moreover, it provides a crucial theoretical foundation and serves as a valuable therapeutic target for further investigations into the antioxidant and anti-brain aging properties of AST Fig. AST plays a protective role in neurons and enhances learning, memory, and cognitive abilities. Additionally, AST curtails senescence and apoptosis in PC12 cells. Further research is required to investigate the antioxidant mechanism of AST and explore its additional beneficial effects in both in vivo and in vitro settings. The data that support the findings of this study are available from the corresponding author upon reasonable request. Ionescu-Tucker A, Cotman CW. Neurobiol ageing. Article CAS Google Scholar. Kandlur A, Satyamoorthy K, Gangadharan G. Oxidative stress in cognitive and epigenetic ageing: a retrospective glance. Front Mol Neurosci. Google Scholar. Uddin MS, Stachowiak A, Mamun A, et al. Front aging Neurosci. Harman D. Free radical theory of ageing: effect of free radical reaction inhibitors on the mortality rate of male LAF1 mice. J Gerontol. Article Google Scholar. Oswald MCW, Garnham N, Sweeney ST, et al. Regulation of neuronal development and function by ROS. FEBS Lett. Article CAS PubMed PubMed Central Google Scholar. Griñán-Ferré C, Vasilopoulou F, Abás S, et al. Behavioral and cognitive improvement induced by novel imidazoline I2 receptor ligands in female SAMP8 mice. Article PubMed Google Scholar. Liu N, Zeng L, Zhang YM, et al. Neural Regen Res. 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Glutaredoxin regulates apoptosis in cardiomyocytes via NFkappaB targets Bcl-2 and Bcl-xL: implications for cardiac ageing. Antioxid Redox Signal. Ghasemi A, Khanzadeh T, Zadi Heydarabad M, et al. Evaluation of BAX and BCL-2 gene expression and apoptosis induction in acute lymphoblastic leukemia cell line CCRFCEM after high-dose prednisolone treatment. Asian Pac J Cancer Prev. CAS PubMed PubMed Central Google Scholar. Yan X, Yu A, Zheng H. Neural Plast. Waldman M, Cohen K, Yadin D, et al. Cardiovasc Diabetol. Wang F, Shang Y, Zhang R, et al. Mol Med Rep. Toklu HZ, Scarpace PJ, Sakarya Y, et al. Appl Physiol Nutr Metab. Guo Z, Fan D, Liu FY, et al. Front Cardiovasc Med. Zhang Q, Song W, Zhao B, et al. Front Neurosci. Somasundaram A, Taraska JW. Local protein dynamics during microvesicle exocytosis in neuroendocrine cells. Mol Biol Cell. Ding D, Enriquez-Algeciras M, Valdivia AO, et al. The role of deimination in regenerative reprogramming of neurons. For more everything you need to know about Astaxanthin, check out our comprehensive information page here. To learn more about our astaxanthin, check out the product page here. Ron Goedeke MD, BSc Hons MBChB, FNZCAM. Ron Goedeke, an expert in the domain of functional medicine, dedicates his practice to uncovering the root causes of health issues by focusing on nutrition and supplement-based healing and health optimisation strategies. An esteemed founding member of the New Zealand College of Appearance Medicine, Dr. Goedeke's professional journey has always been aligned with cutting-edge health concepts. Having been actively involved with the American Academy of Anti-Aging Medicine since , he brings over two decades of knowledge and experience in the field of anti-aging medicine, making him an eminent figure in this evolving realm of healthcare. Throughout his career, Dr. Goedeke has been steadfast in his commitment to leverage appropriate nutritional guidance and supplementation to encourage optimal health. This has allowed him to ascend as one of the most trusted authorities in the arena of nutritional medicine in New Zealand. His expertise in the intricate relationship between diet, nutritional supplements, and overall health forms the backbone of his treatment approach, allowing patients to benefit from a balanced and sustainable pathway to improved wellbeing. Disclaimer : The information provided is for educational purposes only and does not constitute medical advice. Always seek the advice of your physician or qualified healthcare provider with any questions or concerns about your health. Never disregard or delay seeking medical advice because of something you have heard or read on this website. Last updated on the 8th of June Just added to your cart. Continue Shopping. Close search. Home Astaxanthin Astaxanthin for Brain Health: Improving Memory and Cognitive Function. Astaxanthin for Brain Health: Improving Memory and Cognitive Function by Ron Goedeke. Understanding Astaxanthin: A Powerful Antioxidant for Boosting Brain Health Astaxanthin , a carotenoid pigment found in various marine organisms, has attracted considerable attention due to its potential impact on brain health. How Astaxanthin Enhances Memory and Cognitive Function Astaxanthin is not only a powerful antioxidant but has also been linked to enhanced memory and cognitive function. Astaxanthin and Brain Aging: Slowing Down Cognitive Decline Astaxanthin's potent antioxidant and anti-inflammatory properties may also play a significant role in slowing down cognitive decline associated with aging. The Science Behind Astaxanthin: Exploring its Impact on Brain Health Astaxanthin's potential to enhance brain health is underpinned by its unique biochemical characteristics. From Lab to Mind: Astaxanthin's Role in Neuroprotection and Neurogenesis Astaxanthin's neuroprotective properties have been well-documented in numerous animal and in vitro studies. How Astaxanthin Supports Focus and Concentration Astaxanthin's potential benefits for the brain extend beyond neuroprotection and neurogenesis. Protecting the Brain from Oxidative Stress Oxidative stress, caused by an imbalance between free radical production and the body's ability to counteract their harmful effects, can lead to neurodegeneration over time. Astaxanthin's Impact on Mental Acuity and Recall Astaxanthin's potential benefits extend to improving mental acuity and recall, key aspects of cognitive function that often decline with age. Several studies have shown that astaxanthin supplementation can significantly improve these cognitive abilities. One study conducted on healthy older adults found that supplementation with astaxanthin improved their psychomotor speed, processing speed, and memory. This suggests that astaxanthin could be beneficial for maintaining cognitive performance during aging. Another study found that astaxanthin could enhance memory and learning in younger individuals as well. The researchers hypothesized that these benefits might be due to astaxanthin's ability to reduce oxidative stress in the hippocampus, the brain region primarily involved in memory and learning. However, more research is needed to confirm these results and establish the optimal dosage and duration of astaxanthin supplementation for improving mental acuity and recall. It's also important to remember that mental acuity and recall can be influenced by a variety of factors, including sleep, diet, stress, and physical activity. The Role of Astaxanthin in Improving Brain Function Given its antioxidative, anti-inflammatory, and neuroprotective properties, astaxanthin is emerging as a promising supplement for supporting overall brain function. Astaxanthin and Neuroinflammation: Promoting Brain Health from Within Neuroinflammation, characterized by chronic inflammation in the brain, is increasingly recognized as a contributor to neurodegenerative disorders and cognitive decline. Summary Astaxanthin, a potent antioxidant carotenoid, has promising potential for promoting brain health and enhancing cognitive function. Its unique molecular structure enables it to neutralize harmful free radicals and reduce oxidative stress, a key cause of neurodegeneration. Astaxanthin has shown to improve memory and cognitive function, and slow down age-related cognitive decline. Its ability to cross the blood-brain barrier allows it to directly exert neuroprotective effects. Astaxanthin also has anti-inflammatory properties, which could mitigate neuroinflammation—a key contributor to cognitive decline. It promotes neurogenesis or the formation of new neurons, crucial for cognitive health. Some studies have shown astaxanthin's potential in enhancing focus and concentration by improving blood flow to the brain. It also appears to improve mental acuity and recall, essential cognitive functions that often decline with age. Despite these promising findings, more research is needed to confirm astaxanthin's benefits in humans and to establish optimal dosage and duration of treatment. It's important to remember that while astaxanthin can contribute to brain health, a holistic approach that includes a balanced diet, regular exercise, stress management, and adequate sleep is vital for overall cognitive health and wellbeing. Astaxanthin Information For more everything you need to know about Astaxanthin, check out our comprehensive information page here. Related Articles. Supplements For A Healthy Gut Health. Understanding the Role of Supplements in Promoting Optimal Gut Health How Astaxanthin Can Help Improve Your Eyesight. Unveiling the Power of Astaxanthin for Vision Enhancement Astaxanthin is Astaxanthin: Enhancing Sun Protection from Within. Unveiling the Power of Astaxanthin for Sun Protection Astaxanthin, a Protecting Your Cells: How Astaxanthin Supports Overall Well-Being. Harnessing the Power of Astaxanthin: An Introduction to Its Cell-Protective Unlocking the Secrets to a Radiant Complexion With Astaxanthin. The Powerful Antioxidant for Skin Health Astaxanthin, a potent antioxidant, The Power of Astaxanthin And its Health-Boosting Properties. Nature's Super Antioxidant Astaxanthin is a naturally occurring carotenoid, renowned View all. Author Ron Goedeke MD, BSc Hons MBChB, FNZCAM Dr. Understanding Astaxanthin: A Powerful Antioxidant for Boosting Brain Health: Fakhri, S. Astaxanthin: A mechanistic review on its biological activities and health benefits. Pharmacological Research, , DOI: Astaxanthin protects neurons against trauma-induced inflammation and improves the rate of survival. Marine Drugs, 12 11 , Astaxanthin ameliorates aluminum chloride-induced spatial memory impairment and neuronal oxidative stress in mice. European Journal of Pharmacology, , Effects of Composite Supplement Containing Astaxanthin and Sesamin on Cognitive Functions in People with Mild Cognitive Impairment: A Randomized, Double-Blind, Placebo-Controlled Trial. Journal of Alzheimer's Disease, 62 4 , Effects of astaxanthin-rich Haematococcus pluvialis extract on cognitive function: a randomised, double-blind, placebo-controlled study. Journal of Clinical Biochemistry and Nutrition, 51 2 , — Antioxidant effect of astaxanthin on phospholipid peroxidation in human erythrocytes. British Journal of Nutrition, 11 , — Brain foods: the effects of nutrients on brain function. Nature Reviews Neuroscience, 9 7 , — Share Share on Facebook Tweet Tweet on Twitter Pin it Pin on Pinterest. Leave a comment Name. Back to Astaxanthin. |
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Department of Pharmacy, Ningbo Yinzhou No. Department of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, , China. You can also search for this author in PubMed Google Scholar. NZ and HY prepared the manuscript; XL and MZ revised the paper; XY, MZ, YZ and GY performed the experiments; LC, JZ and XY analyzed the data; HL designed the study. All authors read and approved the final manuscript. Correspondence to Hongwei Li. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions. Zhu, N. et al. Astaxanthin protects cognitive function of vascular dementia. Behav Brain Funct 16 , 10 Download citation. Received : 30 January Accepted : 02 November Published : 18 November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Objective The purpose of this study was to evaluate the effect of astaxanthin AST on cognition function, inflammatory response and oxidative stress in vascular dementia VD mice. Method VD mice model was established by left unilateral common carotid arteries occlusion LUCCAO. Results AST improved the discrimination ability of VD mice. Conclusion AST could improve cognitive impairment and hippocampal neurons in VD mice, which may be related to suppression of inflammatory response and oxidative stress. Introduction Vascular dementia VD refers to acquired intelligence disorder syndrome, which is finally caused by the long-term exposure to various risk factors of cerebral vascular diseases such as cerebral ischemia and hypoxic damage [ 1 ]. Object recognition test To assess non-spatial working memory, a 2-day object recognition test was performed on the 31st day after LUCCAO [ 14 ]. Morris water maze test Morris water maze test was performed to evaluate the spatial acquired function of mice on the 33th day after LUCCAO in accordance with previous researches [ 16 , 17 ]. Enzyme-linked immunosorbent assay Protein levels of interleukin-1β IL-1β and interleukin-4 IL-4 in the hippocampus and prefrontal cortex were measured to investigate the regional response of pro-inflammatory and anti-inflammatory cytokine of mice by ELISA kit Beyotime, Shanghai, China. Detected of superoxide dismutase SOD and malondialdehyde MDA To further determine whether AST influences anti-oxidation, we analyzed SOD activity and MDA content in the hippocampus and prefrontal cortex of each group. Statistical analysis All data were statistically analyzed with SPSS Result Weight of mice During the period of dministration, the average body weight of each group increased steadily for 30 days, except for slight fluctuations in the first ten days. The weight of each group mice in the 30 days, with 13 mice per group. Full size image. The hematoxylin and eosin staining results of each group, with 13 mice per group. Bar: um. Discussion The most significant finding of this study was that AST ameliorated the cognitive function and hippocampal neuron in VD mice, which may be associated with the inhibition of inflammatory response and oxidative stress, revealing that the potential value of AST in the treatment of VD. Abbreviations VD: Vascular dementia AST: Astaxanthin CCH: Chronic cerebral hypoperfusion LUCCAO: Left unilateral common carotid artery occlusion ICR: Institute of Cancer Research ELISA: Enzyme-linked immunosorbent assay SOD: Superoxide dismutase MDA: Malondialdehyde IL-1β: Interleukin-1β IL Interleukin-4 IL Interleukin 6 2VO: Bilateral common carotid occlusion. References Kalaria RN. Article PubMed PubMed Central Google Scholar Venkat P, Chopp M, Chen J. Article PubMed PubMed Central Google Scholar Krenk L, Rasmussen LS, Kehlet H. Kritsilis M, Rizou V, S, Koutsoudaki PN. Aging, cellular senescence and neurodegenerative disease. Int J Mol Sci. Wang Q, Ge X, Zhang J, Chen L. Aging Albany NY. 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Structures of astaxanthin and their consequences for therapeutic application. Int J Food Sci. Chou H-Y, Ma D-L, Leung C-H, et al. Purified Astaxanthin from Haematococcus pluvialis promotes tissue regeneration by reducing oxidative stress and the secretion of collagen in vitro and in vivo. Wang X, Zhang T, Chen X, et al. simultaneous inhibitory effects of all-trans astaxanthin on acetylcholinesterase and oxidative stress. Mar Drugs. Download references. We thank the staff of the Laboratory at the First Affiliated Hospital of Jinzhou Medical University for their assistance in this study. This study was supported by grants from the funds for National Natural Science Foundation of China and Natural Science Foundation of Liaoning Province BS from Dr. Ning Liu. Department of Radiology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, , China. Department of Neurology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, , China. You can also search for this author in PubMed Google Scholar. Conceptualization was performed by NL and XL; in vivo experiments were conducted by NL, XL and GL; in vitro experiments were completed by FZ, YC and GL; XL and XZ reviewed and revised the manuscript. NL contributed equally to this work. Correspondence to Xiaohong Lyu. All experimental protocols received approval from the Animal Care and Use Committee of Jinzhou Medical University. Each animal experiment was conducted in accordance with the Guide for the Care and Use of Laboratory Animals 8th ed. This study is reported in accordance with the ARRIVE 2. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions. Liu, N. et al. Cell Biosci 13 , Download citation. Received : 19 April Accepted : 07 September Published : 14 September Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Objective Oxidative stress plays a pivotal role in neurodegenerative diseases. Methods Alzheimer's disease models comprising ICR mice and PC12 cells were established using Aβ25— Results In vivo experiments showed that Aβ25—35 impaired cognitive function, promoted morphological changes in hippocampal neurons, decreased Bcl-2 expression, increased Bax expression, decreased superoxide dismutase and GSH-px levels, and increased reactive oxygen species and malondialdehyde levels. Introduction The biological mechanisms and consequences of aging have captured the attention of numerous scholars, especially considering the rise in life expectancy. Materials and methods Animals Eighty male ICR mice 6 weeks old, weighing 20—25 g were provided by Liaoning Changsheng Co. Full size image. Results AST improved learning, memory, and cognitive function in AD model Results from the Morris water maze test revealed that mice in the Aβ group exhibited spatial learning and memory difficulties, taking longer to locate the submerged platform in the water. Table 2 Oxidative stress indexes in PC12 cells Full size table. Table 3 Apoptotic rate of PC12 cells Full size table. Discussion Effects of AST on senescence and apoptosis of hippocampus neurons in AD model With aging, the brains becomes more vulnerable to early onset of neurodegenerative and neuroinflammation [ 35 , 36 ]. Availability of data and materials The data that support the findings of this study are available from the corresponding author upon reasonable request. References Ionescu-Tucker A, Cotman CW. Article CAS Google Scholar Kandlur A, Satyamoorthy K, Gangadharan G. Google Scholar Uddin MS, Stachowiak A, Mamun A, et al. Google Scholar Harman D. Article Google Scholar Oswald MCW, Garnham N, Sweeney ST, et al. Article CAS PubMed PubMed Central Google Scholar Griñán-Ferré C, Vasilopoulou F, Abás S, et al. Article PubMed Google Scholar Liu N, Zeng L, Zhang YM, et al. Article CAS PubMed Google Scholar El-A SE, Abdel-A AK, Wahdan S, et al. 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Article CAS PubMed Google Scholar Brotosudarmo THP, Limantara L, Setiyono E. See J Alzheimers Dis. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Background Dementia and its first or transitional stage, mild cognitive impairment MCI , is a major concern for the aging Japanese society. Objective 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. Method Twenty-one healthy participants with MCI were recruited in our double-blind placebo-controlled pilot study. 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. Results 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. Conclusion Our results provide support for the use of AS as a dietary supplementation for improving cognitive functions. Free full text Journal of Alzheimer's Disease. J Alzheimers Dis. Published online Mar PMCID: PMC PMID: Naoki Ito a Pharmaceutical and Healthcare Research Laboratories, Research and Development Management Headquarters, FUJIFILM Corporation, Ashigarakami-gun, Kanagawa, Japan, Find articles by Naoki Ito. Hitomi Saito a Pharmaceutical and Healthcare Research Laboratories, Research and Development Management Headquarters, FUJIFILM Corporation, Ashigarakami-gun, Kanagawa, Japan, Find articles by Hitomi Saito. Shinobu Seki a Pharmaceutical and Healthcare Research Laboratories, Research and Development Management Headquarters, FUJIFILM Corporation, Ashigarakami-gun, Kanagawa, Japan, Find articles by Shinobu Seki. Fumitaka Ueda a Pharmaceutical and Healthcare Research Laboratories, Research and Development Management Headquarters, FUJIFILM Corporation, Ashigarakami-gun, Kanagawa, Japan, Find articles by Fumitaka Ueda. Takashi Asada b Memory Clinic Ochanomizu, Bunkyo-ku, Tokyo, Japan, Find articles by Takashi Asada. Author information Article notes Copyright and License information Disclaimer. b Memory Clinic Ochanomizu, Bunkyo-ku, Tokyo, Japan,. E-mail: moc. mlifijuf oti. Accepted Jan Copyright © — IOS Press and the authors. All rights reserved. This is an open access article distributed under the terms of the Creative Commons Attribution CC BY 4. This article has been cited by other articles in PMC. Abstract Background: Dementia and its first or transitional stage, mild cognitive impairment MCI , is a major concern for the aging Japanese society. Objective: 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. Method: Twenty-one healthy participants with MCI were recruited in our double-blind placebo-controlled pilot study. Results: 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. Conclusion: Our results provide support for the use of AS as a dietary supplementation for improving cognitive functions. Keywords: Astaxanthin, CNSVS, cognitive functions, mild cognitive impairment, sesame extract, sesamin. MATERIALS AND METHODS Study design, randomization, and blinding This study was a randomized, double-blind, placebo-controlled, parallel-group comparison trial conducted to evaluate the effects of dietary supplementation with AS on cognitive function in MCI participants. Participants This study included participants aged from 50 to 79 years old in the Tokyo metropolitan area who attended Memory Clinic Ochanomizu, and were diagnosed with MCI. Supplement formulation One AS capsule contained 3 mg of astaxanthin, 5 mg of sesamin, and other components including filling agents such as safflower oil, and dispersants. Cognitive tests The CNSVS is a computerized test that evaluates multiple cognitive functions. Blood sampling and safety evaluation Serum and plasma were obtained from the participants at baseline, after 6 weeks, and after 12 weeks of dietary supplementation. Statistical analysis All results were presented as the mean±standard deviation SD. RESULTS Participants Initially, we recruited 21 participants aged 57—78, 14 males and 7 females in the Tokyo metropolitan area who had been diagnosed with MCI. Open in a separate window. Flow diagram of participants. Table 1 Baseline characteristics of participants who completed 12 weeks test. Cognitive tests The aim of this study was to evaluate the effects of dietary supplementation with AS on cognitive functions. Table 2 Score of cognitive tests. CNS Vital Signs domain scores Week 0 6 12 Group mean±SD mean±SD mean±SD Composite Memory Placebo Blood tests Extensive epidemiological research has demonstrated an association between the risk of cognitive decline and systemic oxidative stress [ 35 ]. Clinical safety We observed several adverse events in both the placebo and AS groups Table 3. Table 3 List of adverse events. Placebo AS Acute low back pain 1 0 Cold 0 3 Cystitis 1 0 Diarrhea 0 1 Dizziness 0 1 Feeling of smothering 2 0 Lassitude 2 0 Lip redness 0 1 Low back pain 1 0 Malaise 1 0 Occult blood in urine 0 1 Protein in urine 0 1 Slight cold 0 1 Sore throat 0 1 Stomatitis 0 1 Tonsillitis 1 0. Neurologia 15 , 93— Arch Toxicol 89 , — RSC Adv 6 , — Mol Neurobiol 53 , — J Nat Prod 69 , — Mar Drugs 12 , — Mol Cryst Liq Cryst , 52— Br J Nutr , — PLoS One 12 , 1— US Patent. Acta Biochim Pol 59 , 43— Atherosclerosis , — Sci Rep 5 , Int J Sports Med 32 , — Mol Nutr Food Res 61 , J Clin Biochem Nutr 51 , — Mar Drugs 13 , — GeroScience 39 , 19— Am J Food Nutr 4 , 21— Int J Biomed Sci 2 , — Biochem Pharmacol Los Angel 4 , Comp Biochem Physiol C Toxicol Pharmacol , — Lipids 34 , — Arch Clin Neuropsychol 21 , — Psychopharmacol Bull 19 , — Evid Based Complement Alternat Med , Jpn Pharmacol Ther 44 , — Arch Neurol 62 , —; discussion Glob J Health Sci 7 , 1— Am J Alzheimers Dis Other Demen 20 , — Alzheimers Dement 1 , S25—S Etude du Vieillissement Artériel. J Am Geriatr Soc 48 , — JAMA Neurol 71 , 55— Food Funct 5 , — Brief Interpretation Guide. Pharmacopsychiatry 36 , — Pharmacol Res 55 , — Alzheimers Dement Amst 6 , — Res Gerontol Nurs 10 , 86— Brain Res , 18— J Med Food 13 , — Brain Res Bull , — Mol Nutr Food Res 60 , — Brain Res , — Food Chem Toxicol 49 , — Acta Pharmacol Sin 38 , — Oxid Med Cell Longev , Rejuvenation Res 15 , — J Neural Transm , — J Clin Biochem Nutr 47 , — Smart citations by scite. ai include citation statements extracted from the full text of the citing article. The number of the statements may be higher than the number of citations provided by EuropePMC if one paper cites another multiple times or lower if scite has not yet processed some of the citing articles. Explore citation contexts and check if this article has been supported or disputed. Astaxanthin: Past, Present, and Future. Nishida Y , Berg PC , Shakersain B , Hecht K , Takikawa A , Tao R , Kakuta Y , Uragami C , Hashimoto H , Misawa N , Maoka T Mar Drugs , 21 10 , 28 Sep Cited by: 0 articles PMID: PMCID: PMC Review Articles in the Open Access Subset are available under a Creative Commons license. Preventive Treatment with Astaxanthin Microencapsulated with Spirulina Powder, Administered in a Dose Range Equivalent to Human Consumption, Prevents LPS-Induced Cognitive Impairment in Rats. Martin M , Pusceddu MM , Teichenné J , Negra T , Connolly A , Escoté X , Torrell Galceran H , Cereto Massagué A , Samarra Mestre I , Del Pino Rius A , Romero-Gimenez J , Egea C , Alcaide-Hidalgo JM , Del Bas JM Nutrients , 15 13 , 23 Jun Cited by: 0 articles PMID: PMCID: PMC Articles in the Open Access Subset are available under a Creative Commons license. Lignan-Rich Sesame Sesamum indicum L. 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