scholarly journals Beneficial Effects of Walnuts on Cognition and Brain Health

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 550 ◽  
Author(s):  
Abha Chauhan ◽  
Ved Chauhan

Oxidative stress and neuroinflammation have important roles in the aging process, mild cognitive impairment (MCI), Alzheimer’s disease (AD), and other brain disorders. Amyloid beta protein (Aβ) is the main component of amyloid plaques in the brains of people with AD. Several studies suggest that Aβ increases the generation of free radicals in neurons, which leads to oxidative damage and cell death. Aβ can also induce neuroinflammation by increasing pro-inflammatory cytokines and enzymes. Walnuts contain several components that have antioxidant and anti-inflammatory effects. Animal and human studies from our and other groups suggest that supplementation with walnuts in the diet may improve cognition and reduce the risk and/or progression of MCI and AD. In the transgenic AD mouse model (AD-tg), we have reported the beneficial effects of a diet with walnuts on memory, learning, motor coordination, anxiety, and locomotor activity. Human clinical trials have also suggested an association of walnut consumption with better cognitive performance and improvement in memory when compared to baseline in adults. Our recent study in AD-tg mice has shown that a walnut-enriched diet significantly improves antioxidant defense and decreases free radicals’ levels, lipid peroxidation, and protein oxidation when compared to a control diet without walnuts. These findings suggest that a diet with walnuts can reduce oxidative stress by decreasing the generation of free radicals and by boosting antioxidant defense, thus resulting in decreased oxidative damage to lipids and proteins. An in vitro study with synthetic Aβ showed that walnut extract can inhibit Aβ fibrillization and solubilize the preformed Aβ fibrils, suggesting an anti-amyloidogenic property of walnuts. Because it takes many years for cognitive impairment and dementia to develop, we suggest that early and long-term dietary supplementation with walnuts may help to maintain cognitive functions and may reduce the risk of developing, or delay the onset and/or slow the progression of, MCI and dementia by decreasing Aβ fibrillization, reducing oxidative damage, increasing antioxidant defense, and decreasing neuroinflammation. Furthermore, several animal and human studies have suggested that walnuts may also decrease the risk or progression of other brain disorders such as Parkinson’s disease, stroke, and depression, as well as of cardiovascular disease and type 2 diabetes. Together, these reports suggest the benefits of a walnut-enriched diet in brain disorders and in other chronic diseases, due to the additive or synergistic effects of walnut components for protection against oxidative stress and inflammation in these diseases.

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3442
Author(s):  
Yaowared Chulikhit ◽  
Wichitsak Sukhano ◽  
Supawadee Daodee ◽  
Waraporn Putalun ◽  
Rakvajee Wongpradit ◽  
...  

The effects of the phytoestrogen-enriched plant Pueraria mirifica (PM) extract on ovari-ectomy (OVX)-induced cognitive impairment and hippocampal oxidative stress in mice were investigated. Daily treatment with PM and 17β-estradiol (E2) significantly elevated cognitive behavior as evaluated by using the Y maze test, the novel object recognition test (NORT), and the Morris water maze test (MWM), attenuated atrophic changes in the uterus and decreased serum 17β-estradiol levels. The treatments significantly ameliorated ovariectomy-induced oxidative stress in the hippocampus and serum by a decrease in malondialdehyde (MDA), an enhancement of superoxide dismutase, and catalase activity, including significantly down-regulated expression of IL-1β, IL-6 and TNF-α proinflammatory cytokines, while up-regulating expression of PI3K. The present results suggest that PM extract suppresses oxidative brain damage and dysfunctions in the hippocampal antioxidant system, including the neuroinflammatory system in OVX animals, thereby preventing OVX-induced cognitive impairment. The present results indicate that PM exerts beneficial effects on cognitive deficits for which menopause/ovariectomy have been implicated as risk factors.


2019 ◽  
Vol 20 (7) ◽  
pp. 1547 ◽  
Author(s):  
Ewa Żebrowska ◽  
Mateusz Maciejczyk ◽  
Małgorzata Żendzian-Piotrowska ◽  
Anna Zalewska ◽  
Adrian Chabowski

This is the first study to analyze the impact of high protein diet (HPD) on antioxidant defense, redox status, as well as oxidative damage on both a local and systemic level. Male Wistar rats were divided into two equal groups (n = 9): HPD (44% protein) and standard diet (CON; 24.2% protein). After eight weeks, glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase-1 (SOD-1), reduced glutathione (GSH), uric acid (UA), total antioxidant (TAC)/oxidant status (TOS) as well as advanced glycation end products (AGE), 4-hydroxynonenal (4-HNE), and malondialdehyde (MDA) were analyzed in the serum/plasma, cerebral cortex, and hypothalamus of HPD and CON rats. HPD resulted in higher UA concentration and activity of GPx and CAT in the hypothalamus, whereas in the cerebral cortex these parameters remained unchanged. A significantly lower GSH content was demonstrated in the plasma and hypothalamus of HPD rats when compared to CON rats. Both brain structures expressed higher content of 4-HNE and MDA, whereas AGE was increased only in the hypothalamus of HPD animals. Despite the enhancement in antioxidant defense in the hypothalamus, this mechanism does not protect the hypothalamus from oxidative damage in rats. Hypothalamus is more susceptible to oxidative stress caused by HPD.


Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 793
Author(s):  
Cheng Schwank-Xu ◽  
Elisabete Forsberg ◽  
Magnus Bentinger ◽  
Allan Zhao ◽  
Ishrath Ansurudeen ◽  
...  

Mitochondrial dysfunction in type 2 diabetes leads to oxidative stress, which drives disease progression and diabetes complications. L-carnosine, an endogenous dipeptide, improves metabolic control, wound healing and kidney function in animal models of type 2 diabetes. Coenzyme Q (CoQ), a component of the mitochondrial electron transport chain, possesses similar protective effects on diabetes complications. We aimed to study the effect of carnosine on CoQ, and assess any synergistic effects of carnosine and CoQ on improved mitochondrial function in a mouse model of type 2 diabetes. Carnosine enhanced CoQ gene expression and increased hepatic CoQ biosynthesis in db/db mice, a type 2 diabetes model. Co-administration of Carnosine and CoQ improved mitochondrial function, lowered ROS formation and reduced signs of oxidative stress. Our work suggests that carnosine exerts beneficial effects on hepatic CoQ synthesis and when combined with CoQ, improves mitochondrial function and cellular redox balance in the liver of diabetic mice. (4) Conclusions: L-carnosine has beneficial effects on oxidative stress both alone and in combination with CoQ on hepatic mitochondrial function in an obese type 2 diabetes mouse model.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Liuqin He ◽  
Haiwen Zhang ◽  
Xihong Zhou

Serine plays an important role in the antioxidant defense system. However, the effects of maternal serine deficiency on the antioxidant ability of weanling offspring have not been reported. In the present study, we investigated the oxidative status of offspring of dams that are maintained on serine-deficient diet and subjected to diquat challenge. Individual pregnant animals were randomly divided into two dietary groups, namely, the control diet group and the serine- and glycine-deficient diet group. Samples were collected from weanling offspring at the age of 3 weeks after diquat challenge. Our results showed that maternal serine deficiency did not affect the levels of antioxidant enzymes and reactive oxygen species, as well as the expression of cellular and mitochondrial stress markers (Hspd1 and Hspa1a), which indicated that maternal serine deficiency did not affect basal oxidative status in weanling offspring. However, the weanling offspring were found to be vulnerable to oxidative challenges. Furthermore, our results suggested that the dysfunctional antioxidant system in response to oxidative stress in offspring of dams fed with serine-deficient diet was primarily caused by reduced availability of nicotinamide adenine dinucleotide phosphate. Furthermore, impairment of the antioxidant defense system caused by maternal serine deficiency was mediated by the Akt/AMPK/Sirt1 pathway. Our results indicated that maternal serine availability is important for maintaining antioxidant defense against oxidative challenge in weanling offspring.


2020 ◽  
Vol 6 (Supplement_1) ◽  
pp. 9-9
Author(s):  
Adisa Rahmat Adetutu ◽  
Sulaimon Lateef Adegboyega ◽  
Okeke Ebele Geraldine ◽  
Ariyo OC ◽  
Abdulkareem Fatimah Biade

PURPOSE Hepatocellular carcinoma (HCC) is a highly malignant cancer, with a high recurrence rate and a poor prognosis. Diethyl nitrosamine (DEN) cirrhosis HCC–induced model has revealed an association of cancer progression with oxidative stress and mitochondrial dysfunction. This study investigated the effects of mitoubiquinol mesylate (MitoQ), a mitochondrial targeted antioxidant derivative from ubiquinone on DEN-induced oxidative damage in HCC Wistar rats. METHODS Fifty male Wistar rats were randomly divided into 5 groups, 10 rats per group. Groups A, B, and C received distilled water 10 mL/kg DEN, and MitoQ orally for 16 weeks, respectively. Animals in group D were pretreated with MitoQ for 1 week followed by coadministration of MitoQ and DEN (protective effect), whereas group E received DEN for 8 weeks, then coadministration of DEN and MitoQ (therapeutic effect) until the end of the study. Survival index, tumor incidence, liver function indices, hematologic profile, mitochondrial respiratory enzymes, and antioxidant defense status were assessed. RESULTS Data obtained show that rats in groups D and E had 80% survival and decreased tumor incidence (40% and 60%, respectively) compared with group B. Similarly, MitoQ significantly ( P < .05) decreased the activities of liver function enzymes, while hemoglobin concentration, red blood cell count, and lymphocytes levels were significantly elevated compared with the DEN-only group. Furthermore, MitoQ significantly ( P < .05) protected the liver from DEN-induced oxidative damage; however, there was no significant difference ( P > .05) between activities of mitochondrial F1F0-ATPase and succinate dehydrogenase of groups A, B, D, and E, respectively, although these enzyme activities were significantly ( P < .05) elevated in group C. Macroscopic and microscopic features indicated a reversal of DEN-induced cellular degeneration in hepatocytes. CONCLUSION These data suggest that MitoQ treatment for 16 weeks attenuated DEN-induced oxidative stress indices via modulation of mitochondrial antioxidant defense systems and could alleviate the burden of HCC as a chemotherapeutic agent.


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Yuji Ishikawa ◽  
Tomohito Gohda ◽  
Mitsuo Tanimoto ◽  
Keisuke Omote ◽  
Masako Furukawa ◽  
...  

Exercise is recommended for the management of type 2 diabetes, but its effects on diabetic nephropathy (DN) are still unknown. We hypothesized that appropriate exercise improves early DN via attenuation of inflammation and oxidative damage. Type 2 diabetic KK-Aymice, a spontaneous DN model, underwent two different kinds of exercise (i.e., moderate and low intensity). Sedentary mice or those undergoing an exercise regimen causing no significant body weight loss were used. We examined the urinary excretion of albumin, number of podocytes and macrophages, renal expressions of HIF-1αand MCP-1, and biomarkers of oxidative stress such as urinary 8-OHdG and serum SOD. Exercise reduced urinary levels of albumin and also maintained the number of podocytes in the exercised KK-Aymice independently of improvements of overweight and hyperglycemia, although moderate-intensity exercise increased expression of HIF-1α. Sedentary KK-Aymice showed increased expression of MCP-1 and infiltration of macrophage, increased urinary 8-OhdG, and decreased serum SOD levels compared with exercised KK-Aymice. On the whole, low-intensity exercise attenuates progression of early DN without affecting marked renal ischemia. Reduction rates of urinary albumin and maintained podocyte numbers, with parallel improvements in oxidative damage and inflammation, are related to beneficial effects of exercise in diabetic kidney disease.


2017 ◽  
Vol 39 (01) ◽  
pp. 21-28 ◽  
Author(s):  
Mohamed Bouzid ◽  
Edith Filaire ◽  
Régis Matran ◽  
Sophie Robin ◽  
Claudine Fabre

AbstractThe hypothesis that aging and regular physical activity could influence oxidative stress has been studied by comparing antioxidant activities (superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GR), ascorbic acid and α-Tocopherol) and malondialdehyde level (MDA) in four groups: young sedentary (n=15; age: 20.3±2.8 years; YS), young active (n=16; age: 21.4±1.9 years; YA), old sedentary (n=15; age: 65.1±3.5 years; OS) and old active (n=17; age: 67.2±4.8 years; OA). Antioxidant activities and MDA level were assessed at rest and after an incremental exercise. There was no difference in resting antioxidant activities and lipid peroxidation between YS and OS. However, resting SOD and GR activities were higher in YA compared to OA (p<0.01 and p<0.05, respectively) and resting MDA level was higher in OA compared to YA (p<0.01). After exercise, a significant increase in SOD and GPX activities was observed in YS, YA and OA (p<0.01). Likewise, after exercise a significant increase of MDA level in YA, OS and OA (p<0.01) was observed. In addition, the comparison of YA to OA and YS to OA revealed similar antioxidant activities and lipid peroxidation between YS and OA, whereas antioxidant activities were higher in YA compared to OA. These data suggest that beneficial effects of regular physical activity in antioxidant defense and lipid peroxidation damage could be impaired by the aging process and that regular physical activity in older adults could maintain age-related decreases in antioxidant defense.


Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 51
Author(s):  
Victoria Valls-Bellés ◽  
Cristina Abad ◽  
María Teresa Hernández-Aguilar ◽  
Amalia Nacher ◽  
Carlos Guerrero ◽  
...  

Mastitis is the inflammation of one or several mammal lobes which can be accompanied by a mammary gland infection, and is the leading cause of undesired early weaning in humans. However, little information exists regarding the changes that this disease may induce in the biochemical composition of human milk, especially in terms of oxidative status. Given that newborns are subject to a significant increase in total ROS burden in their transition to neonatal life and that their antioxidant defense system is not completely developed, the aim of this study was to evaluate antioxidant defense (glutathione peroxidase (GPx), reduced glutathione (GSH), total polyphenol content (TPP), and total antioxidant capacity (TAC)) in milk samples from mothers suffering from mastitis and controls. We also measured the oxidative damage to lipids (malondyaldehyde (MDA)) and proteins (carbonyl group content (CGC)) in these samples. Finally, we tested whether dietary supplementation with cranberries (a product rich in antioxidants) in these breastfeeding mothers during 21 days could improve the oxidative status of milk. GPx activity, TPP, and TAC were increased in milk samples from mastitis-affected women, providing a protective mechanism to the newborn drinking mastitis milk. MDA concentrations were diminished in the mastitis group, confirming this proposal. Some oxidative damage might occur in the mammary gland since the CGC was increased in mastitis milk. Cranberries supplementation seems to strengthen the antioxidant system, further improving the antioxidative state of milk.


2021 ◽  
Author(s):  
Hassan El-Sayyad ◽  
Ali Amin ◽  
Mohammed E El-Beeh

Abstract Aging of mammalian species results in impaired biological function and cognitive decline. The purpose of this study was to determine the capacity of whey supplementation to improve aging –related changes of cognitive impairment markers; tau and amyloid-B and α-amylase in the brain of old rats. These have been conducted in conjunction with histopathology, immunohistochemistry and flow cytometry of apoptosis. Twenty-four male Wistar albino rats (Rattus novergicus) ages 8 and 30-M (months) old were used. They were arranged into four main groups; adult (8-month old) and old rats (30 month old) with or without buffalo whey syrup supplementation. Oral whey supplementations was given daily twice doses of 2 mL3 of whey syrup for two months. At the end of experiment, the rats were sacrificed by light anesthesia. The brain was examined for histological, immunohistochemical of synaptophysin and caspase 3 and biochemical and flow cytometric investigation. Old rats presented with depletion of superoxide dismutase (SOD), adenosine triphosphatase (ATP), dopamine (DA) and serotonin (5-HT). The 30 M old rats also presented with increased lipid peroxidation MDA, inflammatory markers (tumor necrosis factor- α and 5-lpooxygenase), apoptic marker caspase 3, Annexin-v and aging marker tau-protein, amyloid-β and α-amylase. The combination of these findings in old rats predicts cognitive impairment. Among old rats, whey supplementations reduced inflammatory and oxidative stress markers. Whey supplementation also enhanced neurotransmitters and decreased tau-protein, amyloid-β, α- amylase cognitive impairment markers. Improved the histopathology and immunohistochemistry of cerebrum, cerebellum and hippocampus of old rats confirmed these effects of supplementation. The rates of apoptosis were decreased by assessment of Annexin v via flow cytometry. Whey supplementation to 8M old rats resulted in maintenance of the brain structure and function. The authors concluded that whey contains antioxidants and amino acids that decrease brain oxidative stress and restore normal cognitive function. These findings were evaluated by enhanced antioxidant defense and DA and 5-HT neurotransmitters which coincides with improved histology. The authors concluded that whey contains antioxidants and amino acids that decrease brain oxidative stress and restore normal cognitive function. These findings were evaluated by enhanced antioxidant defense and DA and 5-HT neurotransmitters which coincides with improved histology.


Jurnal Medali ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 12
Author(s):  
Annisa Gustiasti Arumsadu ◽  
Niluh Ringga Woroprobosari ◽  
Rina Kartika Sari ◽  
Rochman Mujayanto

Background: Cancer is the second leading cause of death in the world after heart disease. One type of cancer, namely head and neck cancer, can be treated with head and neck radiotherapy. Continuous radiotherapy will cause an increase in oxidative stress and free radicals and damage to the oral mucosa, one of which is oral mucositis. Giving ozone water can help reduce the degree of oral mucositis in patients. Ozone water itself has several beneficial effects such as antioxidant, anti-inflammatory, and antimicrobial. The purpose of this study was to determine the potential of ozone water in reducing the severity of oral mucositis in patients after head and neck radiotherapy.Method: Gargling treatment using ozone water in a ratio of 2:3 for 1 minute with 4 repetitions for 2 weeks showed a significant reduction in pain. Ozone used in gas or liquid form for more than 5 minutes has the potential to cause side effects on the duration of inflammation and for gas can cause infection in the respiratory tract.Conclusion: The conclusion of this review is that the administration of ozone water with a concentration of 2-4 ppm for approximately 5 minutes has the potential to cure oral mucositis due to head and neck radiotherapy


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