Showing papers in "Nutritional Neuroscience in 2012"
TL;DR: The aim of this paper is to present various well-known dietary polyphenols and their mechanisms of neuroprotection with an emphasis on Alzheimer’s disease, Parkinson's disease, and amyotrophic lateral sclerosis.
Abstract: Polyphenols are secondary metabolites with antioxidant properties and are abundant in the diet. Fruits, vegetables, herbs, and various drinks (tea, wine, and juices) are all sources of these molecules. Despite their abundance, investigations into the benefits of polyphenols in human health have only recently begun. Phenolic compounds have received increasing interest because of numerous epidemiological studies. These studies have suggested associations between the consumption of polyphenol-rich aliments and the prevention of chronic diseases, such as cancer, cardiovascular diseases, and neurodegenerative diseases. More specifically, in the last 10 years literature on the neuroprotective effects of a polyphenol-rich diet has grown considerably. It has been demonstrated, in various cell culture and animal models, that these metabolites are able to protect neuronal cells by attenuating oxidative stress and damage. However, it remains unclear as to how these compounds reach the brain, what concentrations are necessary, and what biologically active forms are needed to exert beneficial effects. Therefore, further research is needed to identify the molecular pathways and intracellular targets responsible for polyphenol’s neuroprotective effects. The aim of this paper is to present various well-known dietary polyphenols and their mechanisms of neuroprotection with an emphasis on Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis.
241 citations
TL;DR: The consumption of diets enriched with polyphenols may present the potential of dietary manipulation as a non-invasive, natural, and inexpensive therapeutic means to support a healthy brain.
Abstract: ObjectivesPolyphenols, natural compounds found in plant-based foods, possess special properties that can battle oxidative stress and stimulate the activation of molecules that aid in synaptic plasticity, a process that underlies cognitive function. Unlike many traditional treatments, polyphenols affect a broad range of mechanisms in the brain that can assist in the maintenance of cognitive and mental health, as well as the recovery from neurodegenerative diseases. Examining the molecular basis underlying the link between food intake and brain function has presented the exciting possibility of using diet as a viable method to battle cognitive and psychiatric disorders.MethodsWe will discuss the molecular systems that link polyphenols, the gut, and the brain, as well as introduce published human and animal studies demonstrating the effects of polyphenol consumption on brain plasticity and cognition.ResultsBy influencing cellular energy metabolism and modulating the signaling pathways of molecules in...
150 citations
TL;DR: Diet efficacy among children whose parents reported the presence of GI symptoms, food allergy diagnoses, and suspected food sensitivities included greater improvement in ASD behaviors, physiological symptoms, and social behaviors compared with children whoseParents reported none of these symptoms, diagnoses, or sensitivities.
Abstract: Objectives Studies on the gluten-free and/or casein-free (GFCF) dietary intervention for children with autism spectrum disorders (ASDs) suggest that some children may positively respond to implementation of the dietary intervention. Other research suggests that children diagnosed with ASD can be classified into subpopulations based on various factors, including gastrointestinal (GI) abnormalities and immune function. Methods This study analyzes parental report data collected using a 90-item online questionnaire from 387 parents or primary caregivers of children diagnosed with ASD on the efficacy of the GFCF diet. Parents reported on their child's GI symptoms, food allergy diagnoses, and suspected food sensitivities, as well as the degree and length of their diet implementation. Results Overall, diet efficacy among children whose parents reported the presence of GI symptoms, food allergy diagnoses, and suspected food sensitivities included greater improvement in ASD behaviors, physiological symptoms, and social behaviors compared with children whose parents reported none of these symptoms, diagnoses, or sensitivities (P Discussion These findings suggest that various intricacies related to diet implementation and GI and immune factors may play a role in differentiating diet responders from diet non-responders and substantiate the importance of further investigations into the various, nuanced factors that influence efficacy of the intervention among children with ASDs.
150 citations
TL;DR: The mechanisms by which polyphenols and endogenous antioxidants can produce protection against oxidative stress are reviewed, including: scavenging nitrogen and oxygen reactive species, regulation of signaling pathways associated with cell survival and inflammation, and inhibition of synphilin-1 and alpha-synuclein aggregation.
Abstract: Parkinson’s disease (PD) is a neurodegenerative movement disorder characterized by the degeneration and progressive loss of dopaminergic neurons in the substantia nigra pars compacta. It has been suggested that oxidative stress plays a role in the etiology and progression of PD. For instance, low levels of endogenous antioxidants, increased reactive species, augmented dopamine oxidation, and high iron levels have been found in brains from PD patients. In vitro and in vivo studies of Parkinson models evaluating natural and endogenous antioxidants such as polyphenols, coenzyme Q10, and vitamins A, C, and E have shown protective effects against oxidative-induced neuronal death. In this paper, we will review the mechanisms by which polyphenols and endogenous antioxidants can produce protection. Some of the mechanisms reviewed include: scavenging nitrogen and oxygen reactive species, regulation of signaling pathways associated with cell survival and inflammation, and inhibition of synphilin-1 and alpha-synuclein aggregation.
111 citations
TL;DR: Older adults with MCI had significant improvements in several measures of cognitive function when supplemented with an oily emulsion of DHA-phospholipids containing melatonin and tryptophan for 12 weeks, compared with the placebo.
Abstract: Age-related changes in nutritional status can play an important role in brain functioning. Specific nutrient deficiencies in the elderly may exacerbate pathological processes in the brain. Consequently, the potential of nutritional intervention to prevent or delay cognitive impairment and the development of dementia is an important topic. A randomized, double-blind, placebo-controlled trial has been performed in 25 elderly subjects (86 ± 6 years, 20 females, 5 males) with mild cognitive impairment (MCI). These subjects were randomly assigned to supplement their diet with either an oily emulsion of docosahexaenoic acid (DHA)-phospholipids containing melatonin and tryptophan (11 subjects) or a placebo (14-matched subjects) for 12 weeks. The main aim of this study was to evaluate the efficacy of the dietary supplement on cognition, by the assessment at the start and after 12 weeks of: (1) Orientation and other cognitive functions: Mini-Mental State Examination (MMSE); (2) Short-term memory: digit, ve...
74 citations
TL;DR: Spirulina can reduce the cytotoxicity and inhibit expression of inflammation-related genes of LPS-stimulated BV-2 microglial cells.
Abstract: ObjectiveOur aim was to investigate the effects of Spirulina on BV-2 microglial cell cytotoxicity and inflammatory genes expression.MethodsBV-2 microglial cells were treated with lipopolysaccharide (LPS) (1 µg/ml) and various concentrations of Spirulina platensis water extract or its active component (C-phycocyanin (C-PC)) for 24 hours. Cytotoxicity (lactate dehydrogenase (LDH) release) and expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) mRNAs were assayed.ResultsLPS increased LDH production and up-regulated expression of iNOS, COX-2, TNF-α, and IL-6 by BV-2 microglial cells. However, Spirulina platensis water extract and C-PC significantly reduced LPS-induced LDH release, and expression of iNOS, COX-2, TNF-α, and IL-6 mRNAs.ConclusionSpirulina can reduce the cytotoxicity and inhibit expression of inflammation-related genes of LPS-stimulated BV-2 microglial cells.
60 citations
TL;DR: Folic acid enhances the stimulation by ischemia of Notch signaling and hippocampal neurogenesis in adult brain and lessens the impairment of cognitive function that occurs after experimental stroke.
Abstract: Increasing neurogenesis may restore cognitive functions that are impaired in ischemia stroke. Folic acid has been reported to play an important role in neuronal development and reduce the risk of ischemic stroke in primary prevention. Folic acid supplementation stimulates Notch signaling and cell proliferation in neural progenitor cells cultured from neonatal brain. The present study determined whether folic acid supplementation stimulates Notch signaling and neurogenesis and improves cognitive function after ischemic stroke in adult brain. Rats were randomly assigned to four groups: sham operation plus vehicle (Sham), middle cerebral artery occlusion plus vehicle (MCAO), MCAO plus low-dose folic acid (4 mg/(kg day)), and MCAO plus high folic acid (12 mg/(kg day)). The vehicle and folic acid were administered by oral gavage for 28 days prior to sham or MCAO operation and up to 14 days after surgery. Newborn hippocampal neurons were detected at 3, 7, and 14 days post-MCAO. Cognitive function (learn...
60 citations
TL;DR: Treatment with α-mangostin and curcumin provided a neuroprotective effect against IAA in primary cultures of CGNs, an effect associated with an amelioration of the IAA-induced ROS production.
Abstract: Curcumin is a phenolic yellow curry pigment with anti-inflammatory and antioxidant activities and α-mangostin is a xanthone isolated from mangosteen fruit with antioxidant properties. Iodoacetate (IAA) is an inhibitor of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase that induces a model of metabolic inhibition in neurons where reactive oxygen species (ROS) production is a significant mechanism. Furthermore, it has been shown that the induction of heme oxygenase-1 (HO-1) protects against IAA-induced neuronal death.ObjectivesTo study the effects of α-mangostin and curcumin against the IAA-induced cell death and on HO-1 expression in primary cultures of cerebellar granule neurons (CGNs).MethodsCGNs were treated with curcumin or α-mangostin before the addition of IAA. Cell viability and ROS production were measured 24 and 4 hours after IAA addition, respectively. HO-1 expression was measured by western blot.ResultsBoth α-mangostin and curcumin pretreatment ameliorated the neuronal dea...
56 citations
TL;DR: This evidence is the first demonstration that dietary supplementation with a decaffeinated green coffee preparation may beneficially influence the brain, in particular promoting brain energy metabolic processes.
Abstract: ObjectivesThere is accumulating evidence that coffee consumption may reduce risk for type 2 diabetes, a known risk factor for Alzheimer's and other neurological diseases. Coffee consumption is also associated with reduced risk for Alzheimer's disease and non-Alzheimer's dementias. However, preventive and therapeutic development of coffee is complicated by the cardiovascular side effects of caffeine intake. As coffee is also a rich source of chlorogenic acids and many bioactive compounds other than caffeine, we hypothesized that decaffeinated coffee drinks may exert beneficial effects on the brain.MethodsWe have investigated whether dietary supplementation with a standardized decaffeinated green coffee preparation, Svetol®, might modulate diet-induced insulin resistance and brain energy metabolism dysfunction in a high-fat diet mouse model.ResultsAs expected, dietary supplementation with Svetol® significantly attenuated the development of high-fat diet-induced deficits in glucose-tolerance response...
54 citations
TL;DR: This paper reviews and discusses the last 3-year findings related to the principal molecular mechanisms involved in the control of the balance between apoptosis and cell proliferation exerted by polyphenols.
Abstract: Dietary consumption of fruit, vegetables, fish, and olive oil has been demonstrated to exert beneficial effects on human health. This finding may be due to the high content of antioxidant compounds including polyphenols. Current evidence strongly supports a contribution of polyphenols to the prevention of several chronic degenerative diseases such as cancer, atherosclerosis and cardiovascular diseases, central nervous system disorders, as well as aging. Apoptosis is a genetically controlled and evolutionarily conserved form of cell death of critical importance for the maintenance of tissue homeostasis in the adult organism. The malfunction of the death machinery may play a primary role in various pathologic processes, leading to proliferative or degenerative diseases. Polyphenols can interact with specific steps and/or proteins regulating the apoptotic process in different ways depending on their concentration, the cell system, the type or stage of the pathological process. Because of their abilit...
51 citations
TL;DR: Neither randomized-controlled trials nor observational studies provide conclusive evidence whether Zn in the diet is associated with cognitive decline or AD, and the current state of evidence does not allow conclusions to be drawn on whether supplementation of Zn is beneficial for the prevention or treatment of AD.
Abstract: Objectives This paper reviews evidence of an association between zinc (Zn) nutrition and Alzheimer's disease (AD) or age-associated cognitive decline. The involvement of zinc in the pathology of AD has been reported hundreds of times. It is, however, still a matter of debate whether the disease progression can be influenced by modifying zinc in the diet. Methods We searched Medline, Embase, Biosis, ALOIS, the Cochrane central register of controlled trials, the Cochrane database of systematic reviews, and different publisher databases, and included studies that dealt with zinc in the diet and AD or cognitive decline in elderly subjects. Results Fifty-five studies met the inclusion criteria. Neither randomized-controlled trials nor observational studies provide conclusive evidence whether Zn in the diet is associated with cognitive decline or AD. Case-control and autopsy studies suggest decreased systemic and increased brain Zn levels, respectively. Discussion The current state of evidence does not allow co...
TL;DR: Self-reported conduct problems are elevated in children and adolescents with histories of early childhood malnutrition and later vulnerability to increased conduct problems appears to be mediated by the more proximal neurobehavioral effects of the malnutrition on cognitive function and by adverse conditions in the early home environment.
Abstract: Objectives: The purpose of this study was to compare the prevalence of conduct problems in a welldocumented sample of Barbadian adolescents malnourished as infants and a demographic comparison group and to determine the extent to which cognitive impairment and environmental factors account for this association. Methods: Behavioral symptoms were assessed using a 76-item self-report scale in 56 Barbadian youth (11–17 years of age) with histories of protein–energy malnutrition (PEM) limited to the first year of life and 60 healthy classmates. Group comparisons were carried out by longitudinal and cross-sectional multiple regression analyses at 3 time points in childhood and adolescence. Results: Self-reported conduct problems were more prevalent among previously malnourished youth (P < 0.01). Childhood IQ and home environmental circumstances partially mediated the association with malnutrition. Teacher-reported classroom behaviors at earlier ages were significantly correlated with youth conduct problems, confirming the continuity of conduct problems through childhood and adolescence. Discussion: Self-reported conduct problems are elevated in children and adolescents with histories of early childhood malnutrition. Later vulnerability to increased conduct problems appears to be mediated by the more proximal neurobehavioral effects of the malnutrition on cognitive function and by adverse conditions in the early home environment.
TL;DR: The literature suggests that certain naturally occurring compounds and polysaccharide-rich extracts show promise, when taken orally, in supporting neurologic health and function.
Abstract: Objectives: Current research efforts are centered on delineating the novel health benefits of naturally derived saccharides, including growing interest in their abilities to influence neurologic health. We performed a comprehensive review of the literature to consolidate all controlled studies assessing various roles of exogenous saccharide compounds and polysaccharide-rich extracts from plants, fungi, and other natural sources on brain function, with a significant focus on benefits derived from oral intake. Methods: Studies were identified by conducting electronic searches on PubMed and Google Scholar. Reference lists of articles were also reviewed for additional relevant studies. Only articles published in English were included in this review. Results: Six randomized, double-blind, placebo-controlled clinical studies were identified in which consumption of a blend of plant-derived polysaccharides showed positive effects on cognitive function and mood in healthy adults. A separate controlled clinical study observed improvements in well-being with ingestion of a yeast beta-glucan. Numerous animal and in vitro studies have demonstrated the ability of individual saccharide compounds and polysaccharide-rich extracts to modify behavior, enhance synaptic plasticity, and provide neuroprotective effects. Discussion: Although the mechanisms by which exogenous saccharides can influence brain function are not well understood at this time, the literature suggests that certain naturally occurring compounds and polysaccharide-rich extracts show promise, when taken orally, in supporting neurologic health and function. Additional well-controlled clinical studies on larger populations are necessary, however, before specific recommendations can be made.
TL;DR: Protective mechanism of carnosic acid protected neuronal cells under ischemia/hypoxia through scavenging or reducing of ROS and NO, inhibiting COX-2 and MAPK pathways by anti-inflammatory and anti-oxidative properties.
Abstract: Ischemia/hypoxia induces oxidative stress which is associated with neurodegenerative diseases. The present study investigated protective mechanism of carnosic acid (CA) on ischemia/reperfusion and hypoxia-induced neuronal cell injury. The results showed that CA reduced 52% of the infarct volume from brains under ischemia/reperfusion in vivo and protected the PC12 cells from hypoxic injury in vitro .C A (1.0 μM) enhanced cell viability, prevented lactic dehydrogenase (LDH) release, scavenged reactive oxygen species (ROS), increased superoxide dismutase activity, and attenuated Ca 2+ release, lipid peroxidation, and prostaglandin E2 production in hypoxic PC12 cells. In addition, CA also reduced nitric oxide (NO) and interleukine (IL)-1 and IL-6 production from activated BV-2 microglia. Furthermore, its effect on hypoxia-induced mitogen-activated protein kinases (MAPKs) signaling pathway and caspase-3 was examined. Extracellular signal-regulated protein kinases, c-jun NH2-terminal kinase, and p38 MAPK were activated during hypoxia. CA inhibited MAPKs, caspase-3, and COX-2 activation and correlated well with the diminished LDH release and apoptosis (TUNEL) in PC12 cells under hypoxia. Taken together, CA protected neuronal cells under ischemia/hypoxia through scavenging or reducing of ROS and NO, inhibiting COX-2 and MAPK pathways by anti-inflammatory and anti-oxidative properties.
TL;DR: The antioxidant vitamin complex was effective in reducing oxidative stress in PBMNC of AD patients by lowering ROS production, improving cellular antioxidant capacities and modifying cytokine induced inflammation.
Abstract: Objectives The in vitro effect of a vitamin complex in generating and reducing oxidative species in peripheral blood mononuclear cells (PBMNC) and plasma of patients with Alzheimer's disease (AD) and healthy subjects (HS) was evaluated. Methods Two concentrations of a vitamin complex ([A] and [20A]) with ascorbic acid, alpha-tocopherol, and beta-carotene were incubated with either mononuclear cells or plasma. The generation of oxidizing species was measured in a luminol-dependent chemiluminescence assay and the reducing response by the MTT dye reduction assay. The levels of cytokines (interleukin [IL]-1β, IL-6, and IL-4) were measured by sandwich enzyme-linked immunosorbent assay. Results Our results demonstrated that the increase in the vitamin complex concentration reduced the reactive oxygen species (ROS) production and enhanced cellular reduction capacity in cells of AD patients in concentration [20A]. Plasma reduction capacity rose significantly for both groups (AD and HS). Concentration [A] did not ...
TL;DR: The potential efficacy of a heat-processed form of ginseng on cognitive function and behavioral symptoms in patients with moderately severe Alzheimer's disease is demonstrated.
Abstract: ObjectivesGinseng has been reported to improve cognitive function in animals and in healthy and cognitively impaired individuals. In this study, we investigated the efficacy of a heat-processed form of ginseng that contains more potent ginsenosides than raw ginseng in the treatment of cognitive impairment in patients with moderately severe Alzheimer's disease (AD).MethodsForty patients with AD were randomized into one of three different dose groups or the control group as follows: 1.5 g/day (n = 10), 3 g/day (n = 10), and 4.5 g/day (n = 10) groups, or control (n = 10). The Alzheimer's Disease Assessment Scale (ADAS) and Mini-Mental State Examination (MMSE) were used to assess cognitive function for 24 weeks.ResultsThe treatment groups showed significant improvement on the MMSE and ADAS. Patients with higher dose group (4.5 g/day) showed improvements in ADAS cognitive, ADAS non-cognitive, and MMSE score as early as at 12 weeks, which sustained for 24-week follow-up.DiscussionThese results demonstra...
TL;DR: It is shown that the administration of CUR significantly diminished the oxidative damage in the hippocampus of rats exposed to the OP PAR, suggesting that CUR may be an alternative to prevent neurodegenerative damage after pesticide exposure.
Abstract: One of the main concerns regarding organophosphate pesticides (OP) is their possible toxic effects. Doses that do not produce acute toxicity are capable of altering the structure and biochemistry of different tissues and organs by production of reactive oxygen species (ROS). Curcumin (CUR) is the main substance in Curcuma longa (Zingiberacea) rhizome that has strong antioxidant activity. However, the neuroprotective properties of curcumin against oxidative stress induced by prolonged exposure to parathion (PAR) is not clear. Objective The present work evaluated the protective effect of curcumin against the oxidative damage induced in the rat hippocampus by the OP PAR. Methods Forty female Wistar rats were distributed in four groups as follows: exposed to PAR by inhalation (PAR group); pre-treated with CUR and then exposed to PAR by inhalation, (CUR + PAR group); exposed to environmental air and treated with CUR in the food (CUR group); and exposed to environmental air (the control group). At the end of th...
TL;DR: Omega-3 intake, plasma PC DHA, and plasma PC EPA were all significant positive predictors of memory functioning, consistent with the possibility that omega-3 fatty acid nutrition has an impact on cognitive decline.
Abstract: ObjectivesVarious strands of evidence suggest that low intake of omega-3 fatty acids increases risk of cognitive decline and dementia. The present study investigated differences in dietary intake and blood plasma content of eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3) in individuals with cognitive impairment no dementia (CIND), individuals with Alzheimer's disease (AD), and healthy volunteers (HV).MethodsA total of 135 individuals aged between 55 and 91 years (19 AD, 55 CIND, and 61 HV) were assessed predominantly within a hospital setting.ResultsCompared with age and sex-matched HV, individuals with AD or CIND performed poorly on a majority of tests of cognitive function. Impairment was greatest for delayed and verbal recognition memory. CIND individuals were less impaired than AD individuals. Omega-3 intake and the percentage of EPA and DHA in plasma phosphatidylcholine (PC) showed a similar pattern (AD < HV, with intermediate scores for CIND). Across the whole sa...
TL;DR: The results suggest that alpha-mangostin is able to modulate GPx activity as a potential antioxidant strategy, thereby transiently consuming GSH levels.
Abstract: BackgroundIn a previous report, we have characterized the antiperoxidative properties of alpha-mangostin in different toxic models tested in nerve tissue preparations.ObjectivesHere, the modulatory effects of this xanthone on the glutathione system (reduced glutathione (GSH) levels, glutathione peroxidase (GPx), and glutathione S-transferase (GST) activities) were tested in synaptosomal P2 fractions isolated from rat brains in order to provide further information on key mechanisms exerted by this antioxidant in the nervous system.MethodsSynaptosomes were exposed to increasing concentrations of the xanthone, and also challenged to the toxic actions of a free radical generator, ferrous sulfate (FeSO4). For comparative purposes, the mitochondrial toxin 3-nitropropionic acid (3-NP) was also explored.ResultsAlpha-mangostin significantly decreased the levels of GSH, and increased GPx activity.DiscussionThis finding was interpreted as a modulatory action of the GSH system in preparation to exert antioxid...
TL;DR: It is hypothesized that hypomagnesaemia could be an epiphenomenic biochemical trait in less drug-responsive depressed patients and lower Mg levels and hyperactive traits identify a biological subtype of patients with increased catecholaminergic functioning and a poorer response to aminergic drugs.
Abstract: ObjectivesHigh, normal, or low plasma magnesium (Mg) levels have been observed in depressed patients. The aim of our study was to investigate the relationship of Mg levels with depression severity, specific psychopathological dimensions, and treatment outcome.MethodsA total of 123 outpatients during a major depressive episode were recruited. All patients showed at least two major depressive episodes and did not achieve remission in the former treatment trial. A blood sample was collected to determine total plasma Mg levels. The psychopathological status was assessed using Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, Depression Retardation Rating Scale for psychomotor retardation, and Snaith–Hamilton Pleasure Scale for anhedonia. Hamilton Depression Rating Scale was repeated at 3 months after treatment.ResultsAll patients showed Mg levels mostly within the normal range. No association between Mg levels and psychopathological severity was reported. Patients who responded to antid...
TL;DR: The results confirm the robust effect of chewing gum on reported alertness and show that changes in the effects of chewing Gum on attention require further investigation.
Abstract: Rationale: Chewing gum has been shown to reliably increase subjective alertness whereas the effects on attention are more variable. It has been suggested that chewing gum only enhances attention when the person has been performing a task for some time.
Objectives: The current research aimed to investigate if time-on-task trends enhancing effects of chewing gum could be observed in alertness and attention during and following chewing.
Methods: Study 1 used tests of reported mood, including reported mood, and tests of attention (categoric search, focussed attention, simple reaction time, and vigilance). These tasks were performed shortly after the start of chewing. Study 2 examined effects of previous and current chewing on reported alertness and the attention tests.
Results: Study 1 showed that chewing gum increased reported alertness and hedonic tone and improved performance on the categoric search task. Chewing gum maintained reported alertness across sessions in study 2. In the first experimental session of study 2 gum improved categoric search performance, and during the second session gum broadened focus of attention and quickened vigilance reaction time. This effect on vigilance reaction time was moderated by time-on-task, with an initial negative effect being replaced by a positive effect.
Discussion: The results confirm the robust effect of chewing gum on reported alertness and show that changes in the effects of chewing gum on attention require further investigation. Future research may also determine underlying mechanisms for an alerting effect.
TL;DR: OS has an intimate connection with ND, albeit low levels of ROS seem to protect the brain, and no one knows how to stop or delay ND at present.
Abstract: Oxidative stress (OS) and damages due to excessive reactive oxygen species (ROS) are common causes of injuries to cells and organisms. The prevalence of neurodegenerative diseases (ND) increases with aging and much of the research involving ROS and OS has emerged from works in this field. This text reviews some recent published articles about the role of OS in ND. Since there are many reviews in this field, the focus was centered in articles published recently. The Scientific Journals Directory supported by the Brazilian Ministry of Education Office for the Coordination of Higher Educational Personnel Improvement (CAPES) was used to search, download, and review articles. The search engine looked for the terms 'oxidative stress AND neurodegenerative diseases AND nutrition' in 10 different scientific collections. Biochemical markers for ND lack sensitivity or specificity for diagnosis or for tracking response to therapy today. OS has an intimate connection with ND, albeit low levels of ROS seem to protect the brain. Deleterious changes in mitochondria, OS, calcium, glucocorticoids, inflammation, trace metals, insulin, cell cycle, protein aggregation, and hundreds to thousands of genes occur in ND. The interaction of genes with their environment, may explain ND. Although OS has received much attention over the years, which increased the number of scientific works on antioxidant interventions, no one knows how to stop or delay ND at present. Interventions in vitro, in vivo, and in humans will continue to contribute for a better understanding of these pathologies.
TL;DR: Zinc-modulated apoptosis and the expression of Raf/MEK/ERK at the protein level in hippocampal neurons are demonstrated and it is possible that zinc depletion-induced apoptosis in cultured hippocampusal neurons may be relevant to the changes of Raf-1 kinase/mitogen-activated protein kinase ERK (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway.
Abstract: An experiment was performed to observe the changes in Raf-1 kinase/mitogen-activated protein kinase ERK (MEK)/extracellular signal-regulated kinase (ERK) signaling pathways in cultured hippocampal neurons and its correlation with neurons apoptosis induced by intracellular zinc depletion. Cultured hippocampal neurons were exposed to a cell membrane-permeant zinc chelator TPEN (2 µM), and to TPEN plus zinc sulfate (5 µM) for 24 h. Cultures were then processed to detect neuronal viability by the methyl thiazolyl tetrazolium assay, while apoptosis rate was simultaneously observed by the flow cytometric analysis. Caspase-3, Raf-1, pMEK, pERK1/2, and pCREB protein levels were examined by Western blot assays. The viability in TPEN-incubated neurons was notably decreased, apoptosis rate and expression of caspase-3 significantly increased compared to untreated controls. The significant down-regulation of Raf/MEK/ERK signaling pathway and expression of pCREB were decreased in TPEN-treated neurons. Co-additi...
TL;DR: The results suggest that malnutrition imposed at a critical development period caused an irreversible effect within the auditory primary sensory pathway.
Abstract: The brain that grows and develops under the continued influence of malnutrition presents permanent impairment on functioning and neurotransmitter release. The aim of this study was to investigate the chronic effects of neonatal food restriction on neurochemical and neurodynamical aspects within the primary auditory sensory pathway. Our working hypothesis is that neonatal malnutrition may affect the flow of primary sensory information both at a neurochemical and neurodynamical level. To test this hypothesis, three groups of rats were assigned, from birth to 370 days of life, to the following dietary scheme: a well-nourished (WN) group fed ad libitum lab chow diet; an undernourished (UN) group fed 60% of diet consumed by WN group; and a rehabilitated group, undergoing same dietary restriction as undernourished until 42 days of age and thereafter fed ad libitum until the end of the experiment. At 370 days of age, the animals were submitted to brainstem auditory-evoked potentials (BAEPs) recordings and sacrif...
TL;DR: The data indicate that N21 #125 protected the brain from oxidative damage and inflammation induced by the HFD, and may be through up-regulation of the transcription factor Nrf2 expression.
Abstract: Aims A novel nutritional supplement complex (N21 #125) composed of four well-known compounds (chromium picolinate, phosphatidylserine, docosahexaenoic acid, and boron) was designed to improve memory function and maintain brain health. The present study evaluated the complex's potential mechanism of action and its role in reducing oxidative stress in the brain of obese rats fed a high-fat diet (HFD). Methods Male Wistar rats (n = 40, 8-week-old) were divided into four groups. Group I was fed a standard diet; Group II was fed a standard diet and supplemented with N21 #125; Group III was fed an HFD; and Group IV was fed an HFD and supplemented with N21 #125 for 12 weeks. Results Rats fed HFD had greater serum C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-α) and brain malondialdehyde (MDA) concentrations than rats fed the control diet. Supplementation of N21 #125 decreased CRP, TNF-α, and MDA concentration in rats fed HFD. The levels of brain nuclear factor-E2-related factor-2 (Nrf2), heme oxy...
TL;DR: It is concluded that neuritin mRNA and protein were expressed and down-regulated in Schwann cells under high-glucose concentration and the down-regulation may contribute to apopotosis of Schwann Cells.
Abstract: We aimed to explore neuritin expression in Schwann cells under different glucose conditions. Expression of neuritin at the levels of transcription and translation in purified Schwann cells was detected and measured using reverse transcriptase (RT) (quantitative) polymerase chain reaction (PCR) and western blot. Apoptosis of Schwann cells was measured by flow cytometry using Fluorescence Activated Cell Sorter (FACS) analysis and caspase fluorometric assay. Neuritin mRNA and protein were detected in cultured primary Schwann cells. Neuritin was identified as cell membrane form of protein and predominately as secreted or solube form of protein. Neuritin was significantly lower in 150 mM glucose condition, and more significantly lower in 300 mM glucose, than 5.6 mM glucose condition at 36 hours and especially at 48 hours of the culture, respectively (P < 0.05-0.01). In contrast to 5.6 mM glucose, obvious apoptosis of Schwann cells was demonstrated at 42 hours in 300 mM glucose condition and at 48 hours in 150 mM glucose, respectively (P < 0.05-0.01). Neuritin and apoptosis were correlated in a power regression (P < 0.01). 5.6 mM glucose cultured cells did not show these obvious changes during the experiment. It is concluded that neuritin mRNA and protein were expressed and down-regulated in Schwann cells under high-glucose concentration and the down-regulation may contribute to apopotosis of Schwann cells.
TL;DR: The data suggest that this diet alters insulin signaling differentially in each brain region, and that hippocampal changes induced by this diet could contribute to the understanding of cognitive impairments that are dependent on the hippocampus.
Abstract: Background/objectives Highly palatable food (HPF), which is enriched in simple sugars and saturated fat, contributes to obesity and insulin resistance in humans These metabolic changes are associated with serious complications of the central nervous system, including an elevated risk of cognitive dysfunction We, herein, treated rats with HPF and then examined the insulin-signaling pathway, in particular, the levels of phosphatidylinositol-3 kinase (PI3K), Akt, and insulin receptor substrate-1 (IRS-1) in the hippocampus and hypothalamus Methods Adult Wistar rats fed with HPF (heated or not during preparation) for 4 months and then measured the levels of PI3K, Akt, and IRS-1 in the hippocampus and hypothalamus, by western blotting and quantitative real-time polymerase chain reaction Results We observed changes in body weight, glucose intolerance, and lipidemia, confirming that peripheral metabolic alterations were induced using this model Hippocampal PI3K and hypothalamic Akt were affected in rats that
TL;DR: The main adverse effects of reactive oxygen species (ROS) in the mammalian organism are reviewed, introducing the reader on the worldwide problem of the ROS neurophysiological impact on the developing and the adult brain, and discussing the neuroprotective action of antioxidant molecules.
Abstract: ObjectivesWe review the main adverse effects of reactive oxygen species (ROS) in the mammalian organism, introducing the reader on the worldwide problem of the ROS neurophysiological impact on the developing and the adult brain, and discussing the neuroprotective action of antioxidant molecules.MethodsWe briefly present the electrophysiological phenomenon designated as ‘cortical spreading depression’ (CSD), as a parameter of normal brain functioning. We highlight recent electrophysiological advances obtained in experimental studies from our laboratory and from others, showing how to investigate the ROS effects on the brain by using the CSD phenomenon.ResultsUnder conditions such as aging, ROS production by photo-activation of dye molecules and ethanol consumption, we describe the effects, on CSD, of treating animals with (1) antioxidants and (2) with antioxidant-deficient diets.DiscussionThe current understanding of how ROS affect brain electrophysiological activity and the possible interaction be...
TL;DR: The IC neuronal morphology appearances suggest a possible mechanism for the impairment in information processing of complex phenomena such as taste sensation and hedonic response.
Abstract: The insular cortex (IC) of the rat is a major area for the convergence and integration of olfactory, gustatory, and visual information, and at present it is unclear if perinatal undernutrition interferes with the structure and function of the IC neurons. Golgi–Cox-stained cells of the IC were studied in control and undernourished Wistar rats at 12, 20, and 30 days of age. Pregnant dams were undernourished by the reduction of a balanced diet during a part of the gestational period (G6–G18). After parturition (P1–P23) pups remained for 12 hours with a normal and 12 hours with a nipple-ligated dam. Undernutrition significantly reduced the number, and the arborization of the dendritic arbors, and the perimeter, and cross-sectional area of perikarya. The IC neuronal morphology appearances suggest a possible mechanism for the impairment in information processing of complex phenomena such as taste sensation and hedonic response.
TL;DR: Using two-dimensional electron microscopic analyses of synapses staining with ethanolic phosphotungstic acid, an increment of PSD thickness in severe hypoxic rats is observed, suggesting that hypoxia might cause early misfolding and aggregation of synaptic proteins in severe anoxic animas that could induce long-term neurodegeneration.
Abstract: Perinatal asphyxia (PA) is a medical condition associated with a high short-term morbimortality and different long-term neurological diseases. In previous work we have observed at 6 months post-synaptic densities (PSDs) alterations compatible with neurodegeneration highly correlated with the increment in the ubiquitination. Although alterations in the synaptic organization and function have been related with neuronal death after hypoxia, little is known about the synaptic changes in young animals exposed to PA. The main aim of this work is to study the PSDs changes in striatum of 30-day-old rats subjected to PA. Using two-dimensional electron microscopic analyses of synapses staining with ethanolic phosphotungstic acid we observed an increment of PSD thickness in severe hypoxic rats. These data are consistent with the western blot analysis that showed an increment in ubiquitination levels in the synapses of severe hypoxic rat. We did observe any alterations neither in synaptic structure nor in ubiquitinization in mild asphyctic rats. These data suggest that hypoxia might cause early misfolding and aggregation of synaptic proteins in severe anoxic animas that could induce long-term neurodegeneration.