ascorbic-acid and Cognitive-Dysfunction

Previous studies have suggested that increased antioxidant intakes might reduce risk of cognitive disorders including Alzheimer's disease (AD). Which avenue of antioxidant intake (vitamin E/C) is more effective for decreasing risk, however, is largely unknown.. To quantitatively investigate the relationships between the pattern of antioxidant intakes and risks of dementia and cognitive decline.. We searched all related prospective cohort studies reporting antioxidant intakes (diet and/or supplement) from patients with cognitive disorders. We conducted dose-response meta-analyses to assess potential linear and non-linear dose-response relationships. Summary RRs and 95% CIs were calculated using a random- or fixed-effects model.. The risk of incident AD is significantly reduced by higher consumption of vitamin C by the intake avenue of diet plus supplement.

Topics: Alzheimer Disease; Antioxidants; Ascorbic Acid; Cognitive Dysfunction; Humans; Prospective Studies; Vitamin E; Vitamins

Nutrition has relevant role in the pathogenesis of dementia. However, in Latin American Countries (LAC), it is unknown which type of diet the subjects with dementia and cognitive dysfunction have.. The main purpose of this study was to determine micro- and macronutrients and food frequency intake among the LAC population with mild cognitive impairment (MCI) and dementia.. A systematic review using PubMed, Cochrane, Lilacs, and Scielo databases. Energy intake as well as micro- and macronutrients intake were analyzed using a random-effect model and presented in a forest plot.. Nine articles were included, an estimated energy intake of 1598.47 kcal (95% CI 1351.07-1845.88) was obtained. A daily consumption of 73.64 g/day (95% CI 64.07-83.2) of protein; 262.17 g/day (95% CI 214.51-309.93) of carbohydrates, and 57.91 g/day (95% CI 49.16-66.66) of fats were reported. A micronutrients daily intake consumption of 201.35μg/day of vitamin B9 (95% CI 125.32-277.38); 5.61μg/day of vitamin B12 (95% CI 2.53-8.70), and 139.67 mg/day of vitamin C (95% CI 59.33-220.02). Mineral intake of 637.32 mg/day of calcium (95% CI 288.54-986.11) and 9 mg/day of iron (95% CI 2.28-15.71) was obtained. A low intake of fruits and vegetables was found.. Individuals with MCI and dementia from LAC have a nutritional deficiency characterized by a lower intake of fruits and vegetables, a high consumption of carbohydrates and protein, adequate fats intake and vitamins B12, vitamin C, and iron consumption, but a low intake of vitamin B9 and calcium.

Topics: Ascorbic Acid; Calcium; Cognitive Dysfunction; Dementia; Eating; Energy Intake; Folic Acid; Humans; Iron; Latin America; Vitamin B 12; Vitamins

Vitamin C deficiency may be more common than is generally assumed, and the association between vitamin C deficiency and adverse psychiatric effects has been known for centuries. This paper aims to systematically review the evidence base for the neuropsychiatric effects of vitamin C deficiency.. Relevant studies were identified via systematic literature review.. Nine studies of vitamin C deficiency, including subjects both with and without the associated physical manifestations of scurvy, were included in this review. Vitamin C deficiency, including scurvy, has been linked to depression and cognitive impairment. No effect on affective or non-affective psychosis was identified.. Disparate measurement techniques for vitamin C, and differing definitions of vitamin C deficiency were apparent, complicating comparisons between studies. However, there is evidence suggesting that vitamin C deficiency is related to adverse mood and cognitive effects. The vitamin C blood levels associated with depression and cognitive impairment are higher than those implicated in clinical manifestations of scurvy. While laboratory testing for ascorbic acid can be practically difficult, these findings nonetheless suggest that mental health clinicians should be alerted to the possibility of vitamin C deficiency in patients with depression or cognitive impairment. Vitamin C replacement is inexpensive and easy to deliver, although as of yet there are no outcome studies investigating the neuropsychiatric impact of vitamin C replacement in those who are deficient.

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Cognitive Dysfunction; Depression; Humans; Scurvy; Vitamins

Vitamins and minerals play multiple functions within the central nervous system which may help to maintain brain health and optimal cognitive functioning. Supplementation of the diet with various vitamins and minerals has been suggested as a means of maintaining cognitive function, or even of preventing dementia, in later life.. To evaluate the effects of vitamin and mineral supplementation on cognitive function in cognitively healthy people aged 40 years or more.. We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group's (CDCIG) specialised register, as well as MEDLINE, Embase, PsycINFO, CINAHL, ClinicalTrials.gov and the WHO Portal/ICTRP from inception to 26th January 2018.. We included randomised controlled trials that evaluated the cognitive effects on people aged 40 years or more of any vitamin or mineral supplements taken by mouth for at least three months.. Study selection, data extraction, and quality assessments were done in duplicate. Vitamins were considered broadly in the categories of B vitamins, antioxidant vitamins, and combinations of both. Minerals were considered separately, where possible. If interventions and outcomes were considered sufficiently similar, then data were pooled. In order to separate short-term cognitive effects from possible longer-term effects on the trajectory of cognitive decline, data were pooled for various treatment durations from 3 months to 12 months and up to 10 years or more.. In total, we included 28 studies with more than 83,000 participants. There were some general limitations of the evidence. Most participants were enrolled in studies which were not designed primarily to assess cognition. These studies often had no baseline cognitive assessment and used only brief cognitive assessments at follow-up. Very few studies assessed the incidence of dementia. Most study reports did not mention adverse events or made only very general statements about them. Only 10 studies had a mean follow-up > 5 years. Only two studies had participants whose mean age was < 60 years at baseline. The risk of bias in the included studies was generally low, other than a risk of attrition bias for longer-term outcomes. We considered the certainty of the evidence behind almost all results to be moderate or low.We included 14 studies with 27,882 participants which compared folic acid, vitamin B12, vitamin B6, or a combination of these to placebo. The majority of participants were aged over 60 years and had a history of cardio- or cerebrovascular disease. We found that giving B vitamin supplements to cognitively healthy adults, mainly in their 60s and 70s, probably has little or no effect on global cognitive function at any time point up to 5 years (SMD values from -0.03 to 0.06) and may also have no effect at 5-10 years (SMD -0.01). There were very sparse data on adverse effects or on incidence of cognitive impairment or dementia.We included 8 studies with 47,840 participants in which the active intervention was one or more of the antioxidant vitamins: ß-carotene, vitamin C or vitamin E. Results were mixed. For overall cognitive function, there was low-certainty evidence of benefit associated with ß-carotene after a mean of 18 years of treatment (MD 0.18 TICS points, 95% CI 0.01 to 0.35) and of vitamin C after 5 years to 10 years (MD 0.46 TICS points, 95% CI 0.14 to 0.78), but not at earlier time points. From two studies which reported on dementia incidence, there was low-certainty evidence of no effect of an antioxidant vitamin combination or of vitamin E, either alone or combined with selenium. One of the included studies had been designed to look for effects on the incidence of prostate cancer; it found a statistically significant increase in prostate cancer diagnoses among men taking vitamin E.One trial with 4143 participants compared vitamin D3 (400 IU/day) and calcium supplements to placebo. We found low- to moderate-certainty evidence of no effect. We did not find evidence that any vitamin or mineral supplementation strategy for cognitively healthy adults in mid or late life has a meaningful effect on cognitive decline or dementia, although the evidence does not permit definitive conclusions. There were very few data on supplementation starting in midlife (< 60 years); studies designed to assess cognitive outcomes tended to be too short to assess maintenance of cognitive function; longer studies often had other primary outcomes and used cognitive measures which may have lacked sensitivity. The only positive signals of effect came from studies of long-term supplementation with antioxidant vitamins. These may be the most promising for further research.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; beta Carotene; Calcium; Cholecalciferol; Cognition; Cognitive Dysfunction; Copper; Dementia; Dietary Supplements; Folic Acid; Humans; Middle Aged; Minerals; Randomized Controlled Trials as Topic; Selenium; Vitamin A; Vitamin B 12; Vitamin B 6; Vitamin E; Vitamins; Zinc

Vitamin C plays a role in neuronal differentiation, maturation, myelin formation and modulation of the cholinergic, catecholinergic, and glutaminergic systems. This review evaluates the link between vitamin C status and cognitive performance, in both cognitively intact and impaired individuals. We searched the PUBMED, SCOPUS, SciSearch and the Cochrane Library from 1980 to January 2017, finding 50 studies, with randomised controlled trials (RCTs,

Topics: Ascorbic Acid; Cognition Disorders; Cognitive Dysfunction; Nutritional Status

Oxidative stress is part of the entire pathological process that underlies the development of Alzheimer's disease (AD), including the mild cognitive impairment (MCI) stage. Twendee X (TwX) is a supplement containing a strong antioxidative mix of eight antioxidants, which has been shown to have a clinical and therapeutic benefit in AD model mice. Here, we conducted a multicenter, randomized, double-blind, and placebo-controlled prospective interventional study to evaluate the efficacy of TwX in mitigating MCI. The primary outcomes were differences in Mini-Mental State Examination (MMSE) and Hasegawa Dementia Scale-revised (HDS-R) scores between baseline and six months for placebo and TwX groups. Seventy-eight subjects with MCI were randomized into placebo (n = 37) and TwX (n = 41) groups. MMSE scores at six months differed significantly between the TwX and placebo groups (p = 0.018), and HDS-R scores for the TwX group exhibited a significant improvement at six months relative to baseline (p = 0.025). The TwX group did not show any change in affective or activities of daily living scores at six months. The present study indicates that strong antioxidative supplement TwX is clinical beneficial for cognitive function in subjects with MCI.

Topics: Activities of Daily Living; Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; Cognition; Cognitive Dysfunction; Cystine; Dietary Supplements; Double-Blind Method; Female; Glutamine; Humans; Male; Mental Status and Dementia Tests; Prospective Studies; Treatment Outcome

This study was carried out to investigate the effect of vitamins E and C on cognitive performance among the elderly in Iran.. About 256 elderly with mild cognitive impairment, aged 60-75 years, received 300 mg of vitamin E plus 400 mg of vitamin C or placebo daily just for 1 year.. Demographic characteristics, anthropometric variables food consumption, cognitive function by Mini-Mental State Examination (MMSE), and some of the oxidative stress biomarkers were examined.. Antioxidant supplementation reduced malondialdehyde level (P < 0.001) and raised total antioxidant capacity (P < 0.001) and glutathione (P < 0.01). The serum 8-hydroxydeoxyguanosine remained unchanged (P < 0.4). After adjusting for the covariates effects, MMSE scores following 6- (25.88 ± 0.17) and 12-month antioxidant supplementation (26.8 ± 0.17) did not differ from control group (25.86 ± 0.18 and 26.59 ± 0.18, respectively).. Despite significant improvement in most of the oxidative stress biomarkers, antioxidants' supplementation was not observed to enhance cognitive performance. A large number of kinetic and/or dynamic factors could be suspected.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Aged; Antioxidants; Ascorbic Acid; Cognition; Cognitive Dysfunction; Deoxyguanosine; Dietary Supplements; Double-Blind Method; Female; Glutathione; Humans; Iran; Male; Malondialdehyde; Middle Aged; Oxidative Stress; Vitamin E

Vascular aging is well known to be associated with the breakdown of the neurovascular unit (NVU), which is essential for maintaining brain homeostasis and linked to higher cognitive dysfunction. Oxidative stress is believed to be a significant cause of the vascular aging process. Vitamin C is easily oxidized under physiological conditions, so it loses its potent antioxidant activity. We developed a DNA aptamer that enhances the function of vitamin C. NXP032 is the binding form of the aptamer and vitamin C. In this study, we investigated the effect of NXP032 on neurovascular stabilization through the changes of PECAM-1, PDGFR-β, ZO-1, laminin, and glial cells involved in maintaining the integrity of the blood-brain barrier (BBB) in aged mice. NXP032 was orally administered daily for 8 weeks. Compared to young mice and NXP032-treated mice, 20-month-old mice displayed cognitive impairments in Y-maze and passive avoidance tests. NXP032 treatment contributed to reducing the BBB damage by attenuating the fragmentation of microvessels and reducing PDGFR-β, ZO-1, and laminin expression, thereby mitigating astrocytes and microglia activation during normal aging. Based on the results, we suggest that NXP032 reduces vascular aging and may be a novel intervention for aging-induced cognitive impairment.

Topics: Animals; Ascorbic Acid; Blood-Brain Barrier; Brain; Cognitive Dysfunction; Laminin; Mice

Chronic ethanol exposure causes neurotoxicity and long-term learning and memory impairment along with hippocampal and frontal cortical dysfunction. Flavonoids possess antioxidant and anti-inflammatory properties believed to be contributory factors in reversing cognitive decline. 6-Methoxyflavone (6-MOF), a flavonoid occurring naturally in medicinal plants, has been reported to instigate neuroprotection by reversing cisplatin-induced hyperalgesia and allodynia. Consequently, this study was designed to investigate 6-MOF activity in models of chronic ethanol-induced cognitive impairment along with neurochemical correlates.. Mice were given ethanol orally (2.0 g/kg daily) for 24 days plus either saline, 6-MOF (25-75mg/kg) or donepezil (4mg/kg) and then ethanol was withdrawn for the next 6 days. Animals were subsequently assessed for their cognitive performance in several models on days 1, 12, and 24, during abstinence (Day-26) and on the 7th day of the washout period. Following behavioral assessment, post-mortem dopamine, noradrenaline and vitamin C concentrations were quantified in the frontal cortex, hippocampus and striatum, using HPLC with UV detection.. Chronic ethanol treatment suppressed locomotor activity and impaired cognitive tasks, which included novel object recognition, performance in the Morris water maze as well as the Y-maze, socialization and nest-building behavior throughout the protocol and during withdrawal. These behavioral deficits were at least partially restored by the co-administration of 6-MOF or donepezil with ethanol as were ethanol-induced deficits in frontal cortical and hippocampal dopamine plus noradrenaline, together with striatal dopamine. 6-MOF co-administration with ethanol also modestly restored striatal vitamin C levels.. It is postulated that, apart from donepezil, 6-MOF may be useful not only in the treatment of ethanol withdrawal severity but also in the management of chronic ethanol withdrawal induced cognitive impairment.

Topics: Animals; Ascorbic Acid; Cognitive Dysfunction; Donepezil; Dopamine; Ethanol; Flavones; Hippocampus; Maze Learning; Mice; Norepinephrine

Postoperative cognitive impairment is more likely to occur in elderly patients and in those with neurodegenerative diseases. The mechanisms underlying this impairment include neuroinflammation and oxidative stress. The increase in reactive oxygen species during oxidative stress causes cellular and molecular injury to neurons, including DNA damage, which aggravate brain dysfunction. Vitamin C has antioxidant effects and improves cognitive function in patients with Alzheimer's disease. However, it is unclear whether it can ameliorate surgery-induced cognitive impairment by inhibiting oxidative stress. In this study, 6-month-old mice overexpressing mutant amyloid precursor protein and presenilin-1 (APP/PS1) were subjected to laparotomy. The open field and fear conditioning tests were used to assess cognitive function. Mice that underwent surgery showed cognitive impairment without changes in spontaneous locomotor activity. Oxidative stress, DNA damage and inflammatory mediators were increased in the hippocampus after surgery. The expression levels of non-homologous end-joining DNA repair-associated proteins, including Ku heterodimer, DNA-dependent protein kinase catalytic subunit, X-ray repair cross complementing 4 (XRCC4) and XRCC4-like factor, were increased after surgery. Vitamin C pretreatment effectively attenuated cognitive dysfunction induced by surgery and reduced oxidative stress and DNA damage. Our findings suggest that DNA damage plays an important role in surgery-induced cognitive dysfunction, and that vitamin C pretreatment may have therapeutic potential as a preventative approach for the cognitive impairment.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Ascorbic Acid; Cognitive Dysfunction; Disease Models, Animal; DNA Damage; Mice; Mice, Inbred C57BL; Mice, Transgenic; Presenilin-1

With the dramatically rapid rate of aging worldwide, the maintenance of cognitive function in old age is a major public health priority. The association between total antioxidant capacity (TAC) of midlife diet and cognitive function in late life is still unclear.. The study included 16 703 participants from a prospective cohort study in Singapore. Dietary intakes and selected supplementary use were assessed with a validated 165-item food frequency questionnaire at baseline (1993-1998). Two dietary TACs were calculated from the intake of antioxidant nutrients: the Comprehensive Dietary Antioxidant Index (CDAI) and the Vitamin C Equivalent Antioxidant Capacity (VCEAC). Cognitive function was assessed 20.2 years later using a Singapore-modified version of the Mini-Mental State Examination when subjects were 61-96 years old. Cognitive impairment was defined using education-specific cutoffs. Multivariable logistic regression models were utilized to estimate the associations between dietary TACs, component nutrients, and cognitive impairment.. A total of 2 392 participants (14.3%) were defined to have cognitive impairment. Both CDAI and VCEAC scores were inversely associated with odds of cognitive impairment in a dose-dependent manner. The odds ratio (95% confidence interval; p-trend) comparing the highest with the lowest quartile was 0.84 (0.73, 0.96; p-trend = .003) for the CDAI and 0.75 (0.66, 0.86; p-trend < .001) for the VCEAC. Higher intakes of vitamin C, vitamin E, carotenoids, and flavonoids were all inversely associated with cognitive impairment.. Higher dietary TAC was associated with lower odds of cognitive impairment in later life in a Chinese population in Singapore.

Topics: Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; China; Cognitive Dysfunction; Diet; Humans; Prospective Studies; Singapore

Apolipoprotein E E4 (APOE4) is a risk factor for cognitive decline. A high blood vitamin C (VC) level reduces APOE4-associated risk of developing cognitive decline in women. In the present study, we aimed to examine the effects of functional variants of VC transporter genes expressed in the brain (SLC2A1, SLC2A3, and SLC23A2) on APOE4-associated risk of developing cognitive decline. This case-control study involved 393 Japanese subjects: 252 cognitively normal and 141 cognitively impaired individuals (87 mild cognitive impairment and 54 dementia). Database searches revealed that rs1279683 of SLC23A2, and rs710218 and rs841851 of SLC2A1 are functional variants that are significantly associated with the altered expression of the respective genes and genotyped as three single nucleotide variants (SNVs). When stratified by SNV genotype, we found a significant association between APOE4 and cognitive decline in minor allele carriers of rs1279683 (odds ratio [OR] 2.02, 95% CI, 1.05-3.87, p = 0.035) but not in the homozygote carriers of the major allele. Significant associations between APOE4 and cognitive decline were also observed in participants with major allele homozygotes of rs710218 (OR 2.35, 95% CI, 1.05-5.23, p = 0.037) and rs841851 (OR 3.2, 95% CI, 1.58-6.46, p = 0.0012), but not in minor allele carriers of the respective SNVs. In contrast, the three functional SNVs showed no significant effect on cognitive decline. Our results imply that functional SNVs of VC transporter genes can affect APOE4-associated risk of developing cognitive decline via altered VC levels in the brain.

Topics: Aged; Apolipoprotein E4; Apolipoproteins E; Ascorbic Acid; Case-Control Studies; Cognitive Dysfunction; Female; Genotype; Glucose Transporter Type 1; Glucose Transporter Type 3; Humans; Male; Sodium-Coupled Vitamin C Transporters

Sepsis survivors present long-term cognitive deficits. The present study was to investigate the effect of early administration of high-dose vitamin C on cognitive function in septic rats and explore its possible cerebral protective mechanism. Rat sepsis models were established by cecal ligation and puncture (CLP). Ten days after surgery, the Morris water maze test was performed to evaluate the behavior and cognitive function. Histopathologic changes in the hippocampus were evaluated by nissl staining. The inflammatory cytokines, activities of antioxidant enzymes (superoxide dismutase or SOD) and oxidative products (malondialdehyde or MDA) in the serum and hippocampus were tested 24 h after surgery. The activity of matrix metalloproteinase-9 (MMP-9) and expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1(HO-1) in the hippocampus were measured 24 h after surgery. Compared with the sham group in the Morris water maze test, the escape latency of sepsis rats was significantly (P = 0.001) prolonged in the navigation test, whereas the frequency to cross the platform and the time spent in the target quadrant were significantly (P = 0.003) reduced. High-dose vitamin C significantly decreased the escape latency (P = 0.01), but increased the time spent in the target quadrant (P = 0.04) and the frequency to cross the platform (P = 0.19). In the CLP+ saline group, the pyramidal neurons were reduced and distributed sparsely and disorderly, the levels of inflammatory cytokines of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in the serum and hippocampus were significantly increased (P = 0.000), the blood brain barrier (BBB) permeability in the hippocampus was significantly (P = 0.000) increased, the activities of SOD in the serum and hippocampus were significantly (P = 0.000 and P = 0.03, respectively) diminished while the levels of MDA in the serum and hippocampus were significantly (P = 0.007) increased. High-dose vitamin C mitigated hippocampus histopathologic changes, reduced systemic inflammation and neuroinflammation, attenuated BBB disruption, inhibited oxidative stress in brain tissue, and up-regulated the expression of nuclear and total Nrf2 and HO-1. High-dose vitamin C significantly (P < 0.05) decreased the levels of tumor necrosis factor- (TNF)-α, interleukin-6 (IL-6), MDA in the serum and hippocampus, and the activity of MMP-9 in the hippocampus, but significantly (P < 0.05) increased the levels of SOD, the

Topics: Animals; Ascorbic Acid; Blood-Brain Barrier; Cognitive Dysfunction; Disease Models, Animal; Dose-Response Relationship, Drug; Heme Oxygenase (Decyclizing); Hippocampus; Inflammation; Male; NF-E2-Related Factor 2; Oxidative Stress; Protective Agents; Rats, Sprague-Dawley; Sepsis

Novel hybrids bearing a 2-aminopyrimidine (2-AP) moiety linked to substituted 1,3,4-oxadiazoles were designed, synthesized and biologically evaluated. Among the developed compounds, 28 noncompetitively inhibited human acetylcholinesterase (hAChE; pIC

Topics: Acetylcholinesterase; Animals; Butyrylcholinesterase; Cell Line; Cholinesterase Inhibitors; Cognitive Dysfunction; Dose-Response Relationship, Drug; Drug Design; Humans; Mice; Models, Molecular; Molecular Structure; Oxadiazoles; Pyrimidines; Structure-Activity Relationship

Antioxidants like vitamins C and E may minimize the risk for Alzheimer's disease.. We examined whether vitamins C and E modify the apolipoprotein E (APOE) E4-related risks for developing cognitive decline.. We conducted a population-based prospective study including Japanese residents aged 65 years from Nakajima, Japan. The participants received an evaluation of cognitive function and underwent blood tests including tests for vitamins C and E levels and APOE phenotypes. The APOE E4-by-gender-by-vitamin C or E interactions on developing cognitive decline were analyzed.. Of 606 participants with normal cognitive function determined using a baseline survey (2007-2008), 349 completed the follow up survey between 2014 and 2016. In women with APOE E4, significantly reduced risk for cognitive decline was observed for the highest blood vitamin C concentration tertile [multivariate OR 0.10 (95% CI 0.01-0.93)] compared with the lowest tertile. In men without APOE E4, significantly reduced risk for cognitive decline was observed for the highest blood vitamin E concentration tertile [multivariate OR 0.19 (0.05-0.74)] as compared with the lowest tertile.. Our results demonstrate significant beneficial effects of vitamins C and E in reducing the risk of cognitive decline in women with APOE E4 and men without APOE E4, respectively.

Topics: Aged; Aged, 80 and over; Apolipoprotein E4; Ascorbic Acid; Cognitive Dysfunction; Community Health Planning; Female; Humans; Japan; Male; Neuropsychological Tests; Prospective Studies; Psychiatric Status Rating Scales; Retrospective Studies; Vitamin E; Women's Health

Neuroinflammation is believed to be one of the primary causes of cognitive impairment. Previous studies showed that the antioxidant vitamin C (Vit C) performs many beneficial functions such as immunostimulant and anti-inflammatory actions, but its role in inflammatory cognitive impairment is unclear. In the current study, we investigated the effect and possible mechanism of action of Vit C in lipopolysaccharide (LPS)-induced cognitive impairment. Intracerebroventricular LPS-induced memory impairment was used as the model for neuroinflammatory cognitive dysfunction. Vit C was administered by intracerebroventricular microinjection 30 min prior to LPS exposure. It was found that Vit C significantly protected animals from LPS-induced memory impairment as evidenced by improved performance in the Morris water maze and novel object recognition tests without changes in spontaneous locomotor activity. Vit C pretreatment inhibited the activation of microglia and the production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Furthermore, Vit C pretreatment markedly decreased the malondialdehyde (MDA) level, increased superoxide dismutase (SOD) activity, and modulated the Bax/Bcl-2 ratio and p-p38 MAPK activation in the hippocampus of LPS-treated mice. Together, these results suggest that vitamin C pretreatment could protect mice from LPS-induced cognitive impairment, possibly through the modulation of oxidative stress and inflammatory responses.

Topics: Animals; Anti-Inflammatory Agents; Ascorbic Acid; Cognitive Dysfunction; Cytokines; Disease Models, Animal; Humans; Lipopolysaccharides; Male; Malondialdehyde; Maze Learning; Memory Disorders; Mice; Mice, Inbred C57BL; Neurogenic Inflammation; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Signal Transduction

Topics: Age Factors; Ascorbic Acid; Ascorbic Acid Deficiency; Biomarkers; Cognition; Cognitive Aging; Cognitive Dysfunction; Female; Health Status; Healthy Aging; Humans; Longitudinal Studies; Male; Mental Health; Middle Aged; New Zealand; Prevalence; Prospective Studies; Recommended Dietary Allowances; Risk Factors; Socioeconomic Factors

There are few studies of the association between the use of antioxidant vitamin supplements and the risk of Alzheimer's disease (AD). Cognitive decline is generally viewed as part of the continuum between normal aging and AD.. To evaluate whether the use of vitamin E and C supplements is associated with reduced risks of cognitive impairment, not dementia (CIND), AD, or all-cause dementia in a representative sample of older persons ≥65 years old.. Data from the Canadian Study of Health and Aging (1991-2002), a cohort study of dementia including 3 evaluation waves at 5-yearly intervals, were used. Exposure to vitamins E and C was self-reported at baseline in a risk factor questionnaire and/or in a clinical examination.. The data set included 5269 individuals. Compared with those not taking vitamin supplements, the age-, sex-, and education-adjusted hazard ratios of CIND, AD, and all-cause dementia were, respectively, 0.77 (95% CI = 0.60-0.98), 0.60 (95% CI = 0.42-0.86), and 0.62 (95% CI = 0.46-0.83) for those taking vitamin E and/or C supplements. Results remained significant in fully adjusted models except for CIND. Similar results were observed when vitamins were analyzed separately.. This analysis suggests that the use of vitamin E and C supplements is associated with a reduced risk of cognitive decline. Further investigations are needed to determine their value as a primary prevention strategy.

Topics: Aged; Aging; Alzheimer Disease; Antioxidants; Ascorbic Acid; Canada; Cognitive Dysfunction; Cohort Studies; Dementia; Dietary Supplements; Female; Humans; Male; Proportional Hazards Models; Risk Factors; Surveys and Questionnaires; Vitamin E

The purpose of this study was to determine total water intake and patterns of beverage consumption, and its contribution to total daily micronutrients and calories in older adults with mild memory decline. A descriptive, cross-sectional study was used with 60 independent community-dwelling older adults (71.7 ± 5.4 years) with mild cognitive impairment, who were mostly female, well-educated, and white. Three-day food records were analyzed using the Nutrition Data Systems for Research. Descriptive statistics were conducted for a summary of demographics, the average intakes of beverages, and the contribution of beverages to total calorie and micronutrient intakes. Total daily water intake was 53.6 ± 26.7 fl oz and milk, plain water, and tea/coffee were beverages consumed most frequently. Beverage consumption contributed substantially to the intake of vitamin D (29.4%), calcium (26.4%), riboflavin (22.0%), magnesium (18.9%), and vitamin C (18.1%), but constituted only ∼12.5% of total energy. These findings suggest that nutrient-dense beverages play a fundamental role in overall micronutrient intake, despite comprising a small component of daily caloric intake. Incorporating adequate amounts of such beverages in meals and snacks may help older adults meet their nutrient recommendations.

Topics: Aged; Aging; Animals; Ascorbic Acid; Beverages; Calcium, Dietary; Coffee; Cognitive Dysfunction; Cross-Sectional Studies; Diet; Diet Records; Energy Intake; Female; Humans; Magnesium; Male; Micronutrients; Milk; Nutritional Requirements; Riboflavin; Tea; Vitamin D; Water