ascorbic-acid and Cognition-Disorders

Vitamins and minerals are essential to humans as they play essential roles in a variety of basic metabolic pathways that support fundamental cellular functions. In particular, their involvement in energy-yielding metabolism, DNA synthesis, oxygen transport, and neuronal functions makes them critical for brain and muscular function. These, in turn, translate into effects on cognitive and psychological processes, including mental and physical fatigue. This review is focused on B vitamins (B1, B2, B3, B5, B6, B8, B9 and B12), vitamin C, iron, magnesium and zinc, which have recognized roles in these outcomes. It summarizes the biochemical bases and actions of these micronutrients at both the molecular and cellular levels and connects them with cognitive and psychological symptoms, as well as manifestations of fatigue that may occur when status or supplies of these micronutrients are not adequate.

Topics: Affect; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Cognition; Cognition Disorders; Energy Metabolism; Fatigue; Humans; Iron; Magnesium; Minerals; Nutritional Status; Vitamin B Complex; Vitamin B Deficiency; Vitamins; Zinc

Vitamins and minerals have many functions in the nervous system which are important for brain health. It has been suggested that various different vitamin and mineral supplements might be useful in maintaining cognitive function and delaying the onset of dementia. In this review, we sought to examine the evidence for this in people who already had mild cognitive impairment (MCI).. To evaluate the effects of vitamin and mineral supplementation on cognitive function and the incidence of dementia in people with mild cognitive impairment.. We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group's (CDCIG) specialised register, as well as MEDLINE, Embase, PsycINFO, CENTRAL, CINAHL, LILACs, Web of Science Core Collection, ClinicalTrials.gov, and the WHO Portal/ICTRP, from inception to 25 January 2018.. We included randomised or quasi-randomised, placebo-controlled trials which evaluated orally administered vitamin or mineral supplements in participants with a diagnosis of mild cognitive impairment and which assessed the incidence of dementia or cognitive outcomes, or both. We were interested in studies applicable to the general population of older people and therefore excluded studies in which participants had severe vitamin or mineral deficiencies.. We sought data on our primary outcomes of dementia incidence and overall cognitive function and on secondary outcomes of episodic memory, executive function, speed of processing, quality of life, functional performance, clinical global impression, adverse events, and mortality. We conducted data collection and analysis according to standard Cochrane systematic review methods. We assessed the risk of bias of included studies using the Cochrane 'Risk of bias' assessment tool. We grouped vitamins and minerals according to their putative mechanism of action and, where we considered it to be clinically appropriate, we pooled data using random-effects methods. We used GRADE methods to assess the overall quality of evidence for each comparison and outcome.. We included five trials with 879 participants which investigated B vitamin supplements. In four trials, the intervention was a combination of vitamins B6, B12, and folic acid; in one, it was folic acid only. Doses varied. We considered there to be some risks of performance and attrition bias and of selective outcome reporting among these trials. Our primary efficacy outcomes were the incidence of dementia and scores on measures of overall cognitive function. None of the trials reported the incidence of dementia and the evidence on overall cognitive function was of very low-quality. There was probably little or no effect of B vitamins taken for six to 24 months on episodic memory, executive function, speed of processing, or quality of life. The evidence on our other secondary clinical outcomes, including harms, was very sparse or very low-quality. There was evidence from one study that there may be a slower rate of brain atrophy over two years in participants taking B vitamins. The same study reported subgroup analyses based on the level of serum homocysteine (tHcy) at baseline and found evidence that B vitamins may improve episodic memory in those with tHcy above the median at baseline.We included one trial (n = 516) of vitamin E supplementation. Vitamin E was given as 1000 IU of alpha-tocopherol twice daily. We considered this trial to be at risk of attrition and selective reporting bias. There was probably no effect of vitamin E on the probability of progression from MCI to Alzheimer's dementia over three years (HR 1.02; 95% CI 0.74 to 1.41; n = 516; 1 study, moderate-quality evidence). There was also no evidence of an effect at intermediate time points. The available data did not allow us to conduct analyses, but the authors reported no significant effect of three years of supplementation with vitamin E on overall cognitive function, episodic memory, speed of processing, clinical global impression, functional performance, adverse events, or mortality (five deaths in each group). We considered this to be low-quality evidence.We included one trial (n = 256) of combined vitamin E and vitamin C supplementation and one trial (n = 26) of supplementation with chromium picolinate. In both cases, there was a single eligible cognitive outcome, but we considered the evidence to be very low-quality and so could not be sure of any effects.. The evidence on vitamin and mineral supplements as treatments for MCI is very limited. Three years of treatment with high-dose vitamin E probably does not reduce the risk of progression to dementia, but we have no data on this outcome for other supplements. Only B vitamins have been assessed in more than one RCT. There is no evidence for beneficial effects on cognition of supplementation with B vitamins for six to 24 months. Evidence from a single study of a reduced rate of brain atrophy in participants taking vitamin B and a beneficial effect of vitamin B on episodic memory in those with higher tHcy at baseline warrants attempted replication.

Topics: Aged; Aged, 80 and over; alpha-Tocopherol; Ascorbic Acid; Cognition; Cognition Disorders; Dementia; Dietary Supplements; Executive Function; Humans; Memory, Episodic; Middle Aged; Mortality; Picolinic Acids; Quality of Life; Randomized Controlled Trials as Topic; Trace Elements; Vitamin B Complex; Vitamins

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

The objective of this review was to evaluate the evidence from human studies on the intake of vitamins, either as monotherapies or in combination with other vitamins, as neuroprotective agents that may delay the onset of cognitive decline in older adults.. Evidence-based methodologies were used to capture and evaluate the highest levels of evidence.. The current evidence available showed no association for cognitive benefits of vitamins B6 or B12 as a monotherapy, and recent systematic reviews provide no clear evidence that supplementation with vitamin B6, B12 and/or folic acid improves dementia outcomes or slows cognitive decline, even though it may normalise homocysteine levels. Meta-analyses from systematic reviews have shown an association between low vitamin D levels and diminished cognitive function, although causality cannot be confirmed from the available evidence. There is no convincing evidence for an association of vitamin A, vitamin C or vitamin E either as a monotherapy or in combination with other antioxidant vitamins such as β-carotene and the prevention of cognitive decline. The appraisal of nineteen systematic reviews and meta-analyses has highlighted the heterogeneity between studies, and the need for better consensus on definitions of cognitive decline, duration of testing and agreement on which specific endpoints are clinically relevant.. Evaluation of the totality of the currently available evidence indicates that intake of the above vitamins, either as a monotherapy, or in combination with other vitamins, has no clinically-relevant effect on delaying cognitive decline or delaying the onset of dementia in older adults.

Topics: Aged; Antioxidants; Ascorbic Acid; beta Carotene; Cognition; Cognition Disorders; Dementia; Dietary Supplements; Folic Acid; Homocysteine; Humans; Meta-Analysis as Topic; Vitamin A; Vitamin B 12; Vitamin B 6; Vitamin D; Vitamin D Deficiency; Vitamin E; Vitamins

This review is focused upon the role of ascorbic acid (AA, vitamin C) in the promotion of healthy brain aging. Particular attention is attributed to the biochemistry and neuronal metabolism interface, transport across tissues, animal models that are useful for this area of research, and the human studies that implicate AA in the continuum between normal cognitive aging and age-related cognitive decline up to Alzheimer's disease. Vascular risk factors and comorbidity relationships with cognitive decline and AA are discussed to facilitate strategies for advancing AA research in the area of brain health and neurodegeneration.

Topics: Aging; Alzheimer Disease; Animals; Ascorbic Acid; Brain; Cognition; Cognition Disorders; Disease Models, Animal; Humans; Observational Studies as Topic; Randomized Controlled Trials as Topic; Risk Factors

Vitamin C is a pivotal antioxidant in the brain and has been reported to have numerous functions, including reactive oxygen species scavenging, neuromodulation, and involvement in angiogenesis. Absence of vitamin C in the brain has been shown to be detrimental to survival in newborn SVCT2(-/-) mice and perinatal deficiency have shown to reduce hippocampal volume and neuron number and cause decreased spatial cognition in guinea pigs, suggesting that maternal vitamin C deficiency could have severe consequences for the offspring. Furthermore, vitamin C deficiency has been proposed to play a role in age-related cognitive decline and in stroke risk and severity. The present review discusses the available literature on effects of vitamin C deficiency on the developing and aging brain with particular focus on in vivo experimentation and clinical studies.

Topics: Aging; Animals; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Brain; Cognition; Cognition Disorders; Female; Humans; Pregnancy; Prenatal Nutritional Physiological Phenomena; Stroke; Vitamins

To further inform the debate on the possible cognitive benefits of antioxidant nutrients in the elderly, we systematically reviewed available prospective studies while paying a special attention to their methodological quality.. This is a systematic review of studies involving major antioxidant nutrients and change in cognitive performance. Abstracts were independently reviewed; studies were selected based on prespecified criteria. Methodological quality of primary studies was assessed using a methodological checklist for cohort studies. Findings were presented using a narrative synthesis and tabulation of results.. Eight-hundred and fifty potentially eligible studies were identified; 10 met the inclusion criteria and were retained for data extraction and appraisal. The main supportive evidence came from two studies, both judged to be of high quality: The first observed an accelerated decline in global cognition, attention, and psychomotor speed over 9 years, concomitant to a decrease in plasma selenium levels over the same period; the second study reported a slower rate of global cognitive decline over 3 years in persons in the highest quartile of intake of vitamins C, E, and carotenes. All associations persisted after adjustment for confounding factors. Evidence in favor of beneficial associations of higher dietary intake of vitamin E and flavonoids, as well as higher serum beta carotene levels, came from further studies of only adequate quality.. There is a possibility for protective effects of antioxidant nutrients against decline in cognition in older people although the supportive evidence is still limited in number. This association deserves further examination in additional quality investigations.

Topics: Aged; Antioxidants; Ascorbic Acid; Carotenoids; Cognition; Cognition Disorders; Databases, Factual; Diet; Flavonoids; Humans; Meta-Analysis as Topic; Observational Studies as Topic; Randomized Controlled Trials as Topic; Selenium; Vitamin E

Antioxidants in the diet have long been thought to confer some level of protection against the oxidative damage that is involved in the pathology of Alzheimer's disease as well as general cognitive decline in normal aging. Nevertheless, support for this hypothesis in the literature is equivocal. In the case of vitamin C (ascorbic acid) in particular, lack of consideration of some of the specific features of vitamin C metabolism has led to studies in which classification of participants according to vitamin C status is inaccurate, and the absence of critical information precludes the drawing of appropriate conclusions. Vitamin C levels in plasma are not always reported, and estimated daily intake from food diaries may not be accurate or reflect actual plasma values. The ability to transport ingested vitamin C from the intestines into blood is limited by the saturable sodium-dependent vitamin C transporter (SVCT1) and thus very high intakes and the use of supplements are often erroneously considered to be of greater benefit that they really are. The current review documents differences among the studies in terms of vitamin C status of participants. Overall, there is a large body of evidence that maintaining healthy vitamin C levels can have a protective function against age-related cognitive decline and Alzheimer's disease, but avoiding vitamin C deficiency is likely to be more beneficial than taking supplements on top of a normal, healthy diet.

Topics: Aging; Alzheimer Disease; Antioxidants; Ascorbic Acid; Cognition Disorders; Dietary Supplements; Humans; Sodium-Coupled Vitamin C Transporters

The objective of this review was to elucidate the relationship between VaD and various nutritional factors based on epidemiological studies.. Vascular dementia (VaD) is the second most common type of dementia. The prevalence of VaD continues to increase as the US population continues to grow and age. Currently, control of potential risk factors is believed to be the most effective means of preventing VaD. Thus, identification of modifiable risk factors for VaD is crucial for development of effective treatment modalities. Nutrition is one of the main modifiable variables that may influence the development of VaD.. A systematic review of literature was conducted using the PubMed, Web of Science, and CINAHL Plus databases with search parameters inclusive of vascular dementia, nutrition, and vascular cognitive impairment (VCI).. Fourteen articles were found that proposed a potential role of specific nutritional components in VaD. These components included antioxidants, lipids, homocysteine, folate, vitamin B12, and fish consumption. Antioxidants, specifically Vitamin E and C, and fatty fish intake were found to be protective against VaD risk. Fried fish, elevated homocysteine, and lower levels of folate and vitamin B12 were associated with increased VaD. Evidence for dietary lipids was inconsistent, although elevated midlife serum cholesterol may increase risk, while late-life elevated serum cholesterol may be associated with decreased risk of VaD.. Currently, the most convincing evidence as to the relationship between VaD and nutrition exists for micronutrients, particularly Vitamin E and C. Exploration of nutrition at the macronutrient level and additional long term prospective cohort studies are warranted to better understand the role of nutrition in VaD disease development and progression. At present, challenges in this research include limitations in sample size, which was commonly cited. Also, a variety of diagnostic criteria for VaD were employed in the studies reviewed, indicating the need for constructing a correct nosological definition of VaD for consistency and conformity in future studies and accurate clinical diagnosis of VaD.

Topics: Animals; Antioxidants; Ascorbic Acid; Cholesterol; Cognition Disorders; Dementia, Vascular; Diet; Disease Progression; Fishes; Folic Acid; Humans; Meat; Nutritional Status; Prevalence; Risk Factors; Vitamin B 12; Vitamin E

Although several studies show the importance of oxidative stress in the pathogenesis of Alzheimer's disease (AD), there are few evidences on the role of free radicals in Mild Cognitive Impairment (MCI). Our results showing a marked decrease of the main components of the antioxidant defense system of the organism support the hypothesis that in MCI there is a condition of oxidative stress. This work also gives an overview on the existing evidence of the early occurrence of oxidative processes in the development of dementing disorders of the Alzheimer type. Since MCI represents a condition of increased risk for AD, use of antioxidants in MCI could be of importance for prevention.

Topics: Aged; Alzheimer Disease; Ascorbic Acid; Cognition Disorders; Erythrocytes; Humans; Oxidative Stress; Vitamin A; Vitamin E

Demographic changes, together with improvements in nutrition, general health, and life expectancy, will greatly change the social and economic structures of most industrialized and developing countries in the next 50 years. Extended life expectancy has increased the number of chronic illnesses and disabilities, including cognitive impairments. Inflammatory processes and vascular dysfunctions appear to play important roles in the pathogenesis of age-associated pathologies including Alzheimer's and Parkinson's disease. A large body of evidence shows that both vitamins E and C are important for the central nervous system and that a decrease in their concentrations causes structural and functional damage to the cells. Several studies reveal a link between diets rich in fruits and vegetables containing generous amounts of vitamins E and C and lower incidence of certain chronic diseases.

Topics: Aged; Antioxidants; Ascorbic Acid; Cognition; Cognition Disorders; Female; Humans; Male; Middle Aged; Neurodegenerative Diseases; Vitamin E

Topics: Aged; Aging; Animals; Antioxidants; Ascorbic Acid; beta Carotene; Cognition; Cognition Disorders; Humans; Oxidative Stress; Vitamin E

Few studies have investigated the long-term impact of overall dietary patterns (DP) on cognition. We evaluated the association between empirically derived DP in midlife and cognitive performance 13 y later. Dietary data were based on 24-h dietary records obtained from a subsample of the Supplémentation en Vitamines et Minéraux Antioxydant Study. Cognitive performance was assessed via a battery of neuropsychological tests that included verbal fluency, the RI-48 cued recall test, the trail-making test, and forward and backward digit span. Three composite variables, for global cognitive function, verbal memory, and executive functioning, were built. The multivariate analyses were adjusted for baseline characteristics (age, gender, intervention group, education, alcohol and energy intake, number of dietary records, physical activity, BMI, tobacco use, self-reported memory troubles, diabetes, hypertension, and, for women, menopausal status and hormone therapy use), follow-up time, history of cardiovascular disease, and depressive symptoms. Adjusted means ± SEM of composite variables across quartiles (Q4 vs. Q1) of DP were estimated using ANCOVA. A healthy and a traditional DP were identified. In the multivariate model, the healthy pattern was associated with better global cognitive function (50.1 ± 0.7 vs. 48.9 ± 0.7; P-trend = 0.001) and verbal memory (49.7 ± 0.4 vs. 48.7 ± 0.4; P-trend = 0.01). These relationships were stronger in participants scoring below the gender-specific median values for energy intake (<2490 kcal for men and <1810 for women) than in those scoring at or above those values. Adherence to a healthy DP in middle life may help preserve global cognitive function, especially verbal memory, when total energy intake is regulated.

Topics: Aged; Antioxidants; Ascorbic Acid; beta Carotene; Cognition; Cognition Disorders; Energy Metabolism; Feeding Behavior; Female; Follow-Up Studies; Humans; Male; Memory; Middle Aged; Neuropsychological Tests; Selenium; Verbal Learning; Vitamin E; Vitamins; Zinc

Cardiovascular factors are associated with cognitive decline. Antioxidants may be beneficial.. The Women's Antioxidant Cardiovascular Study was a trial of vitamin E (402 mg every other day), beta carotene (50 mg every other day), and vitamin C (500 mg daily) for the secondary prevention of cardiovascular disease. From 1995 to 1996, women > or =40 years of age with cardiovascular disease or > or =3 coronary risk factors were randomized. From 1998 to 1999, a cognitive function substudy was initiated among 2824 participants > or =65 years of age. With 5 cognitive tests, cognition was assessed by telephone 4 times over 5.4 years. The primary outcome was a global composite score averaging all scores; repeated-measures analyses were used to examine cognitive change over time. Vitamin E supplementation and beta carotene supplementation were not associated with slower rates of cognitive change (mean difference in change for vitamin E versus placebo, -0.01; 95% confidence interval, -0.05 to 0.04; P=0.78; for beta carotene, 0.03; 95% confidence interval, -0.02 to 0.07; P=0.28). Although vitamin C supplementation was associated with better performance at the last assessment (mean difference, 0.13; 95% confidence interval, 0.06 to 0.20; P=0.0005), it was not associated with cognitive change over time (mean difference in change, 0.02; 95% confidence interval, -0.03 to 0.07; P=0.39). Vitamin C was more protective against cognitive change among those with new cardiovascular events during the trial (P for interaction=0.009).. Antioxidant supplementation did not slow cognitive change among women with preexisting cardiovascular disease or cardiovascular disease risk factors. A possible late effect of vitamin C or beta carotene among those with low dietary intake on cognition warrants further study.

Topics: Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; beta Carotene; Cardiovascular Diseases; Cognition Disorders; Female; Follow-Up Studies; Humans; Memory Disorders; Middle Aged; Neuroprotective Agents; Neuropsychological Tests; Oxidative Stress; Risk Factors; Single-Blind Method; Treatment Failure; Vitamin E

Participants in the Age-Related Eye Disease Study were randomly assigned to receive daily antioxidants (vitamin C, 500 mg; vitamin E, 400 IU; beta carotene, 15 mg), zinc and copper (zinc, 80 mg; cupric oxide, 2 mg), antioxidants plus zinc and copper, or placebo. A cognitive battery was administered to 2,166 elderly persons after a median of 6.9 years of treatment. Treatment groups did not differ on any of the six cognitive tests (p > 0.05 for all). These results do not support a beneficial or harmful effect of antioxidants or zinc and copper on cognition in older adults.

Topics: Aged; Antioxidants; Ascorbic Acid; beta Carotene; Cognition Disorders; Copper; Female; Humans; Male; Middle Aged; Vitamin E; Zinc

In order to assess peripheral levels and activities of a broad spectrum of non-enzymatic and enzymatic antioxidants in elderly subjects with mild cognitive impairment (MCI) and Alzheimer's disease (AD), plasma levels of water-soluble (Vitamin C and uric acid) and of lipophilic (Vitamin A, Vitamin E and carotenoids including lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha- and beta-carotene) antioxidant micronutrients as well as activities of plasma and red blood cell (RBC) superoxide dismutase (SOD) and of plasma glutathione peroxidase (GPx) were measured in 25 patients with MCI, 63 AD patients and 53 controls. Peripheral levels and activities of antioxidants were similarly lower in MCI and AD patients as compared to controls. As MCI may represent a prodromal stage of AD, and oxidative damage appears to occur as one of the earliest pathophysiological events in AD, an increased intake of antioxidants in patients with MCI could be helpful in lowering the risk of conversion to dementia.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; Antioxidants; Apolipoproteins E; Ascorbic Acid; Carotenoids; Cognition Disorders; Erythrocytes; Female; Glutathione Peroxidase; Humans; Male; Matched-Pair Analysis; Oxidative Stress; Plasma; Reference Values; Superoxide Dismutase; Uric Acid; Vitamin A; Vitamin E

In a prospective, randomized, controlled study an intravenous vitamin B complex and vitamin C preparation was administered pre- and post-operatively to 28 elderly patients with a fractured proximal femur and compared with 32 nonsupplemented postoperative controls. Vitamin supplementation significantly, though only transiently, improved postoperative thiamine status (P less than 0.001), but had no influence on mental state or outcome during the postsurgical period. Therefore, the use of parenteral vitamins for postoperative confusion cannot be justified on a routine basis.

Topics: Aged; Aged, 80 and over; Ascorbic Acid; Cognition Disorders; Confusion; Female; Femoral Fractures; Humans; Male; Middle Aged; Postoperative Complications; Premedication; Prospective Studies; Random Allocation; Thiamine; Vitamin B Complex

Topics: Aged; Anemia; Ascorbic Acid; Avitaminosis; Cognition Disorders; Contusions; Diagnosis, Differential; Diet; Dizziness; Hemoglobins; Humans; Male; Melena; Scurvy

Menopause is associated with increased oxidative stress and memory impairment. Based on the antioxidant property of ascorbic acid (AA), It's effect on cognitive function, the serum level of the brain-derived neurotrophic factor (BDNF) and the activity of antioxidant enzymes within the brain in ovariectomized (OVX) mice was investigated.. AA (100, 300 and 500 mg/kg), was orally administrated per day in OVX mice for 30 days. Tactile learning and working memory were evaluated by the novel object recognition task and T-maze continuous alternation task, respectively. The levels of serum BDNF were measured and animals' brains were analyzed for the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity.. AA prevented from the deleterious effects of ovariectomy on learning memory (300 and 500 mg/kg) and working memory (100 and 500 mg/kg). The serum BDNF level was also increased in OVX animals treated with AA (100 and 500 mg/kg). Furthermore, AA (500 mg/kg) increased the SOD and GPx activity in the brain of OVX animals.. Collectively, the results of the present study suggest that AA might be an appropriate choice in loss or reduction of estradiol for the amelioration of cognitive impairment.

Topics: Animals; Antioxidants; Ascorbic Acid; Behavior, Animal; Brain; Brain-Derived Neurotrophic Factor; Cognition; Cognition Disorders; Disease Models, Animal; Female; Glutathione Peroxidase; Maze Learning; Memory, Short-Term; Menopause; Mice; Ovariectomy; Oxidative Stress; Recognition, Psychology; Superoxide Dismutase

Long-term d-galactose injection induces accelerated aging in experimental rodent models. The aim of this study was to determine the effects of dietary fructo-oligosaccharide (FO) on the brain β-amyloid (Aβ), amyloid-associated enzymes, cognitive function, and plasma antioxidant levels in d-galactose-treated Balb/c mice.. The subcutaneous (s.c.) injection and the dietary treatment were conducted simultaneously for 49 days. Mice (12 weeks of age) were divided into five groups (n = 14/group): control (s.c. saline, control diet) serving as a young control, DG (s.c. 1.2 g d-galactose/kg body weight, control diet), DG + LFO (2.5% w/w FO, low-dose FO diet), DG + HFO (5% w/w FO, high-dose FO diet), and DG + E (α-tocopherol 0.2% w/w, vitamin E diet) as an antioxidant reference group. Another group of older mice (64 weeks of age) without any injection served as a natural aging (NA) group.. The DG and NA groups had greater Aβ levels in the cortex, hippocampus, and the whole brain. High-dose FO, similar to α-tocopherol, attenuated the d-galactose-induced Aβ density in the cortex and hippocampus. In addition, FO attenuated the d-galactose-induced protein expression of Aβ and beta-site amyloid precursor cleaving enzyme of the whole brain in a dose-response manner. Either dose of FO supplementation, similar to α-tocopherol, attenuated the d-galactose-induced cognitive dysfunction. In addition, FO improved the plasma ascorbic acid level in a dose-response manner.. Dietary FO (2.5-5% w/w diet) could attenuate the development of Alzheimer's disease, which was likely to be associated with its systematic antioxidant effects.

Topics: alpha-Tocopherol; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Antioxidants; Ascorbic Acid; Brain; Cognition; Cognition Disorders; Disease Models, Animal; Dose-Response Relationship, Drug; Galactose; Male; Mice; Mice, Inbred BALB C; Oligosaccharides

We previously reported lower lymphocyte vitamin C levels in individuals with type 2 diabetes mellitus and in individuals with severe Parkinson's disease. Oxidative stress has been proposed to play a key role in the progression of Alzheimer's disease. Thus, the objective of this study was to investigate the association between peripheral levels of vitamin C and the progression of cognitive dysfunction in Alzheimer's disease. Fifty individuals with Alzheimer's disease being treated at Shizuoka General Hospital were consecutively enrolled in this study from December 2009 to March 2015 (76.0±9.7 y of age [mean±SD]; 32 men and 18 women; Mini-Mental State Examination Japanese version (MMSE-J) score range, 8-27). Plasma and lymphocyte vitamin C levels in fasting blood samples were measured. The association between the MMSE-J scores and vitamin C levels was estimated using Spearman's rank correlation coefficient (ρ) and the criteria defined by Swinscow. Spearman's ρ for the relationship between peripheral vitamin C levels and the MMSE-J score was ρ=0.17 for plasma vitamin C and ρ=0.26 for lymphocyte vitamin C. Thus, the associations were relatively weak based on the criteria. In contrast with type 2 diabetes mellitus and Parkinson's disease, lymphocyte vitamin C levels in the peripheral blood may not directly reflect the progression of cognitive dysfunction in Alzheimer's disease. Additional longitudinal studies are needed to evaluate the clinical importance of changes of peripheral vitamin C status in Alzheimer's disease.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; Ascorbic Acid; Body Mass Index; Cognition Disorders; Cross-Sectional Studies; Disease Progression; Female; Humans; Male; Middle Aged; Oxidative Stress

Anesthetic isoflurane has been reported to induce caspase-3 activation. The underlying mechanism(s) and targeted intervention(s), however, remain largely to be determined. Vitamin C (VitC) inhibits oxidative stress and apoptosis. We therefore employed VitC to further determine the up-stream mechanisms and the down-stream consequences of the isoflurane-induced caspase-3 activation. H4 human neuroglioma cells overexpressed human amyloid precursor protein (H4-APP cells) and rat neuroblastoma cells were treated either with (1) 2% isoflurane or (2) with the control condition, plus saline or 400 μM VitC for 3 or 6 h. Western blot analysis and fluorescence assay were utilized at the end of the experiments to determine caspase-3 activation, levels of reactive oxygen species and ATP, and mitochondrial function. The interaction of isoflurane (1.4% for 2 h) and VitC (100 mg/kg) on cognitive function in mice was also assessed in the fear conditioning system. Here, we show for the first time that the VitC treatment attenuated the isoflurane-induced caspase-3 activation. Moreover, VitC mitigated the isoflurane-induced increases in the levels of reactive oxygen species, opening of mitochondrial permeability transition pore, reduction in mitochondrial membrane potential, and the reduction in ATP levels in the cells. Finally, VitC ameliorated the isoflurane-induced cognitive impairment in the mice. Pending confirmation from future studies, these results suggested that VitC attenuated the isoflurane-induced caspase-3 activation and cognitive impairment by inhibiting the isoflurane-induced oxidative stress, mitochondrial dysfunction, and reduction in ATP levels. These findings would promote further research into the underlying mechanisms and targeted interventions of anesthesia neurotoxicity.

Topics: Adenosine Triphosphate; Animals; Ascorbic Acid; Caspase 3; Cell Line, Tumor; Cognition Disorders; Humans; Isoflurane; Membrane Potential, Mitochondrial; Mice, Inbred C57BL; Mitochondria; Reactive Oxygen Species

Subclinical vitamin C deficiency is widespread in many populations, but its role in both Alzheimer's disease and normal aging is understudied. In the present study, we decreased brain vitamin C in the APPSWE/PSEN1deltaE9 mouse model of Alzheimer's disease by crossing APP/PSEN1(+) bigenic mice with SVCT2(+/-) heterozygous knockout mice, which have lower numbers of the sodium-dependent vitamin C transporter required for neuronal vitamin C transport. SVCT2(+/-) mice performed less well on the rotarod task at both 5 and 12 months of age compared to littermates. SVCT2(+/-) and APP/PSEN1(+) mice and the combination genotype SVCT2(+/-)APP/PSEN1(+) were also impaired on multiple tests of cognitive ability (olfactory memory task, Y-maze alternation, conditioned fear, Morris water maze). In younger mice, both low vitamin C (SVCT2(+/-)) and APP/PSEN1 mutations increased brain cortex oxidative stress (malondialdehyde, protein carbonyls, F2-isoprostanes) and decreased total glutathione compared to wild-type controls. SVCT2(+/-) mice also had increased amounts of both soluble and insoluble Aβ1-42 and a higher Aβ1-42/1-40 ratio. By 14 months of age, oxidative stress levels were similar among groups, but there were more amyloid-β plaque deposits in both hippocampus and cortex of SVCT2(+/-)APP/PSEN1(+) mice compared to APP/PSEN1(+) mice with normal brain vitamin C. These data suggest that even moderate intracellular vitamin C deficiency plays an important role in accelerating amyloid pathogenesis, particularly during early stages of disease development, and that these effects are likely modulated by oxidative stress pathways.

Topics: Aging; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Anxiety; Ascorbic Acid; Ascorbic Acid Deficiency; Brain; Cognition Disorders; Disease Models, Animal; Female; Learning; Male; Memory; Mice, Transgenic; Motor Activity; Oxidative Stress; Peptide Fragments; Presenilin-1; Sodium-Coupled Vitamin C Transporters

To assess the relationship between dietary intake of antioxidants (vitamin C, vitamin E, β-carotene, lutein, flavonoids and lignans) and cognitive decline at middle age, analyses were performed on data from the population based Doetinchem Cohort Study. Habitual diet and cognitive function were assessed twice with a 5-year interval in 2613 persons aged 43-70 year at baseline (1995-2002). Diet was assessed with a validated 178-item semi-quantitative FFQ. Cognitive function was assessed with a neuropsychological test battery, consisting of the 15 Words Learning Test, the Stroop Test, the Word Fluency test, and the Letter Digit Substitution Test. Scores on global cognitive function, memory, processing speed, and cognitive flexibility were calculated. In regression analyses, quintiles of antioxidant intake were associated with change in cognitive domain scores. Results showed that higher lignan intake was linearly associated with less decline in global cognitive function (P= 0.01), memory (P< 0.01) and processing speed (P= 0.04), with about two times less declines in the highest v. the lowest quintile. In the lowest quintile of vitamin E intake, decline in memory was twice as fast as in all higher quintiles (P< 0.01). Global cognitive decline in the highest lutein intake group was greater than in the lowest intake group (P< 0.05). Higher flavonoid intake was associated with greater decline in cognitive flexibility (P for trend = 0.04). Intakes of other antioxidants were not associated with cognitive decline. We conclude that within the range of a habitual dietary intake, higher intake of lignans is associated with less cognitive decline at middle age.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; beta Carotene; Cognition; Cognition Disorders; Cohort Studies; Diet; Dietary Supplements; Feeding Behavior; Female; Flavonoids; Humans; Lignans; Lutein; Male; Middle Aged; Neuropsychological Tests; Surveys and Questionnaires; Vitamin E

Lead (Pb) is a neurotoxic metal that is widely distributed in the environment. In experimental animals, chronic exposure to this neurotoxicant resulted in impaired synaptic plasticity and cognitive function. In this study, we examined the protective effects of vitamin C (ascorbic acid) against Pb exposure-induced impairment of long-term potentiation (LTP). Forty-four adult male Wistar rats were divided into six groups and subjected to the following treatments for three months: (1) vehicle (distilled water); (2) Pb; (3) ascorbic acid; (4) Pb+ascorbic acid; (5) Pb (two months) followed by ascorbic acid; and (6) ascorbic acid (one month) followed by Pb. After treatment, the population spike (PS) amplitude and slope of excitatory postsynaptic potentials (EPSP) were measured in the dentate gyrus(DG) of rats in vivo. Following these measurements, blood samples were collected for the following biochemical assays: malondialdehyde (MDA), total antioxidant capacity (TAC), and total oxidant status (TOS). There was a significant increase in plasma MDA and TOS in the Pb-intoxicated group compared to the control group. There was a significant increase in TAC levels in the ascorbic acid group. Our results also show that Pb exposure caused a decrease in the EPSP slope and PS amplitude when compared with the control group, whereas vitamin C increased these parameters. Co-administration of Pb with vitamin C inhibited the effects of Pb. These findings suggested that Pb exposure caused impairment in LTP, that may have been mediated through oxidative damage. Vitamin C ameliorated the Pb-induced impairment of synaptic plasticity in the DG via antioxidant activity.

Topics: Animals; Antioxidants; Ascorbic Acid; Cognition Disorders; Dentate Gyrus; Excitatory Postsynaptic Potentials; Male; Malondialdehyde; Neuronal Plasticity; Neuroprotective Agents; Organometallic Compounds; Oxidative Stress; Random Allocation; Rats, Wistar

The authors examined long-term antioxidant intake in relation to cognitive decline among older women. Beginning in 1980, Nurses' Health Study (NHS) participants completed dietary assessments every 4 years; in 1995-2001, 16,010 participants aged ≥70 years completed initial cognitive assessments, which were repeated 3 times at 2-year intervals. Long-term antioxidant intake was averaged from 1980 through the time of initial cognitive interviews. Multivariable-adjusted linear regression was used to estimate mean differences in rates of cognitive decline across categories of vitamin E, vitamin C, and carotenoid intake; statistical tests were 2-sided. No associations were evident for vitamin E or total carotenoid intake and cognitive decline (e.g., after multivariable adjustment, P-trend = 0.44 and P-trend = 0.51, respectively, for a global composite score averaging all 6 cognitive tests), although higher lycopene intake and lower vitamin C intake were related to slower cognitive decline. In alternative analyses of overall cognitive status at older ages (averaging all 4 cognitive assessments), results for vitamins E and C were generally null, but higher carotenoid intake was related to better cognition. Overall, long-term vitamin E and C intakes were not consistently related to cognition, although greater consumption of carotenoids may have cognitive benefits in older adults.

Topics: Aged; Aging; Antioxidants; Ascorbic Acid; Carotenoids; Cognition Disorders; Female; Humans; Nurses; Vitamin E; Women's Health

Learning and memory deficits occur in depression and other stress related disorders. Although the pathogenesis of cognitive impairment after stress has not been fully elucidated, factors such as oxidative stress and neurotrophins are thought to play possible roles. Here we investigated the effect of treatment with vitamin E (40 mg/kg) and vitamin C (100 mg/kg) on the effects elicited by chronic variable stress on rat performance in Morris water maze. Brain-derived neurotrophic factor (BDNF) immunocontent was also evaluated in hippocampus of rats. Sixty-day old Wistar rats were submitted to different stressors for 40 days (stressed group). Half of stressed group received administration of vitamins once a day, during the period of stress. Chronically stressed rats presented a marked decrease in reference memory in the water maze task as well as a reduced efficiency to find the platform in the working memory task. Rats treated with vitamins E and C had part of the above effects prevented, suggesting the participation of oxidative stress in such effects. The BDNF levels were not altered in hippocampus of stressed group when compared to controls. Our findings lend support to a novel therapeutic strategy, associated with these vitamins, to the cognitive dysfunction observed in depression and other stress related diseases.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain-Derived Neurotrophic Factor; Cognition Disorders; Male; Maze Learning; Memory Disorders; Rats; Rats, Wistar; Stress, Psychological; Vitamin E

This experiment was designed to assess the protective effect of betacyanins from Portulaca oleracea L. against the D-galactose (D-gal)-induced neurotoxicity in mice. Betacyanins from Portulaca oleracea markedly reversed the D-gal-induced learning and memory impairments, as measured by behavioral tests. The activities of superoxide dismutases (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) in D-gal-treated mice were enhanced, while the content of the lipid peroxidation product malondialdehyde (MDA) was decreased by betacyanin administration. Furthermore, significant negative correlations were found between mouse latency in finding the platform and the activities of SOD, CAT GR and GPx in the mouse brain, but the level of MDA correlated positively with the latency. These results suggest that the neuroprotective effect of betacyanins against D-gal-induced neurotoxicity might be caused, at least in part, by an increase in the activities of antioxidant enzymes with a reduction in lipid peroxidation. In comparison with vitamin C (VC), the betacyanins had a more pronounced effect on ameliorating cognition deficits in mice.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Carbocyanines; Cognition Disorders; Disease Models, Animal; Enzymes; Galactose; Lipid Peroxidation; Male; Malondialdehyde; Maze Learning; Memory; Mice; Mice, Inbred Strains; Neurotoxins; Oxidative Stress; Phytotherapy; Plant Extracts; Portulaca

Besides low mortality and morbidity rates in cardiac surgery, the associated cognitive dysfunction is the focus of interest. One possible reason is microembolisation.. The authors analysed the crystallogenesis in the calcium-containing prime, inspired by their observation that the fluid sometimes becomes turbid during the priming process. Lactated Ringer-based prime solutions were tested, adding mannitol, NaHCO(3), and heparin. The oxygenator was ventilated with compressed medical air. Samples were taken for dynamic light scattering particulate level analysis. The priming was furthermore modelled in the laboratory by mixing the components and then ventilating the mixture through with compressed air. Turbid solutions from the operating room contained 100-6500 nm crystals, while clear solutions contained 20-473 nm particles. In the model, continuous pH measurement showed pH 6.4-7.4 after blending the solutions, which then elevated the pH to 7.5-8.0 after ventilation with concomitant turbidity. The pH of the prime can be stabilized by the addition of ascorbic acid (1-2 mg/ml) and, also, the turbidity may be prevented.. Ventilating the lactated Ringer-based calcium-containing primes after blending is not advisible because of alkalization and crystallogenesis. Ascorbic acid stabilizes the pH and prevents crystallogenesis in the prime. Pre-bypass filtration is recommended.

Topics: Alkalies; Ascorbic Acid; Calcium; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Cognition Disorders; Crystallization; Embolism; Humans; Hydrogen-Ion Concentration; Isotonic Solutions; Microcirculation; Nephelometry and Turbidimetry; Particle Size; Ringer's Lactate

Lycium barbarum (Fructus Lycii, Wolfberry, or Gouqi) belongs to the Solanaceae. The red-colored fruits of L. barbarum have been used for a long time as an ingredient in Chinese cuisine and brewing, and also in traditional Chinese herbal medicine for improving health. However, its effects on cognitive function have not been well studied. In the present study, prevention of a milk-based wolfberry preparation (WP) on cognitive dysfunction was tested in a prenatal stress model with rats and the antioxidant mechanism was tested by in vitro experiments. We found that prenatal stress caused a significant decrease in cognitive function (Morris water maze test) in female offspring. Pretreatment of the mother rats with WP significantly prevented the prenatal stress-induced cognitive dysfunction. In vitro studies showed that WP dose-dependently scavenged hydroxyl and superoxide radicals (determined by an electron spin resonance spectrometric assay), and inhibited FeCl(2)/ascorbic acid-induced dysfunction in brain tissue and tissue mitochondria, including increases in reactive oxygen species and lipid peroxidation and decreases in the activities of complex I, complex II, and glutamate cysteine ligase. These results suggest that dietary supplementation with WP may be an effective strategy for preventing the brain oxidative mitochondrial damage and cognitive dysfunction associated with prenatal stress.

Topics: Animals; Antioxidants; Ascorbic Acid; Cognition Disorders; Female; Ferrous Compounds; Free Radical Scavengers; Glutamate-Cysteine Ligase; Lipid Peroxidation; Lycium; Male; Maze Learning; Milk; Mitochondria; Oxidative Stress; Plant Extracts; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Sprague-Dawley; Restraint, Physical; Stress, Psychological

The brain maintains high levels of ascorbic acid (AA) despite a concentration gradient favoring diffusion from brain to peripheral tissues. Dietary antioxidants, including AA, appear to modify the risk of Alzheimer's disease (AD). The objective of this study was to test the hypothesis that neurodegeneration in AD is modified by brain levels of AA. Thirty-two patients with mild to moderate AD participated in a biomarker study involving standardized clinical assessments over one year. Cerebrospinal fluid (CSF) and serum were collected at baseline for AA and albumin content. Cognitive measures were collected at baseline and one year. CSF and plasma AA failed to predict cognitive decline independently, however, CSF: plasma AA ratio did. After adding CSF Albumin Index (an established marker of blood-brain barrier integrity) to the regression models the effect of CSF: plasma AA ratio as a predictor of cognitive decline was weakened. CSF: plasma AA ratio predicts rate of decline in AD. This relationship may indicate that the CSF: plasma AA ratio is an index of AA availability to the brain or may be an artifact of a relationship between blood-brain barrier impairment and neurodegeneration.

Topics: Aged; Alzheimer Disease; Antioxidants; Ascorbic Acid; Blood-Brain Barrier; Brain Chemistry; Cognition Disorders; Data Interpretation, Statistical; Disease Progression; Female; Humans; Male; Neuropsychological Tests; Prospective Studies

This was a cross-sectional study of the ability of independently living healthy elders to follow a medication regimen. Participants were divided into a group with High Cognitive Function (HCF) or Low Cognitive Function (LCF) based on their scores on the ADAS-Cog.. Thirty-eight participants aged 65 or older and living independently in the community followed a twice-daily vitamin C regimen for 5 weeks. Adherence was measured using an electronic 7-day pillbox.. The LCF group had significantly poorer total adherence than the HCF group (LCF: 63.9 +/- 11.2%, HCF: 86.8 +/- 4.3%, t( 36) = 2.57, p = .007), and there was a 4.1 relative risk of non-adherence in the LCF group as compared to the HCF group.. This study has important implications for the conduct of clinical drug trials, as it provides strong evidence that even very mild cognitive impairment in healthy elderly has a detrimental impact on medication adherence.

Topics: Activities of Daily Living; Aged; Aged, 80 and over; Ascorbic Acid; Cognition; Cognition Disorders; Cross-Sectional Studies; Female; Geriatric Assessment; Health Status; Humans; Male; Medication Adherence; Oregon; Psychiatric Status Rating Scales; Self Administration; Self Care

Mangos are a source of bioactive compounds with potential health-promoting activity. The present work was undertaken to evaluate the ethanolic extract of Mangifera indica L. fruit on cognitive performances. The models used to study the effect on cognitive performances are step down passive avoidance task and elevated plus maze task in mice. Chronic treatment (7 days) of extract and vitamin C significantly (p < 0.05) reversed the aging and scopolamine induced memory deficits in both paradigms. Preliminary phytochemical screening revealed the presence of free sugars, saponins, tannins, and flavonoids. The results suggestthe extract contained pharmacologically active principles that are memory-enhancing in nature.

Topics: Animals; Ascorbic Acid; Cognition Disorders; Female; Fruit; Male; Mangifera; Mice; Phytotherapy; Plant Extracts; Scopolamine

Alzheimer's disease (AD) has become one of the major health problems of the developed world. Previous studies have shown that oxidant-induced changes occur in cerebral tissue in AD and in late-onset amnestic mild cognitive impairment. The oxidative damage begins early and involves free radical-mediated effects that cause lipid peroxidations and oxidative protein and nucleic acid damages which begin before the cardinal neuropathologic manifestations. Impaired cerebral iron homeostasis and iron accumulation are postulated to be primary and seminal in the pathogenesis.. To demonstrate that the Fenton reaction involving hydrogen peroxide and iron at very low concentrations as has been found in human plasma and cerebrospinal fluid may produce promptly oxidations which may be inhibited by preventive use of uric acid and ascorbic acid as hydrophilic antioxidants.. A photometric study in vitro at physiologic pH using concentrations of uric acid and ascorbic acid readily attainable in human extracellular fluids.. Uric acid levels of 0.5 and 6.0 mg/dl (below the saturation level for urate precipitation) and ascorbic acid at a level readily attainable in blood plasma inhibited significantly and completely, respectively, oxidations caused by reactions of 20 microM concentrations of hydrogen peroxide with free bivalent iron at 9.8 muM and at a low hemoglobin level of 12 mg/dl of saline.. Results suggest that supplemental use orally of ascorbic acid combined with use of metabolic precursor to uric acid, like inosine or hypoxanthine, has the potential for preventing or attenuating the progression of AD and amnestic mild cognitive impairment.

Topics: Alzheimer Disease; Antioxidants; Ascorbic Acid; Cognition Disorders; Hemoglobins; Hydrogen Peroxide; Iron; Oxidation-Reduction; Photometry; Uric Acid

Glutathione (GSH) metabolism dysfunction is one risk factor in schizophrenia. A transitory brain GSH deficit was induced in Wistar (WIS) and mutant (ODS; lacking ascorbic acid synthesis) rats using BSO (l-buthionine-(S,R)-sulfoximine) from post-natal days 5-16. When GSH was re-established to physiological levels, juvenile BSO-ODS rats were impaired in the water maze task. Long after treatment cessation, adult BSO-WIS/-ODS rats showed impaired place discrimination in the homing board with distributed visual or olfactory cues. Their accuracy was restored when a single cue marked the trained position. Similarly, more working memory errors were made by adult BSO-WIS in the radial maze when several olfactory cues were present. These results reveal that BSO rats did not suffer simple sensory impairment. They were selectively impaired in spatial memory when the task required the integration of multimodal or olfactory cues. These results, in part, resemble some of the reported olfactory discrimination and cognitive impairment in schizophrenia.

Topics: Aging; Animals; Animals, Newborn; Ascorbic Acid; Brain; Cognition Disorders; Cues; Disease Models, Animal; Female; Glutathione; Male; Maze Learning; Memory Disorders; Nerve Degeneration; Olfaction Disorders; Orientation; Oxidative Stress; Rats; Rats, Mutant Strains; Rats, Wistar; Schizophrenia; Sex Characteristics; Smell

There are conflicting reports about the potential role of vitamin antioxidants in preventing and/or slowing the progression of various forms of cognitive impairment including Alzheimer's disease (AD). We examined longitudinal data from the Canadian Study of Health and Aging, a population-based, prospective 5-year investigation of the epidemiology of dementia among Canadians aged 65+ years. Our primary objective was to examine the association between supplemental use of antioxidant vitamins and subsequent risk of significant cognitive decline (decrease in 3MS score of 10 points or more) among subjects with no evidence of dementia at baseline (n=894). We also explored the relationship between vitamin supplement use and incident vascular cognitive impairment (VCI; including a diagnosis of vascular dementia, possible AD with vascular components and VCI but not dementia), dementia (all cases) and AD. After adjusting for potential confounding factors assessed at baseline, subjects reporting a combined use of vitamin E and C supplements and/or multivitamin consumption at baseline were significantly less likely (adjusted OR 0.51; 95% CI 0.29-0.90) to experience significant cognitive decline during a 5-year follow-up period. Subjects reporting any antioxidant vitamin use at baseline also showed a significantly lower risk for incident VCI (adjusted OR 0.34, 95% CI 0.13-0.89). A reduced risk for incident dementia or AD was not observed. Our findings suggest a possible protective effect for antioxidant vitamins in relation to cognitive decline but randomized controlled trials are required for confirmation.

Topics: Aged; Antioxidants; Ascorbic Acid; Cognition Disorders; Dementia; Drug Therapy, Combination; Female; Follow-Up Studies; Humans; Male; Neuropsychological Tests; Population Surveillance; Prospective Studies; Vitamin E

Experimental data suggest that oxygen free radicals are probably involved in the deterioration of cognitive processes.. Our objective was to investigate the relation of high-dose antioxidant supplements to cognition.. Information on the use of specific supplements containing vitamins E and C was collected biennially via mailed questionnaires beginning in 1980 from 14 968 community-dwelling women who participated in the Nurses' Health Study. From 1995 to 2000, telephone tests of cognitive function [Telephone Interview of Cognitive Status (TICS), delayed recall of the TICS 10-word list, immediate and delayed recall of a short paragraph, a test of verbal fluency, and a digit span backwards test] were administered to the women, who were 70-79 y of age at that time. We used linear and logistic regression models to calculate multivariate-adjusted mean differences in test scores and relative risks of a low score for specific supplement users compared with nonusers.. Long-term, current users of vitamin E with vitamin C had significantly better mean performance, as judged by a global score that combined individual test scores, than did women who had never used vitamin E or C (P = 0.03); there was a trend for increasingly higher mean scores with increasing durations of use (P = 0.04). These associations were strongest among women with low dietary intakes of alpha-tocopherol. Benefits were less consistent for women taking vitamin E alone, with no evidence of higher scores with longer durations of use. Use of specific vitamin C supplements alone had little relation to performance on our cognitive tests.. The use of specific vitamin E supplements, but not specific vitamin C supplements, may be related to modest cognitive benefits in older women.

Topics: Aged; alpha-Tocopherol; Antioxidants; Ascorbic Acid; Cognition; Cognition Disorders; Cohort Studies; Diet; Dietary Supplements; Female; Health Surveys; Humans; Logistic Models; Nurses; Risk; Telephone; Vitamin E

The role of oxidative stress in the pathogenesis of diseases such as macular degeneration, certain types of cancer, and Alzheimer's disease has received much attention. Thus, there is considerable interest in the potential contribution of antioxidants to the prevention of these diseases.. The objective of this study was to determine whether use of supplemental antioxidants (vitamins A, C, or E, plus selenium or zinc) was associated with a reduced risk of development of cognitive impairment or cognitive decline in a representative sample of the community-dwelling elderly.. The sample consisted of 2082 nonproxy subjects from the Duke Established Populations for Epidemiologic Studies of the Elderly who were not cognitively impaired at the 1989-1990 interview (baseline for the present analysis). Medication use was determined during in-home interviews. Cognitive function was assessed 3 and 7 years from baseline in terms of incident cognitive impairment, as measured on the Short Portable Mental Status Questionnaire (SPMSQ) using specific cut points (number of errors) based on race and education, and cognitive decline, defined as an increase of > or = 2 errors on the SPMSQ. Multivariate analyses were performed using weighted data adjusted for sampling design and controlled for sociodemographic characteristics, health-related behaviors, and health status.. At baseline, 224 (10.8%) subjects were currently taking a supplement containing an antioxidant. During the follow-up period, 24.0% of subjects developed cognitive impairment and 34.5% experienced cognitive decline. Current antioxidant users had a 34.0% lower risk of developing cognitive impairment compared with non-antioxidant users (adjusted relative risk [RR], 0.66; 95% CI, 0.44-1.00) and a 29.0% lower risk of experiencing cognitive decline (adjusted RR, 0.71; 95% CI, 0.49-1.01).. The results of this analysis suggest a possible beneficial effect of antioxidant use in terms of reducing cognitive decline among the community-dwelling elderly.

Topics: Age Factors; Aged; Antioxidants; Ascorbic Acid; Cognition; Cognition Disorders; Cohort Studies; Dose-Response Relationship, Drug; Female; Humans; Male; Oxidative Stress; Selenium; Sex Factors; Surveys and Questionnaires; Treatment Outcome; Vitamin A; Vitamin E; Zinc

Propionic acidemia is an inherited neurometabolic disorder characterized by progressive neurological deterioration with psychomotor delay/mental retardation, convulsions and coma, and whose pathophysiology is poorly unknown. In the present study, we investigated the effect of chronic administration (from the 5th to the 28th days of life) of propionic acid (PA), the major metabolite accumulating in tissues of patients affected by propionic acidemia, on the cognitive performance of adult rats in the Morris water maze task. PA doses ranged from 1.44 to 1.92 micromol/g body weight as a function of animal age. Control rats were treated with saline in the same volumes. Chronic postnatal days (5-28) PA treatment had no effect on body weight. However, it impaired spatial performance in the water maze. We also determined the effect of ascorbic acid (AA) administered, alone or combined with PA, on the same behavioral parameters in order to test whether free radicals could be responsible for the behavioral alterations observed in PA-treated animals. AA was able to prevent the behavioral alterations provoked by PA, implying that oxidative stress may be involved in these effects. Furthermore, we also investigated the total radical-trapping antioxidant potential (TRAP) in the hippocampus of the animals. We observed that TRAP was significantly reduced in the brain of propionic acidemic rats and that co-administration of AA prevented this effect. The results provide evidence that early PA treatment induces long-lasting behavioral deficits, which are possibly caused by oxygen reactive species generation, and suggest that oxidative stress may be involved in the neuropathology of propionic acidemia.

Topics: Animals; Ascorbic Acid; Body Weight; Cognition Disorders; Free Radical Scavengers; Hippocampus; Male; Maze Learning; Propionates; Rats; Rats, Wistar; Reactive Oxygen Species; Reversal Learning; Swimming

To assess the cross-sectional association of dietary and supplemental antioxidant (carotenoids, vitamins C and E) intake with cognitive function in 12 187 individuals, aged 48-67 years, participating in the Atherosclerosis Risk in Communities (ARIC) Study.. Dietary intake of antioxidant vitamins, as assessed by a food frequency questionnaire, and use of supplements were analysed in relation to the results of three cognitive tests, the delayed word recall test, the Wechsler adult intelligence scale, revised (WAIS-R) digit symbol subtest and the word fluency test.. After adjustment for covariates previously found to be associated with cognition in this sample, we found no consistent associations between dietary antioxidant vitamin intake or supplement use and any of the cognitive tests.. This study suggests little, if any, association between antioxidant vitamin intake and better cognitive function in middle-aged adults.

Topics: Aged; Antioxidants; Ascorbic Acid; Carotenoids; Cognition; Cognition Disorders; Cohort Studies; Cross-Sectional Studies; Dietary Supplements; Female; Humans; Male; Middle Aged; Multicenter Studies as Topic; Prospective Studies; Surveys and Questionnaires; Vitamin E

To test the hypothesis that vitamin C protects against cognitive impairment, the authors conducted a cohort study (n=117) in a retirement community in Sydney, Australia. Vitamin C intake was assessed at baseline (1991) with a semiquantitative food frequency questionnaire, and cognitive function was assessed 4 years later (1995). After adjustment for age, sex, smoking, education, total energy intake, and use of psychotropic medications, consumption of vitamin C supplements was associated with a lower prevalence of more severe cognitive impairment (based on scores on the Mini-Mental State Examination; adjusted odds ratio=0.39, 95% confidence interval 0.18-0.84). There were no associations between vitamin C intake and scores on tests of verbal and category fluency. This study suggests that vitamin C might protect against cognitive impairment.

Topics: Aged; Aged, 80 and over; Ascorbic Acid; Cognition; Cognition Disorders; Cohort Studies; Dementia; Dietary Supplements; Female; Humans; Male; Neuropsychological Tests; Prevalence; Regression Analysis

Aging processes, and among them brain aging, are thought to be associated with free radical action. It is hypothesized that plasma antioxidant vitamin levels correlate with cognitive performance in healthy older subjects.. Longitudinal and cross-sectional comparisons.. The city of Basle, considered representative of the older urban population in Switzerland.. A total of 442 subjects aged 65 to 94 years (mean: 75 years; 312 male, 132 female) was selected from a random sample.. In 1993, participants were tested for memory, and plasma vitamin levels were measured for the three antioxidants alpha-tocopherol, ascorbic acid, and beta-carotene. These vitamin parameters, measured previously in 1971 in the same sample, were integrated in our analyses. In addition, plasma cholesterol, ferritin, and systolic blood pressure were taken into account. Memory variables were priming, working-memory, free recall, recognition and the WAIS-R vocabulary test (semantic memory).. Correlations showed significant stability of the plasma antioxidants over the time lag of 22 years (alpha-tocopherol: r = .47, P < or = .001; beta-carotene: r = .43, P < .001; ascorbic acid: r = .22, P < .001). Free recall, recognition, and vocabulary (but not priming and working-memory) correlated significantly with ascorbic acid and beta-carotene in the cross-sectional 1993 data as well as in the longitudinal 1971-1993 analysis. These two antioxidants remained significant predictors, especially of semantic memory, after controlling for possible confounding variables like age, education, and gender using multiple regression analyses and ANOVAs.. Among people aged 65 and older, higher ascorbic acid and beta-carotene plasma level are associated with better memory performance. These results indicate the important role played by antioxidants in brain aging and may have implications for prevention of progressive cognitive impairments.

Topics: Aged; Aging; Antioxidants; Ascorbic Acid; beta Carotene; Cognition Disorders; Cross-Sectional Studies; Female; Free Radicals; Humans; Longitudinal Studies; Male; Memory; Regression Analysis; Vitamin E; Wechsler Scales

To investigate the relation between cognitive function and cause specific mortality in people aged 65 and over. DESIGN-A 20 year follow up study of a cohort of randomly selected elderly people living in the community who in 1973-4 had taken part in a nutritional survey funded by the Department of Health and Social Security.. Eight areas in Britain (five in England, two in Scotland, and one in Wales).. 921 men and women whose cognitive function was assessed by a geriatrician in 1973-4 and for whom data on health, socioeconomic circumstances, and diet had been recorded.. Cognitive impairment was associated with increased mortality, in particular death from ischaemic stroke. Those who scored 7 or less on the Hodkinson mental test had a relative risk of dying from stroke of 2.8 (95% confidence interval 1.4 to 5.5), compared with those who gained the maximum score (10), after adjustment for age, sex, blood pressure, serum cholesterol concentration, and vitamin C intake. These associations were independent of illness or social class. At the time of the nutritional survey, cognitive function was poorest in those with the lowest vitamin C status, whether measured by dietary intake or plasma ascorbic acid concentration. The relation between vitamin C status and cognitive function was independent of age, illness, social class, or other dietary variables.. The relation between cognitive function and risk of death from stroke suggests that cerebrovascular disease is an important cause of declining cognitive function. Vitamin C status may be a determinant of cognitive function in elderly people through its effect on atherogenesis. A high vitamin C intake may protect against both cognitive impairment and cerebrovascular disease.

Topics: Aged; Aged, 80 and over; Ascorbic Acid; Cause of Death; Cerebrovascular Disorders; Cognition Disorders; Cohort Studies; Diet; Female; Follow-Up Studies; Humans; Male; Mortality; Multivariate Analysis; Risk Factors; Socioeconomic Factors; United Kingdom

Topics: Aged; Ascorbic Acid; Ascorbic Acid Deficiency; Avitaminosis; Cognition Disorders; Female; Humans; Leukocytes; Male; Pellagra; Pyruvates; Thiamine Deficiency; Vitamin B Complex; Vitamin B Deficiency