ascorbic-acid and Learning-Disabilities

Glucose transporter type1 (GLUT-1) deficiency may be rare, but it is a preventable cause of severe learning difficulties; and therefore there is an urgency in making an early diagnosis. Suspicions must be roused when intractable seizures occur in infancy. These may be associated with acquired microcephaly and developmental delay. The finding of low glucose sugar levels in the cerebrospinal fluid, but not in the blood will identify the condition. The gene encoding the GLUT-1 protein is located on the short arm of chromosome 1, and inheritance is by a dominant trait. Patients with this syndrome can have heterozygous mutations, with one allele being a normal wild type and one being mutant. An efficient transport of glucose across the blood-brain barrier is essential as it is such an important fuel for the brain, and this is provided by glucose transporter type1 in the endothelial cells of the brain capillaries. Another minor contribution to the symptomatology of GLUT-1 may be impaired transport of an oxidised form of vitamin C. Treatment with anti-epileptic drugs may be needed, and the ketogenic diet may reduce symptoms, as ketosis can provide an alternative source of fuel for the brain. It has also been suggested that antioxidant thioctic acid may be of benefit. Substances such as caffeine and phenobarbitone should be avoided as they inhibit glucose transport.

Topics: Anticonvulsants; Antioxidants; Ascorbic Acid; Blood-Brain Barrier; Caffeine; Central Nervous System Stimulants; Chromosomes, Human, Pair 1; Glucose; Glucose Transporter Type 1; Humans; Ketosis; Learning Disabilities; Monosaccharide Transport Proteins; Mutation; Phenobarbital; Seizures; Thioctic Acid

Preliminary to a stimulant comparison study, 31 children with minimal brain dysfunction randomly received either placebo or a megavitamin combination. During a two-week trial, only two children responded so well that stiumlants were not considered necessary; both were in the placebo group. Change scores from pretest to posttest on four blind ratings by teachers and parents did not show a significant difference between the placebo and vitamin groups.

Topics: Ascorbic Acid; Attention Deficit Disorder with Hyperactivity; Child; Female; Glutamates; Humans; Hyperkinesis; Learning Disabilities; Male; Nicotinic Acids; Orthomolecular Therapy; Pantothenic Acid; Pyridoxine

Learning and memory deficits occur in diabetes mellitus. Although the pathogenesis of cognitive impairment in diabetes has not been fully elucidated, factors such as metabolic impairments, vascular complications and oxidative stress are thought to play possible roles. Here we investigated the effect of chronic treatment with vitamin C (50mg/kg, p.o), vitamin E (100mg/kg, p.o) and both together on passive avoidance learning (PAL) and memory in male Wistar control and diabetic rats. Treatments were begun at the onset of hyperglycemia. Passive avoidance learning was assessed 30 days later. Retention was tested 24h after training. At the end, animals were weighed and blood samples were drawn for plasma glucose measurement. Diabetes caused impairment in acquisition and retrieval processes of PAL and memory. The combination of vitamin C and E improved learning and memory in controls and reversed learning and memory deficits in diabetic rats. Combined treatment also affected the body weight and plasma glucose level of diabetic treated animals compared to untreated diabetic animals. Hypoglycemic effects and antioxidant properties of the vitamins may be involved in the nootropic effect of such treatment. These results show that combined treatment with vitamins C and E improved PAL and memory of control rats. In addition, combined vitamins administration to rats for 30 days from onset of diabetes alleviated the negative influence of diabetes on learning and memory. Therefore, combined vitamins treatment may provide a new potential alternative for prevention of impaired cognitive functions associated with diabetes and may warrant further clinical study.

Topics: Animals; Ascorbic Acid; Avoidance Learning; Blood Glucose; Body Weight; Diabetes Mellitus, Experimental; Drug Therapy, Combination; Learning Disabilities; Male; Memory; Memory Disorders; Neuropsychological Tests; Nootropic Agents; Rats; Rats, Wistar; Time Factors; Vitamin E

We carried out animal experiments based on the orthogonal design L(8)(2(7)) setting seven factors with two different levels of each and 10 groups of rats. The nutrients tested were tyrosine, glycine, methionine, taurine, ascorbic acid, thiamine and zinc.. The objective of this study was to explore the optimal combinations of nutrients for prevention or amelioration of lead-induced learning and memory impairment.. Rats were supplemented with nutrients by gavage once a day in two experiments: one was simultaneous nutrient supplementation with lead acetate administration (800 mg l(-1)) for 8 weeks (prophylactic supplementation) and the other was nutrient supplementation for 4 weeks after the cessation of 4 weeks of lead administration (remedial supplementation). Morris water maze was initiated at ninth week. Rats were terminated for assays of levels of Pb in blood, activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS) in hippocampus, levels of nitric oxide (NO) in hippocampus and expressions of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine monophosphate (cAMP) response element-binding protein messenger RNA in hippocampus.. Results showed that in prophylactic supplementation, methionine, taurine, zinc, ascorbic acid and glycine were the effective preventive factors for decreasing prolonged escape latency, increasing SOD and NOS activities and NO levels in the hippocampus, respectively. On the other hand, in remedial supplementation, taurine was the effective factor for reversing Pb-induced decrease in activities of SOD, NOS and levels of NO.. In conclusion, the optimum combinations of nutrients appear to be methionine, taurine, zinc, ascorbic acid and glycine for the prevention of learning and memory impairment, while taurine and thiamine appear to be the effective factors for reversing Pb neurotoxicity.

Topics: Animals; Antioxidants; Ascorbic Acid; Food; Glycine; Hippocampus; Lead Poisoning; Lead Poisoning, Nervous System; Learning Disabilities; Male; Maze Learning; Memory Disorders; Methionine; Models, Animal; Organometallic Compounds; Rats; Rats, Sprague-Dawley; Taurine; Thiamine; Tyrosine; Zinc

Vitamin C (ascorbate) has important antioxidant functions that can help protect against oxidative stress in the brain and damage associated with neurodegenerative disorders such as Alzheimer's disease. When administered parenterally ascorbate can bypass saturable uptake mechanisms in the gut and thus higher tissue concentrations can be achieved than by oral administration. In the present study we show that ascorbate (125 mg/kg) administered intraperitoneally (i.p.) 1-h before testing, partially attenuated scopolamine-induced (1 mg/kg i.p.) cognitive deficits in Morris water maze performance in young mice. Cumulative search error, but not escape latency nor path length, was significantly improved during acquisition in ascorbate plus scopolamine-treated mice although performance did not equal that of control mice. During the probe trial, scopolamine led to increased search error and chance level of time spent in the platform quadrant, whereas mice pre-treated with ascorbate prior to scopolamine did not differ from control mice on these measures. Ascorbate had no effect on unimpaired, control mice and neither did it reduce the peripheral, activity-increasing effects of scopolamine. Ascorbate alone increased acetylcholinesterase activity in the medial forebrain area but had no effect in cortex or striatum. This change, and its action against the amnestic effects of the muscarinic antagonist scopolamine, suggest that ascorbate may be acting in part via altered cholinergic signaling. However, further investigation is necessary to isolate the cognition-enhancing effects of ascorbate.

Topics: Acetylcholinesterase; Animals; Ascorbic Acid; Cerebral Cortex; Corpus Striatum; Escape Reaction; Female; Learning Disabilities; Liver; Locomotion; Male; Maze Learning; Mice; Mice, Inbred Strains; Nootropic Agents; Prosencephalon; Scopolamine; Space Perception; Time Factors

The effects of long-term treatment with both antioxidants and a program of behavioral enrichment were studied as part of a longitudinal investigation of cognitive aging in beagle dogs. Baseline performance on a battery of cognitive tests was used to assign 48 aged dogs (9-12 years) into four cognitively equivalent groups, of 12 animals per group: Group CC (control food-control environment), group CE (control food-enriched environment); Group AC (antioxidant fortified food-control environment); Group AE (fortified food-enriched environment). We also tested a group of young dogs fed the control food and a second group fed the fortified food. Both groups of young dogs received a program of behavioral enrichment. To evaluate the effects of the interventions on cognition after 1 year, the dogs were tested on a size discrimination learning task and subsequently on a size discrimination reversal learning task. Both tasks showed age-sensitivity, with old dogs performing more poorly than young dogs. Both tasks were also improved by both the fortified food and the behavioral enrichment. However, in both instances the treatment effects largely reflected improved performance in the combined treatment group. These results suggest that the effectiveness of antioxidants in attenuating age-dependent cognitive decline is dependent on behavioral and environmental experience.

Topics: Aging; Animals; Antioxidants; Ascorbic Acid; Behavior, Animal; Carnitine; Diet; Discrimination Learning; Dogs; Environment; Food, Fortified; Learning Disabilities; Longitudinal Studies; Models, Biological; Reversal Learning; Thioctic Acid; Vitamin E

Topics: Ascorbic Acid; Child; Female; Humans; Learning Disabilities; Male; Methylphenidate; Niacinamide

Topics: Ascorbic Acid; Attention Deficit Disorder with Hyperactivity; Birth Weight; Child; Dietary Proteins; Female; Follow-Up Studies; Gestational Age; Humans; Infant; Infant, Newborn; Infant, Premature; Intelligence; Intelligence Tests; Learning Disabilities; Male; Perceptual Disorders; Psychological Tests; Tyrosine