a byproduct of methcathinone synthesis if potassium permanganate is used as an oxidiser. symptoms include apathy, bradykinesia, gait disorder with postural instability, and spastic-hypokinetic dysarthria. another street drug sometimes contaminated with manganese is the so-called "bazooka", prepared by free-base methods from cocaine using manganese carbonate. reports also mention such sources as contaminated drinking water, and fuel additive methylcyclopentadienyl manganese tricarbonyl (mmt), which on combustion becomes partially converted into manganese phosphates and sulfate that go airborne with the exhaust, and manganese ethylene-bis-dithiocarbamate (maneb), a pesticide. pathological mechanisms manganese may affect liver function, but the threshold of acute toxicity is very high. on the other hand, more than 95% of manganese is eliminated by biliary excretion. any existing liver damage may slow this process, increasing its concentration in blood plasma. the exact neurotoxic mechanism of manganese is uncertain but there are clues pointing at the interaction of manganese with iron, zinc, aluminum, and copper. based on a number of studies, disturbed iron metabolism could underlie the neurotoxic action of manganese. it participates in fenton reactions and could thus induce oxidative damage, a hypothesis corroborated by the evidence from studies of affected welders. a study of the exposed workers showed that they have significantly fewer children. this may indicate that long-term accumulation of manganese affects fertility. pregnant animals repeatedly receiving high doses of manganese bore malformed offspring significantly more often compared to controls. manganism mimics schizophrenia. it is found in large quantities in paint and steelmaking. treatment the current mainstay of manganism treatment is levodopa and chelation with edta. both have limited and at best transient efficacy. replenishing the deficit of dopamine with levodopa has been shown to initially improve extrapyramidal symptoms, but the response to treatment goes down after 2 or 3 years, with worsening condition of the same patients noted even after 10 years since last exposure to manganese. enhanced excretion of manganese prompted by chelation therapy brings its blood levels down but the symptoms remain largely unchanged, raising questions about efficacy of this form of treatment. increased ferroportin protein expression in human embryonic kidney (hek293) cells is associated with decreased intracellular mn concentration and attenuated cytotoxicity, characterized by the reversal of mn-reduced glutamate uptake and diminished lactate dehydrogenase (ldh) leakage. locations the red river delta near hanoi has high levels of manganese or arsenic in the water. approximately 65 percent of the region's wells contain high levels of arsenic, manganese, selenium and barium. this was also published in the proceedings of the national academy of sciences. magnesium magnesium is necessary for the function of many metabolic enzymes and also serves as a key regulator of calcium channels involved in neurotransmission (e.g. nmda receptor). magnesium supplementation facilitates nerve regeneration after injury. although unpolished grains contain magnesium, phytic acid in grains can inhibit its absorption. leafy greens are an excellent source of magnesium. vitamins deficiency or excess intake of many vitamins can affect the brain contributing to developmental and degenerative diseases. vitamin a vitamin a is an essential nutrient for mammals which takes form in either retinol or the provitamin beta-carotene. it helps regulation of cell division, cell function, genetic regulation, helps enhance the immune system, and is required for brain function, chemical balance, growth and development of the central nervous system and vision. learning memory in an experiment by chongqing medical university pregnant rats were either plentiful in vitamin a or were of a vitamin a deficiency (vad) due to their diet. the offspring of these rats were then tested in a water maze at 8 weeks old and it was found the vad offspring had a harder time finishing the maze which helps show that these rats, even while having a deficiency from in utero, have more problems with learning memory. young rats in a separate study by the same university also showed impaired long-term potentiation in the hippocampus when they were vad which shows neuronal impairment. when the patient is vad for too long, the effects of the damage to the hippocampus can be irreversible. spatial memory vitamin a affects spatial memory most of the time because the size of the nuclei in hippocampal neurons are reduced by approximately 70% when there is a deficiency which affects a person's abilities for higher cognitive function. in a study by the university of cagliari, italy, vad rats had more trouble learning a radial arm maze than rats who had normal levels of the vitamin. the healthy rats were able to correctly solve the maze within the 15-day training period and other rats that were once deficient but had vitamin a restored to normal levels were also able to solve it. here it was found that the retinoid receptors which help transport vitamin a were of normal function. prevention, treatment and symptoms eating foods high in vitamin a or taking dietary supplements, retinol or retinal will prevent a deficiency. the foods highest in vitamin a are any pigmented fruits and vegetables and leafy green vegetables also provide beta-carotene. there can be symptoms of fat loss and a reduction of any weight gain that would be considered normal for an individual, especially developmental weight gains such as in infants which would occur if the infant was deprived of vitamin a in utero and/or if it was deprived postnatal for an extensive period of time. the deficiency can also cause conditions such as blindness or night blindness, also known as nyctalopia. night blindness is due to the inability to regenerate rhodopsin in the rods which is needed in dim light in order to see properly. a treatment of supplements of retinoic acid which is a part of vitamin a can help replenish levels and help bring learning to normal, but after 39 weeks this is ineffective even if the treatment is daily because it will not bring the retinoid hypo-signalling back to normal. relationship with zinc zinc is needed to maintain normal vitamin a levels in blood plasma. it also helps vitamin a become metabolized by the liver. however evidence suggests that when someone is deficient in both vitamin a and zinc, memory is more improved when just vitamin a is increased than when just zinc is increased. of course memory has the largest improvement when both are increased. when one of these nutrients is not balanced, the other is most likely to be affected because they rely on each other for proper functioning in learning. thiamin (vitamin b1) vitamin b1, also known as thiamine, is a coenzyme essential for the metabolism of carbohydrates. this vitamin is important for the facilitation of glucose use, thus ensuring the production of energy for the brain, and normal functioning of the nervous system, muscles, and heart. thiamine is found in all living tissues, and is uniformly distributed throughout mammalian nervous tissue, including the brain and spinal cord. metabolism and coenzyme function of the vitamin suggest a distinctive function for thiamin within the nervous system. the brain retains its thiamine content in the face of a vitamin-deficient diet with great tenacity, as it is the last of all nervous tissues studied to become depleted. a 50% reduction of thiamine stores in rats becomes apparent after only 4 days of being put on a thiamine-deficient diet. however, polyneuritic signs do not begin to appear until about 4 or 5 weeks have passed. similar results have been found in human subjects. deficiencies the body has only small stores of b1; accordingly, there is risk of deficiency if the level of intake is reduced only for a few weeks. thiamin deficiency during critical periods of early development can disrupts neurogenesis in animal models. lack of thiamin later in life causes the disease known as beriberi. there are two forms of beriberi: "wet", and "dry". dry beriberi is also known as cerebral beriberi. characteristics of wet beriberi include prominent edema and cardiac involvement, whereas dry beriberi is mainly characterized by a polyneuritis. in industrialized nations, thiamine deficiency is a clinically significant problem in individuals with chronic alcoholism or other disorders that interfere with normal ingestion of food. thiamine deficiency within developed nations tends to manifest as wernicke–korsakoff syndrome. chronic alcoholism can disrupt thiamin absorption and thiamin deficiency contributes to neurodegeneration and memory loss in alcoholics known as wernicke's encephalopathy. individuals with chronic alcoholism may fall short on minimum daily requirements of thiamine in part due to anorexia, erratic eating habits, lack of available food, or a combination of any of these factors. thiamine deficiency has been reported in up to 80% of alcoholic patients due to inadequate nutritional intake, reduced absorption, and impaired utilization of thiamine. alcohol, in combination with its metabolite acetaldehyde, interacts with thiamine utilization at the molecular level during transport, diphosphorylation, and modification processes. for this reason, chronic alcoholics may have insufficient thiamine for maintenance of normal brain function, even with seemingly adequate dietary intake. symptoms clinical signs of b1 deficiency include mental changes such as apathy, decrease in short-term memory, confusion, and irritability. moderate deficiency in thiamine may reduce growth in young populations, in increase chronic illness in both young and middle-aged adults. in addition, moderate deficiency of thiamine may increase rates of depression, dementia, falls, and fractures in old age. the lingering symptoms of neuropathy associated with cerebral beriberi are known as korsakoff's syndrome, or the chronic phase of wernicke-korsakoff's. wernicke encephalopathy is a neurological disorder resulting from a deficiency in thiamine, sharing the same predominant features of cerebral beriberi, as characterized by ocular abnormalities, ataxia of gait, a global state of confusion, and neuropathy. the state of confusion associated with wernicke's may consist of apathy, inattention, spatial disorientation, inability to concentrate, and mental sluggishness or restlessness. clinical diagnosis of wernicke's disease cannot be made without evidence of ocular disturbance, yet these criteria may be too rigid. korsakoff's likely represents a variation in the clinical manifestation of wernicke encephalopathy, as they both share similar pathological origin. korsakoff's syndrome is often characterized by confabulation, disorientation, and profound amnesia. characteristics of the neuropathology are varied, but generally consist of bilaterally symmetrical midline lesions of brainstem areas, including the mammillary bodies, thalamus, periaqueductal region, hypothalamus, and the cerebellar vermis. treatment immediate treatment of wernicke encephalopathy involves the administration of intravenous thiamine, followed with long-term treatment and prevention of the disorder through oral thiamine supplements, alcohol abstinence, and a balanced diet. improvements in brain functioning of chronic alcoholics may occur with abstinence-related treatment, involving the discontinuation of alcohol consumption and improved nutrition. wernicke's encephalopathy is life-threatening if left untreated. however, a rapid reversal of symptoms may result from prompt administration of thiamine. prevention fortification of flour is practiced in some countries to replace the thiamine lost during processing. however, this method has been criticized for missing the target population of chronic alcoholics, who are most at risk for deficiency. alternative solutions have suggested the fortification of alcoholic beverages with thiamine. ingesting a diet rich in thiamine may stave off the adverse effects of deficiency. foods providing rich sources of thiamine include unrefined grain products, ready-to-eat cereals, meat (especially pork), dairy products, peanuts, legumes, fruits and eggs. niacin (vitamin b3) vitamin b3, also known as niacin, includes both nicotinamide as well as nicotinic acid, both of which function in many biological oxidization and reduction reactions within the body. these functions include the biochemical degradation of carbohydrates, fats and proteins. niacin is also involved in the synthesis of fatty acids and cholesterol, which are known mediators of brain biochemistry, and in effect, of cognitive function. sufficient niacin intake is either obtained from diet, or synthesized from the amino acid tryptophan. deficiencies pellagra initially presents as dermatitis severe niacin deficiency typically manifests itself as the disease pellagra. synthesis of b3 from tryptophan involves vitamin b2 and b6, so deficiencies in either of these nutrients can lead to niacin deficiency. an excess of leucine, an essential amino acid, in the diet can also interfere with tryptophan conversion and subsequently result in a b3 deficiency. pellagra is most common to populations within developing countries in which corn is the dietary staple. the disease has virtually disappeared from industrialized countries, yet still appears in india and parts of china and africa. this is in part due to the bound form of niacin that unprocessed corn contains, which is not readily absorbed into the human body. the processes involved in making corn tortillas, can release the