origin. it 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. 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. vitamin b3 (niacin) 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. niacin is involved in the synthesis of fatty acids and cholesterol, known mediators of brain biochemistry, and in effect, of cognitive function. pellagra is a niacin deficiency disease. pellagra is classically characterized by four 4 "d's": diarrhea, dermatitis, dementia, and death. neuropsychiatric manifestations of pellagra include headache, irritability, poor concentration, anxiety, hallucinations, stupor, apathy, psychomotor unrest, photophobia, tremor, ataxia, spastic paresis, fatigue, and depression. symptoms of fatigue and insomnia may progress to encephalopathy characterized by confusion, memory loss, and psychosis. those afflicted with pellagra may undergo pathological alterations in the nervous system. findings may include demylenation and degeneration of various affected parts of the brain, spinal cord, and peripheral nerves. oral nicotinamide has been promoted as an over-the-counter drug for the treatment of alzheimer's dementia. conversely, no clinically significant effect has been found for the drug, as nicotinamide administration has not been found to promote memory functions in people with mild to moderate dementia of either alzheimers', vascular, or fronto-temporal types. this evidence suggests that nicotinamide may treat dementia as related to pellagra, but administration does not effectively treat other types of dementia. though treatment with niacin does little to alter the effects of alzheimer's dementia, niacin intake from foods is inversely associated with the disease. vitamin b9 (folic acid) folate and vitamin b12 play a vital role in the synthesis of s-adenosylmethionine, which is of key importance in the maintenance and repair of all cells, including neurons. in addition, folate has been linked to the maintenance of adequate brain levels of cofactors necessary for chemicals reactions that lead to the synthesis of serotonin and catecholamine neurotransmitters. concentrations of blood plasma folate and homocysteine concentrations are inversely related, such that an increase in dietary folate decreases homocysteine concentration. thus, dietary intake of folate is a major determinant of homocysteine levels within the body. the relationship between folate and b12 is so interdependent that deficiency in either vitamin can result in megaloblastic anemia, characterized by organic mental change. the link between levels of folate and altered mental function is not large, but is sufficient enough to suggest a causal association. deficiency in folate can cause an elevation of homocysteine within the blood, as the clearance of homocysteine requires enzymatic action dependent on folate, and to a lesser extent, vitamins b6 and b12. elevated homocysteine has been associated with increased risk of vascular events, as well as dementia. differences lie in the presentation of megaloblastic anemia induced by either folate or b12 deficiency. megaloblastic anemia related to deficiency in b12 generally results in peripheral neuropathy, whereas folate-related anemia often results in affective, or mood disorders. neurological effects are not often associated with folate-related megaloblastic anemia, although demyelinating disorders may eventually present. in one study, mood disturbances were recorded for the majority of people with megaloblastic anemia in the absence of b12 deficiency. in addition, folate concentrations within blood plasma have been found to be lower in people with both unipolar and bipolar depressive disorders when compared with control groups. in addition, depressive groups with low folate concentrations responded less well to standard antidepressant therapy than did those with normal levels within plasma. however, replication of these findings are less robust. intake of the vitamin has been linked to deficits in learning and memory, particularly within the elderly population. elderly people deficient in folate may present with deficits in free recall and recognition, which suggests that levels of folate may be related to efficacy of episodic memory. lack of adequate folate may produce a form of dementia considered to be reversible with administration of the vitamin. indeed, there is a degree of improvement in memory associated with folate treatment. in a 3-year longitudinal study of men and women aged 50–70 years with elevated homocysteine plasma concentration, researchers found that a daily oral folic acid supplementation of 800μg resulted in an increase in folate levels and a decrease in homocysteine levels within blood plasma. in addition to these results, improvements of memory, and information-processing speed, as well as slight improvements of sensorimotor speed were observed, which suggests there is a link between homocysteine and cognitive performance. however, while the amount of cognitive improvement after treatment with folate is correlated with the severity of folate deficiency, the severity of cognitive decline is independent of the severity of folate deficiency. this suggests that the dementia observed may not be entirely related to levels folate, as there could be additional factors that were not accounted for which might have an effect. because neurulation may be completed before pregnancy is recognized, it is recommended that women capable of becoming pregnant take about 400μg of folic acid from fortified foods, supplements, or a combination of the two in order to reduce the risk of neural tube defects. these major anomalies in the nervous system can be reduced by 85% with systematic folate supplementation occurring before the onset of pregnancy. the incidence of alzheimer's and other cognitive diseases has been loosely connected to deficiencies in folate. it is recommended for the elderly to consume folate through food, fortified or not, and supplements in order to reduce risk of developing the disease. additionally, folic acid has also been found to improve the memory of older people. there is some evidence that deficiency in folic acid may increase the risk of dementia, especially alzheimer's disease and vascular dementia, but there is debate about whether it lowers risk of cognitive impairment in the older population. folic acid supplementation is shown to lower blood homocysteine levels, while folic acid deficiency can lead to a condition of high levels of homocysteine (hcy) in the bloodstream called hyperhomocysteinemia (hhcy). hhcy is related to several vascular diseases such as coronary artery disease, peripheral vascular disease, and stroke. vitamin b12 (cobalamin) also known as cobalamin, b12 is important for the maintenance of neurological function and psychiatric health. b12 deficiency, also known as hypocobalaminemia, often results from complications involving absorption into the body. an assortment of neurological effects can be observed in 75–90% of individuals of any age with clinically observable b12 deficiency. cobalamin deficiency manifestations are apparent in the abnormalities of the spinal cord, peripheral nerves, optic nerves, and cerebrum. these abnormalities involve a progressive degeneration of myelin, and may be expressed behaviorally through reports of sensory disturbances in the extremities, or motor disturbances, such as gait ataxia. combined myelopathy and neuropathy are prevalent within a large percentage of cases. cognitive changes may range from loss of concentration to memory loss, disorientation, and dementia. all of these symptoms may present with or without additional mood changes. mental symptoms are extremely variable, and include mild disorders of mood, mental slowness, and memory defect. memory defect encompasses symptoms of confusion, severe agitation and depression, delusions and paranoid behavior, visual and auditory hallucinations, dysphasia, violent maniacal behavior and epilepsy. it has been suggested that mental symptoms could be related to a decrease in cerebral metabolism, as caused by the state of deficiency. mild to moderate cases of pernicious anemia may show poor concentration. in severe cases of pernicious anemia, individuals may present with various cognitive problems such as dementia, and memory loss. it is not always easy to determine whether b12 deficiency is present, especially within older adults. people may present with violent behavior or more subtle personality changes. they may also present with vague complaints, such as fatigue or memory loss, that may be attributed to normative aging processes. cognitive symptoms may mimic behavior in alzheimer's and other dementias as well. people who are deficient in b12 despite normal absorption functionality may be treated through oral administration of at least 6 µg/day of the vitamin in pill form. people who suffer from irreversible causes of deficiency, such as pernicious anemia or old age, will need lifelong treatment with pharmacological doses of b12. strategy for treatment is dependent on the person's level of deficiency as well as their level of cognitive functioning. treatment for those with severe deficiency involves 1000 µg of b12 administered intramuscularly daily for one week, weekly for one month, then monthly for the rest of the person's life. the progression of neurological manifestations of cobalamin deficiency is generally gradual. as a result, early diagnosis is important or else irreversible damage may occur. people who become demented usually show little to no cognitive improvement with the administration of b12. there is risk that folic acid administered to those with b12 deficiency may mask anemic symptoms without solving the issue at hand. in this case, people would still be at risk for neurological deficits associated with b12 deficiency-related anemia, which are not associated with anemia related to folate deficiency. vitamin a deficiency and impaired memory 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. iron deficiency and cognition oxygen transportation, dna synthesis, myelin synthesis, oxidative phosphorylation, and neurotransmitter synthesis and metabolism are all biological processes that require iron; however, an iron imbalance can result in neurotoxicity causing oxidation and modification of lipids, proteins, carbohydrates, and dna. hypoxic conditions in severely anemic individuals may cause brain damage resulting in cognitive impairment. when iron levels in the brain are disrupted neurophysiological mechanisms and cognition are affected, potentially resulting in long-term behavioral changes and may affect attention span, intelligence, sensory perception functions, mood, and behavior. neuropathies such as adhd, autism, depression, anxiety, schizophrenia, and bipolar disorder are seen in iron deficient individuals. however, excessive iron accumulation can be seen in neurodegenerative diseases including alzheimer’s and huntington’s disease. iron is needed to develop the central nervous system (cns), endocrine system, autoimmune system, and brain. iron is involved with the development and functioning of different neurotransmitter systems and large iron quantities are required for the myelination of white brain matter. abnormal myelination of white matter due to iron deficiency during development may be related to the onset of psychological disorders in adolescents. decreased iron concentration results in a reduction of neurotransmitter levels, in turn leading to poor myelination and delayed neuromaturation. aging and cognitive disease foods that are rich in omega-3 fatty acids have been shown to decrease risk of getting alzheimer's disease. omega-3 fatty acids omega-3 fatty acids, primarily docosahexaenoic acid (dha), which is the most prevalent omega-3 fatty acid found in neurons, have been studied extensively for use in possible prevention and therapy of alzheimer's disease. some studies (cross-sectional) suggest that reduced intake or low brain levels of dha are associated with earlier development of cognitive deficits or development of dementia, including alzheimer's disease. several clinical trials suggest that omega-3 fatty acid supplementation does not have significant effects in the treatment of alzheimer's disease—which in turn may suggest that the protective benefits of omega-3 fatty acid supplementation could depend on the scope of the disease and other confounding factors. a diet that is rich in antioxidants will also help get rid of free radicals in the body, which could be a cause for alzheimer's. the buildup of beta amyloid plaques, a marker highly associated with alzheimer's disease, generates cell damaging free radicals. therefore, the role of antioxidants as protectants against alzheimer's disease has become a hot topic of study. simple dietary modification, towards fewer highly processed carbohydrates and relatively more fats ad cholesterol, is likely a protective measure against alzheimer's disease.