All of the essential minerals are important for cellular functions in brain, as they are elsewhere in the body. These are sodium, potassium, calcium, magnesium, iron, copper, zinc, manganese, cobalt, and molybdenum. While most function as cofactors in enzymatic reactions, sodium and potassium are key ions in electrical conduction in neuronal membranes, calcium functions as a second messenger within neurons, and magnesium is an important component of certain neurotransmitter receptors. The diet normally provides more than adequate amounts of almost all minerals, except possibly for calcium, iron, magnesium, and zinc. The BBB permeability to most metals is quite low. For example, although the brain extracts 20-30% of the glucose in blood in a single capillary transit, it extracts <0.3% of any metal. The mechanisms of transport into brain for most metals are unknown. However, some details regarding the transport and/ or functions of iron, calcium, and copper are available.

Iron circulates bound to the protein transferrin. Iron uptake into brain occurs primarily at the BBB, and involves a transferrin receptor-mediated endo-cytosis of the iron-transferrin complex by capillary endothelial cells. Iron dissociates from transferrin inside the cell, and is delivered into the brain interstitial fluid; the transferrin is returned to the circulation. Brain iron associates with ferretin, and is stored intracellularly. The bulk of the iron-ferretin stored in brain resides in glial cells and is laid down early in postnatal life. Marked regional differences in iron and ferretin concentrations occur in brain; levels in some areas are as high as those in liver. This distribution, however, does not correlate with the density of transferrin receptors in brain capillaries; it is presently unknown how or why the unequal distribution of iron develops. Numerous enzymes in brain are iron requiring, including several hydroxylases involved in neurotransmitter production, and a key metabolic enzyme, monoamine oxidase.

Iron deficiency can cause impairments in attention and cognition in children. Similar effects are seen in animals. In iron-deficient rats, brain iron concentrations decline, with newborn and infant animals showing more rapid declines than older animals. Iron repletion in brain occurs in infant and adult rats with iron supplementation, but not in animals depleted at birth. While outside of the brain, the activities of many iron-dependent enzymes are depressed by iron deficiency, their activities are unaffected inside the brain. However, a reduction in certain dopamine receptors occurs, along with aberrations in dopamine-dependent behaviors (dopamine is a CNS neurotransmitter). The inability of brain iron stores to recover in rats made iron deficient as newborns coincides with a persistence of dopamine-linked behavioral deficits, despite normal repletion of iron stores elsewhere in the body. Restoration of normal behavior with iron supplementation, along with brain iron stores, is seen in animals made iron deficient at other ages.

Iron deficiency also interferes with myelinization. Since marked glial proliferation and myelin formation occur early in infancy, iron deficiency during this period could prevent the optimal development of neuronal communications (glial cells provide insulation for axons and synapses). This effect could account for some of the behavioral deficits associated with neonatal iron deficiency.

Calcium is actively transported into the CNS, primarily via the blood-CSF barrier, and is not vitamin D sensitive. Since calcium concentrations in the circulation are regulated, under most circumstances, this process should also help to maintain brain calcium uptake and levels in the face of vagaries in calcium intake. Deficiencies in brain calcium should thus be a relatively rare occurrence.

Copper functions as a cofactor for numerous enzymes, including dopamine fi-hydroxylase (DBH), which converts dopamine to noradrenaline. Dietary copper deficiency in humans is fairly rare. When produced in animals, it leads to reduced DBH activity in neurons and cells anywhere in the nervous system that synthesize noradrenaline. The mechanism of copper transport into the brain is presently unknown. Copper deficiency occurs as an X-linked genetic disease of copper transport in Menkes' syndrome, in which tissue and brain copper levels become extremely low, and produce neurodegeneration. Children with Menkes' syndrome die at a very young age.

See also: Amino Acids: Chemistry and Classification; Metabolism; Specific Functions. Ascorbic Acid: Physiology, Dietary Sources and Requirements. Biotin. Calcium. Choline and Phosphatidylcholine.

Cobalamins. Copper. Fatty Acids: Metabolism. Folic Acid. Glucose: Metabolism and Maintenance of Blood Glucose Level. Niacin. Pantothenic Acid. Protein: Synthesis and Turnover. Riboflavin. Thiamin:

Physiology. Vitamin A: Physiology; Biochemistry and Physiological Role. Vitamin E: Metabolism and Requirements.

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