Neutral amino acids are taken up from plasma into brain by a single high-affinity transport system at brain capillaries. Transport affinity differs among neutral amino acids by 700 fold and is determined primarily by amino acid side chain hydrophobicity. At normal plasma concentrations the transport system is saturated, forcing individual amino acid to compete for available transport sites. Competition makes the brain susceptible to inbalances in plasma concentrations. Neutral amino acid transport into rat brain decreases between 1 week and 3 months of age and then remains constant between 3 and 24 months. Changes in amino acid transport with development and aging correlate with changes in brain protein synthesis. The nonmetabolizable amino acid, l-aminocyclohexanecarboxylic acid, is transported by the cerebrovascular neutral amino acid carrier and may be a suitable in vivo probe of amino acid transport in humans using positron emission tomography. Calcium influx into cerebrospinal fluid is maintained constant during chronic hypocalcemia by saturable, Vitamin D-independent transport at the choroid plexus epithelium. In contrast, calcium transport across brain capillaries may not be regulated during hypocalcemia. An electron beam X-ray microanalysis method was developed to determine metal concentrations in human brain tissue. Analysis of samples from patients with Alzheimer's disease demonstrated that aluminum is not accumulated significantly in senile plaques as compared to surrounding brain tissue.
