Metals in Brain - Biological Inorganic Chemistry - page 394

is essential for a number of enzymes, including tryptophan hydroxylase (serotonin) tyrosine hydroxylase
(noradrenaline and dopamine). Long-term follow-up studies of iron deficiency in the human infant brain indicate that
such alterations in myelination result in slower conduction in both the auditory and visual systems. Both of these
sensory systems are rapidly myelinating during the period of iron deficiency and are critical for learning and social
interaction. Together with the reduced energy, impaired glial function, altered activation of monoamine circuits, this
may alter experience dependent processes which are critical to brain structure and function during early development.
In contrast, an inevitable consequence of ageing is an elevation of brain iron in specific brain regions, e.g., in
the putamen, motor cortex, prefrontal cortex, sensory cortex, and thalamus, localised within H- and L-ferritin and
neuromelanin with no apparent adverse effect. However, as we will see in Chapter 21, ill-placed excessive
amounts of iron in specific intracellular compartments, like mitochondria, or in specific regions of the brain, such
as the substantia nigra and lateral globus pallidus, will lead to neurodegenerative diseases (Friedreich's ataxia, or
Parkinson's disease, respectively). Increases in both copper and zinc are also observed in the ageing brain.

CONCLUDING REMARKS
As the reader can appreciate, extremely low concentrations of metal ions are able to orchestrate a multitude of
activities in the brain, controlling the opening of various ion channels as well as activating various neurotrans-
mitter receptors. Clearly, changes in the concentrations of such metal ions will induce adverse effects and induce
the demise of neurons and other cell types. This will be considered in the next chapter.

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