In some cases the brain is not physically broken by injury, stroke, or other insult, but nonetheless is still dysfunctional. With conditions such as depression, anxiety, amnesia, and schizophrenia it seems that the chemical communication systems of the brain, not its nerve pathways, are affected. Most common of all is depression, a debilitating condition that some 20-40 per cent of adults will experience at some time in their lives.
You will recall that there are two quite different types of chemical messengers or neurotransmitters in the brain. There are those that establish the brain's wiring diagram, ensuring either rapid excitatory or inhibitory connections between neurons in complex networks. These fast transmitters work by binding to special receptor molecules that directly activate the flow of electrically charged ions into or out of the affected neuron. It is thought that depression does not arise from a disruption to the brain's neural network. Rather it seems that the problem resides among the indirect neurotransmitters and it seems depression is a condition that reflects an abnormality of brain chemistry rather than brain structure. Strongly implicated in depressive disorders are the slow monoamine transmitters serotonin, noradrenalin, and dopamine. In the brain of a depressed person there is an insufficiency of these transmitters. Precisely how this causes the symptoms of depression, including loss of interest in life, lowered appetite, sleep disruption, and suicidal tendencies is not fully understood, though we do know that drugs that elevate the brain's monoamine levels can be an effective treatment for this illness.
This important class of drug is known as monoamine selective re-uptake inhibitors, a name that refers to their mode of action. In Chapter 3 we saw that, following the release of neurotransmitters, E their action must be rapidly terminated so that a following chemical J! message is not confused with the previous one. The process of transmitter action termination is known as inactivation. Inactivation for serotonin and noradrenalin involves their removal from the region of the synapse by a selective re-uptake mechanism. By inhibiting a neurotransmitter's re-uptake it tends to accumulate in the brain, its concentration is increased, and over a period of weeks the depressive symptoms are reversed or ameliorated.
Antidepressants, the first of which were discovered more than 50 years ago, are now the most widely prescribed drugs. But depression remains the most prevalent of all psychological diseases and not all experts are convinced by the efficacy of commonly prescribed antidepressants, all of which increase the level of monoamine transmitters in the brain. In fact there is growing concern that the monoamine hypothesis is wrong and that some antidepressants may increase the likelihood of suicide. The fact is we know very little about the fundamental neurobiology of depression. It is very unlikely to be due simply to an insufficiency of monoamines. If this were the case, it would be difficult to understand why antidepressant drugs that raise monoamine levels quickly take several weeks to have a significant effect on depressive symptoms. This delay suggests that antidepressants work indirectly and that depression is caused by biochemical dysfunction that is only distantly linked to monoamine function. Indeed, in their search for new targets for antidepressant drugs, pharmaceutical companies are now exploring alternative biochemical pathways, such as those associated with the regulation of the brain's stress hormone cortisol. Growing concerns about the safety and side effects of the monoamine uptake inhibitors are a driving force behind the search for more effective new treatments for this baffling illness of the brain.
In this chapter we have seen how the broken brain might be fixed by a combination of brain-machine interface technology, the neutralization of inhibitors of regeneration, or by manipulating the r
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