Academic journal article
By Whitehouse, Peter J.; Juengst, Eric; Mehlman, Maxwell; Murray, Thomas H.
The Hastings Center Report , Vol. 27, No. 3
Human beings have often sought to enhance their cognitive performance: to remember more, think faster, reason more clearly, judge more wisely. Most of these efforts have relied on a combination of tools and training, such as the Chinese abacus and mercantile apprenticeships or our personal computers and university degrees. Since Adam and Eve's apple, however, the most controversial means of cognitive enhancement have always been the enhancers we take rather than the ones we invent or earn: the supernatural gifts, magic potions, or medical drugs that promise to expand our abilities without requiring us to exert ourselves unduly in the process. It is just this class of "unnatural cognitive enhancers that is now becoming interesting again in neuroscience circles. As we learn more about how our brains work, the possibility of developing pharmaceutical enhancers for cognition becomes more plausible. Moreover, as the complexity of our information-rich world increases, the need for enhanced cognitive function seems to grow. It is a good time to begin thinking aloud about the ethical and social issues that biting this new apple might raise.
We will focus on drugs that have as their principal aim cognitive enhancement, leaving aside the important class of new drugs that affect emotions, even though the clinical and conceptual distinctions between cognition and emotion are difficult to make and the neural systems for these behaviors overlap with each other. We do not consider, for example, mood elevators such as Prozac or psychoactive compounds such as LSD, even though both classes of drugs have been used in psychotherapy to produce mental states that are claimed to expand an individual's cognitive abilities.
The Biological Basis of Cognition: Recent Developments
The term "cognition" is used in many different ways by clinicians and researchers. It usually is considered to be a combination of skills, including attention, learning, memory, language, praxis (skilled motor behaviors), and so-called executive functions, such as decisionmaking, goal setting, planning, and judgment. Most of the clinical literature on cognitive enhancement concerns the development of compounds to improve either attention or memory. In daily life, individuals frequently complain that their memory is inadequate or that they cannot pay attention in certain cognitively demanding situations.
A drug that enhanced memory alone, however, such as the ability to remember lists of words, would not be as valuable as a drug that had more general effects on cognition, particularly on executive functions. Perhaps the highest order of executive functions is what we call wisdom. Can we imagine a cognitive enhancer that would make people wiser? Although this seems unlikely, drugs that improve the speed of processing, the allocation of attention in complex multitask situations, or the ability to integrate cognitive and emotional functions might actually improve executive functions.
The neural substrates of cognition are complex and still poorly understood. The brain is composed of individual nerve cells interconnected in complex patterns. Synapses are small junctions between nerve cells over which chemical messages, called neurotransmitters, travel. At each synapse, different neurotransmitter messages of different strengths are integrated, allowing information to be processed. The biological substrate of cognitive impairment is the dysfunction of nerve cells and their synapses, which impairs the interactions among the neurotransmitters and their receptors on the postsynaptic cell. In normal aging, as in disease, cognitive impairment is thought to be due to a loss of neurotransmitter molecules and their receptors, which in turn may be caused by the death of nerve cells. Some of the neurotransmitters discussed later (acetylcholine and noradrenaline) may be biological substrates of both cognition and emotions.)
If the concentration of the neurotransmitter acetylcholine is reduced, as it is in the brains of patients with Alzheimer disease and other dementias, a short-term therapeutic strategy would be to increase levels of acetylcholine. …