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Constructive Memory and Memory Enhancement

In Jorge Luis Borges’ short story, “Funes the Memorious,” the character Ireneo Funes sustains a brain injury from an equestrian accident. Consistent with Borges’ penchant for irony, Funes does not develop amnesia but instead a condition in which he remembers every detail of everything he experiences. Speaking to the narrator, Funes says, “My memory, sir, is like a garbage disposal.” Funes becomes an invalid, a prisoner of a hyperactive system of memory consolidation and recall, unable to learn new things and anticipate the future because he cannot tolerate any additional experience. The narrator suspects that Funes “was not very capable of thought. To think is to forget a difference, to generalize, to abstract. In the overly replete world of Funes, there were nothing but details, almost contiguous details.” Because of his overloaded memory, Funes is unable to execute such cognitive tasks as problem-solving and decision-making. He is also unable to anticipate and plan for the future because be cannot forget the particular features of his experience.

The most famous actual case of this condition was neurologist A. R. Luria’s patient Shereshevkii, described in Luria’s book The Mind of a Mnemonist. His formidable ability to remember a vast amount of facts and events resulted in his inability to process new information. He was prevented from doing any work other than as a traveling mnemonist.

Research into the mechanisms of memory suggests that novel pharmacological agents could enhance the encoding and storage of long-term episodic and semantic memory of events and facts. “Smart” drugs targeting the transcription factor cyclic response element binding protein (CREB), which influences the encoding and storage of long-term memory, might increase memory capacity in our brains.1 This effect might also be achieved through drugs that increased acetylcholine, the main neurotransmitter involved in the regulation of memory. Other pharmacological agents that might have a similar effect are ampakines, which can influence the neurotransmitter glutamate and promote better communication between synapses in the cortex. These agents might also enhance the retrieval of remembered facts and events from the hippocampus and other sites in the medial temporal lobes by the prefrontal cortex for short-term working memory in executive cognitive functions. Insofar as it would involve people with normal memory functions, enhancement would be different from the therapeutic use of drugs (such as the cholinesterase inhibitor donepezil and the glutamate antagonist memantine) to retard memory loss in Alzheimer disease. Memory enhancement could result in more effective cognitive capacities such as problem-solving and decision-making.

Yet there are other critical features of memory, consisting in more than mechanisms of encoding, storage, and retrieval. It is unclear what effects drugs designed to enhance these mechanisms might have on these other features of our ability to recall the past. It is possible that the drugs might do more to impair than improve the usefulness and value of memory.

A recent study by Demis Hassabis, published in the Proceedings of the National Academy of Sciences, sheds some light on the problem exemplified by Borges’ fictional character and Luria’s patient. The Hassabis study compared people with bilateral hippocampal amnesia with people whose episodic memory was intact. Whatever episodic memory the amnesiacs retained consisted in recalling trivial details of past events. They were unable to express the general meaning of these events and unable to imagine new experiences. This supports the hypothesis that remembering the past and imagining the future are interrelated mental capacities. Unlike the amnesiacs, Funes and Shereshevkii had a preternatural capacity for recall. Yet the fact that none of these individuals was able to capture the gist of the past suggests that what matters is not just how much one can recall, but how one recalls it. The ability to meaningfully recall the past and anticipate the future appears to depend as much on qualitative than on quantitative aspects of our episodic memory. Hassabis’s study suggests that increasing the quantity of memory might interfere with the qualitative capacity to make sense of past experience and simulate future experience. Among other things, this dual constructive capacity enables us to have an integrated and unified set of psychological properties necessary for our experience of ourselves as subjects that persist through time. While this requires a certain amount of memory storage and retrieval, it is more than a function of how many memories of specific details our brains can store, or how efficiently our brains can retrieve them for immediate cognitive tasks.

As Daniel Schacter and Donna Rose Addis point out in a recent essay in Nature, “Many researchers believe that remembering the gist of what happened is an economical way of storing the most important aspects of our experiences without cluttering memory with trivial details.” This is precisely what Funes, Shereshevkii, and Hassabis’s amnesiacs were unable to do. Schacter and Rose Addis also note that “information about the past is useful only to the extent that it allows us to anticipate what may happen in the future.” The extent to which we can learn new things depends on the meaning we can construct from our past. Memory is not just a reproduction of past events. The brain and mind do not function as a video recorder, or as a bank from which we withdraw particular memories of facts and events stored in specific sites. In addition to the hippocampus in the temporal lobe, regions in the frontal and parietal lobes play an important role in the dual capacity to give meaning to past experience and simulate future experience. The parietal lobe regulates our orientation to space and time. Together with the hippocampus, it provides a holistic representation of the environmental setting necessary for us to have and exercise the relevant dual capacity.

Even if drugs targeting CREB or similar factors could strengthen memory consolidation, increase memory storage, and expedite memory retrieval, it is unclear how these drugs could improve the spatial, temporal, and phenomenological framework in which past and future events are meaningful to and can be imagined by us. It is also unclear how they could influence the way the brain regions mediating memory respond to the external environment. If these drugs only affected quantitative and not also qualitative, constructive, aspects of memory, they could clutter the mind with trivial details and could impair at least some of our cognitive and other mental capacities.

The limits we have in our capacity to remember only so many fact and events may be necessary for an optimal balance between the storage and retrieval of memory. This balance in turn may be necessary for the neural framework that enables us to construct a holistic interpretation of our episodic memories and project ourselves into the future. One can question whether artificial manipulation of naturally designed memory systems that have served us so well stand much chance of improving and not impairing these systems. Although it is speculative, these agents might disrupt the balance between quantitative and qualitative aspects of different memory systems.

As memory researcher James McGaugh noted in testimony delivered to the President’s Council on Bioethics, we should be wary of inferring that if a certain amount of memory is good, then more memory is better. Our capacity to form and store more memories might leave us too focused on the past, which might alter our phenomenological experience of persisting from the past to the future. Our identities as persons and some of our cognitive capacities could be diminished by our ability to recall more facts and events that had no little or no meaning or purpose for us. Before we pharmacologically tinker with memory systems, we need to consider the different brain regions and the cognitive and imaginative mental capacities that mediate the content and meaning of memory. This is necessary to adequately assess the potential benefits and potential risks of memory-enhancing drugs. We should look to Funes, Shereshevkii, and the individuals with bilateral hippocampal amnesia as examples of the consequences we would want to avoid.

1. For some background see G. Lynch, “Memory Enhancement: The Search for Mechanism-Based Drugs,” Nature Neuroscience 5 (2002): 1035-1038, and T. Tully et al., “Targeting the CREB Pathway for Memory Enhancers,” Nature Reviews Drug Discovery 2 (2003): 267-277.

Published on: May 21, 2007
Published in: Bioethics, Emerging Biotechnology, Psychology

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