The Triple Helix @ UChicago

Winter 2017

"Modifying Memory: A Construction of a New Mental Life" by Clara Sava-Segal


We currently live in an “age of ‘technology of consciousness,”[1] in which medical improvements and modern technology are being used to develop psychotropic substances, or chemical agents that are capable of altering brain function. While a lot of these drugs are still at their preliminary levels, memory augmentation drugs are being researched at rapid rates, which is introducing imperative potential medical benefits, as well as various ethical discussions.

How it Works

At a basic level, neurons interact with one another to spread signals throughout the nervous system. When it comes to learning and memory, information--the signal--is often carried by neurotransmitters. It is useful to think of neurons as a web along which signals are transmitted. The space between neurons that the neurotransmitters transverse is termed a “synapse.” Furthermore, the ability of signaling to occur relies on action potentials (electrical potential changes) to relay the information by permitting neurotransmitters to be released. Acetylcholine and glutamate are two kinds of neurotransmitters that will be noted here.

As neural signals spread from place to place along the neuron web, they activate or create response when they arrive at a neuron with the right receptors and decrease as they go on to the next neuron. Increasing and decreasing the level of neurotransmitter that carries the signal doesn’t only depend on the aforementioned action potentials, but also on intracellular mechanisms. For instance, to decrease neurotransmitter levels, specific enzymes often break them down. These changes in neurotransmitter levels are what modify the strength of signaling and therefore, their mechanisms are often the target of drugs.

But how does memory work?

Mechanistically, neuroscientists are looking at the actual procurement of memory via long-term potentiation (LTP) or the underlying mechanism by which memories are not only formed within the brain, but also stored for long-term retrieval and usage [2], [3]. Simply, LTP is the reason that information that we learn is consolidated or becomes a “memory.” Memory consolidation is the stabilization or maintenance of a memory trace after its initial presentation.

LTP is linked to an amplified efficiency within synapses due to an increased stimulation of the same neural pathway. So when the same information is being processed intensely or over multiple instances, this augmented pathway in the brain is said to be “strengthened.” Hebb’s famous phrase- “Neurons that fire together, wire together” comes to mind. Neurons that are firing together in the creation of a memory will have increased signal strength for weeks to come. The created memory will progress into long-term memory storage. For instance, if you are constantly being asked to remember the name of something, you will be activating the same pathway each time and this consistent exercise will strength it. As such, due to this LTP, your memory will be more solidified and stronger: you will likely be able to remember it long-term. 

LTP depends on two mechanisms- (1) induction- the initial setting of the signal and (2) maintenance (of the signal) [4]. These two mechanisms are dependent on the aforementioned molecules and are examined in drug research and creation.

Research on LTP

Psychotropic agents are being developed to strengthen synapses artificially. As discussed, having “stronger” neural patterning relates to a prolonged and stronger consolidation of memory. Therefore, to treat neurodegenerative diseases, such as Alzheimer’s, Dementia and Parkinson’s, that are characterized by progressive memory loss, LTP can be improved. However, to counter memory formation or the development of PTSD, neural signaling can be hindered. To strengthen consolidation, “induction” is modified, while “maintenance” is the focus for research looking at decreasing LTP.

Degenerative Diseases- Targeting Memory “Induction”

Long-term memory enhancement drugs are not only trying to enhance memory, but also trying to maximize plasticity. Plasticity generally means that the region will be more adaptable and, in this particular case, suggests that memories will be encoded more easily. Therefore, these drugs look at enhancing LTP and are therefore crucial for postponing neurodegenerative diseases. It should be noted that cells with receptors for acetylcholine (a neurotransmitter), which are called cholinergic cells, are the first to die in Alzheimer patients [5]. Therefore, mechanisms that deal with acetylcholine are involved in memory formation and cholinergic cells are generally the subjects of research for memory stimulants.

As noted, cells need a method to increase and decrease the presence of a neurotransmitter in order to spread the signal. Therefore, drugs moderate these mechanisms. For instance, Racetams, such as Piracetam, work by modifying membrane fluidity to increase neurotransmitter release and receptor binding. In addition, Piracetam activates acetylcholine, which takes up oxygen, improves blood flow and increases neurogenesis, as well as synaptogenesis [6]. This growth of neurons and synapses encourages LTP and memory consolidation. Another example are anticholinesterase drugs, which inhibit acetylcholinesterase--the enzyme that breaks down acetylcholine. By preventing the breakdown of acetylcholine and thereby increasing its action, these drugs have been shown to have a mild effect on preventing the decline of memory degradation in Alzheimer’s patients [5].

PTSD- Targeting Memory “Maintenance”

On the other hand, trying to diminish memory consolidation targets the “maintenance” aspect of LTP. Protein Kinase Mzeta (PKMzeta) has been found to be necessary in maintaining memory consolidated. Research on mice has found that inhibiting PKMzeta reverses LTP. Interestingly, even after the inhibitor has been removed, the given memory remains erased. However, new memories are able to form [4]. This study targeted traumatic memories in mice, specifically. Thus, such research is imperative to targeting debilitating memories in PTSD patients, but allowing them to continue with their everyday memory function.

Cures or Supplements: Ethical Implications

Memory-modification drugs can have critical medical application. It should be noted, however, that the main target group for the companies that are creating and developing memory enhancement drugs are 40-60 year olds that are beginning to experience aging and want to counter their cognitive impairment [1]. Therefore, we must wonder if this is the ethically correct use for such drugs. What is the distinction between medical and lifestyle supplement usage?

Looking at the widespread usage of Attention Deficit Hyperactivity Disorder (ADHD) medications with prescriptions [1], it is no stretch of the imagination to assume that memory-altering drugs can become a method of self-medication and self-improvement for both aging adults and stressed out college students. The market will likely continue to expand as these drugs gain cosmetic value.

But, isn’t memory decline in everyday life natural? The present memory system, with its lapses, is constructive in nature and structurally holds a lot of evolutionary benefit [8]. There exists a natural balance and need between memory loss and gain. Human brains process so many experiences in an hour alone that increasing the consolidation of each of these memories and their remembrance would not only use too much energy, but would require much larger brains, and could even be painful. Drugs have the potential for serious long-term adverse effects, as they might increase the capacity of working memory at the expense of higher-order, long-term ability [1].

As such, while the growing research has incredible medical implications, in the case of non-life threatening memory loss, a conversation needs to be had at a global level to discuss both the beneficial and adverse effects of memory-modification.


[1] Fuchs, Thomas. “Ethical Issues in Neuroscience.” Current Opinion in Psychiatry 19, no. 6 (November 2006): 600–607. doi:10.1097/01.yco.0000245752.75879.26.

[2] Malenka, RC and RA Nicoll. “Long-Term Potentiation--a Decade of Progress?” Science (New York, N.Y.). 285, no. 5435 (September 18, 1999): 1870–74. Accessed February 13, 2017.

[3] Shors, TJ and LD Matzel. “Long-Term Potentiation: What’s Learning Got to Do with It?” The Behavioral and brain sciences. 20, no. 4 (March 31, 1999): 597–614. Accessed February 13, 2017.

[4] Sacktor, TC. “PKMzeta, LTP Maintenance, and the Dynamic Molecular Biology of Memory Storage.” Progress in brain research. 169 (April 9, 2008): 27–40. Accessed February 13, 2017.

[5] Dekkers, Wim and Marcel Olde Rikkert. Memory Enhancing Drugs and Alzheimer’s Disease: Enhancing the Self or Preventing the Loss of It? 10, no. 2 (May 8, 2007). Accessed February 13, 2017.

[6] “Piracetam - Usage, Side Effects and Dosage Guide.” 2014. Accessed February 13, 2017.

[7] “Enhancing Cognitive Function with Pregnenolone.” 2017. Accessed February 13, 2017.

[8] Schacter, Daniel L. “The Seven Sins of Memory: Insights from Psychology and Cognitive Neuroscience.” American Psychologist 54, no. 3 (1999): 182–203. doi:10.1037//0003-066x.54.3.182.

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