If you have taken modules (or know a thing or two) about neuroscience and memory, please do share with me what you know. Here is my take on the study, which essentially argues that we must be careful when extrapolating these findings to explain forgetting in human beings. And this is because the “forgetting” that is studied in rats is different from “forgetting” as we know in human beings.
According to this video, neurogenesis (i.e. the formation of new neurons) in the hippocampus is responsible for the phenomenon we know as forgetting. To test this hypothesis, researchers examined forgetting (dependent variable) against the rate of neurogenesis (independent variable). In other words, researchers aimed to understand the relationship between neurogenesis in the hippocampal formation and forgetting.
So here was how they studied the two variables. First, the researchers measured forgetting in terms of whether the rodents froze in response to a novel environment. As the mice were previously classically conditioned to freeze in response to that particular environment, the presence of freezing behaviour suggests that they retained the memory. On the other hand, the absence of freezing behaviour suggests that they had lost the memory.
Second, the researchers manipulated the rate of neurogenesis by using different types of rodents (they used other methods as well, which will not be discussed here). For simplicity, we shall name these two types of rodents R1 and R2, where the rate of neurogenesis is faster in R1 as compared to R2. If it were true that neurogenesis is largely responsible for forgetting, and that the rate of neurogenesis is significantly larger in R1 than in R2, then it must be true that R1 retains the learnt association for a shorter period of time (since they forget faster) than R2.
According to the results, this was precisely what the researchers had found. Within a fixed period of time t, the researchers demonstrated that R1 forgot the learnt association more rapidly as compared to R2. As such, the authors concluded that rapid brain development in infants is responsible for what we know as infantile amnesia, or the phenomenon that human individuals are generally unable to remember events that had occured behaviour the age of approximately 2 to 4 years old. Moreover, the researchers ended with the possibility that artificially increasing neurogenesis in human beings is sufficient to induce forgetting.
The problem with this interpretation, and extrapolation of findings from nonhuman animals to humans, is that the meaning of the term “forgetting” becomes extremely tricky. What this study shows is that neurogenesis is likely to diminish a fear response that would otherwise have been elicited if neurogenesis had not occured at all, or as rapidly. However, the absence of a fear response, or any emotional response for that matter, does not necessarily imply that the memory has been lost altogether. To paraphrase, it is possible for humans to no longer have an emotional response to a particular stimulus, but still “remember” the stimulus.
And we see this all the time around us – episodic memories (memories that are usually associated an experiential component) are constantly “converted” into semantic memories (memories that are not usually associated with an experiential component) over time. For example, immediately after your birthday celebration, your recollection of the event comprises both a factual component, as well as an experiential component where you can “feel” how you had felt during the event. Over time, the experiential component fades, and what remains is a set of propositions regarding the event (e.g. “I remember that …”). Similarly, events that frighten us continue to elicit fear within us for some time after its occurrence. However, we eventually stop experiencing such intense fear when recollecting the event, and can simply talk about the event in a way that the layman would describe as “objective” (N.B. this phenomenon may be different among abnormal populations). What these examples aim to argue is that the causal link between an absence of a fear response and forgetting put forth by the authors is weak, and that extrapolating their behavioural observations in mice to explain forgetting in human beings is a scientifically risky move to make.
So what do I propose has occurred (and, once again, if you have taken modules on neuroscience or memory, please to share with me what you know)? In memory research, there is this process known as consolidation. During consolidation, a physical neural connection is formed between two areas of the brain – one where the information was first processed (let us call this A1), and another where the information is going to be stored (let us call this A2). Consolidation is said to be complete when information can flow from A2 to A1 without the help of the hippocampus. During the process of consolidation, the hippocampus is necessary for remembering (i.e. information flows from A2 to hippocampus to A1). After consolidation, the hippocampus is no longer necessary for remembering (i.e. information flows from A2 to A1). As such, I would suggest that neurogenesis increases the rate of memory consolidation, but does not increase the rate of forgetting (as the authors have suggested). And a possible reason why the authors could have arrived at such a conclusion is because they viewed the rodents’ behaviour as indicative of the absence of both episodic and semantic memories. It is possible that fear responses are tied to the “episodic memory” equivalent in rats, and it is highly unlikely that we have any means of identifying the presence of semantic memories in rodents.
So what does my hypothesis imply (i.e. under what conditions is my claim falsified)? My hypothesis would imply that increasing the rate of neurogenesis in a human subject would result in a target memory being consolidated more rapidly. Assume that we have two willing human subjects H1 and H2. While the researchers artificially increase the rate of neurogenesis in H1, they do not artificially increase the rate of neurogenesis in H2. Subsequently, both participants are given a stimulus to learn. As the participants are repeatedly tested over time, there will arrive a point during which H1 can remember the target stimulus without hippocampal activation, while H2 cannot remember the target stimulus without hippocampal activation. If this result cannot be found, then my hypothesis is necessarily falsified. Alternatively, if there is no evidence that neurogenesis is associated with consolidation, then my hypothesis is also falsified.
In conclusion, I feel that when the authors claim that neurogenesis leads to forgetting, they neglect how the entire phenomenon of memory and forgetting is rich and complex so that it is difficult to ascertain if a memory is truly lost. As we have seen in the paragraph on consolidation, even if the brain no longer uses the hippocampus to retrieve a particular memory, it is still possible that the individual is still able to retrieve the memory, albeit through a different neural route. Moreover, the authors’ assumption that the absence of a fear response implies forgetting is necessarily invalid, for reasons that have been argued for above. Moving forward, more needs to be known (both on my part and on the part of the scientific community) about what neurogenesis does to our memories. At this point, I should add that I do not think the authors’ claim wrong in its entirety. In fact, it is possible that only some memories are consolidated while others are not. And to the extent that the fear response belongs to the latter category of memories (i.e. memories that are not consolidated), the authors could be right in their argument that neurogenesis results in the loss of memory.
Target article:
http://www.latimes.com/science/la-sci-sn-brain-growth-memories-disappear-20140508-premiumvideo.html
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