Where did our childhood memories go?
We can barely recall the very first years of our life. Have these memories disappeared, or do they remain hidden somewhere in the brain?
The paradox of early amnesia
In his Dictionary of received ideas, French novelist Gustave Flaubert wrote, at the entry “Memory”: “Memory. To complain about one’s own, and even to boast of not having any”. That said, concerning early childhood, everyone is in the same boat: we barely remember it.
We would hardly say that we can accurately recall an episode lived before the age of 2. We would assume that it is a product of imagination rather than of memory. An imagination derived, for example, from anecdotes reported by our older relatives.
This early amnesia phenomenon has been known for a long time, and was already described by Freud: it’s referred to as infantile amnesia.
Besides infantile amnesia, memory research has shown that very few memories are recalled for events experienced between the ages of 2 and 6. More specifically, memories of events experienced during this period are subject to accelerated forgetting. They are also much less detailed and vivid than memories of events experienced afterwards. This is referred to as childhood amnesia.
Still, events experienced at an early age, such as traumatic events, can have a considerable influence on later emotional and intellectual development. How can early experiences influence our life if we don’t remember them? How to explain this paradox of early amnesia?
The hippocampus: a brain region key to memory
It would be wrong to say that we forget absolutely everything we experienced before the age of two. At the age of two, we know, for example, the names and faces of our family members, or the meaning of many words. All this is not forgotten. But we are talking here about another type of memory: that of facts and concepts, i.e. semantic memory.
The memory of infantile amnesia and childhood amnesia, on the other hand, is the memory of personal experiences, of specific events that we remember having lived in a given spatial and temporal context: for example, a friend’s birthday, something that happened in a particular place at a particular time. It is the memory of events that we can relive and review in our heads, i.e. episodic memory.
Episodic memory is mainly dependent on a brain region called the hippocampus. The hippocampus is the region targeted by Alzheimer’s disease. Following a stroke, severe impairment of the hippocampus leads to the inability to form new episodic memories (while one can continue to learn new semantic information).
Logically, given the crucial role of the hippocampus in memory, the forgetting of early childhood memories must be related, in one way or another, to the hippocampus.
The slow maturation of the hippocampus during childhood
The brain takes a long time to develop. This is sometimes referred to as ‘cerebral adolescence’, which is thought to last until the age of 25. By brain development or maturation, we mean that we observe cerebral changes (for example, the multiplication of connections between neurons) that explain a progressive increase in intellectual capacity as we grow up; after this point, we just grow old.
Cerebral maturation is asynchronous: not all brain regions develop at the same time, nor the same rate. Until relatively recently, the hippocampus was thought to reach this state of maturation relatively quickly. The hippocampus sees its volume double during the first two years of life, during infantile amnesia, before stagnating thereafter. Everything thus suggested that the hippocampus was mature from the age of two years. This explained the absence of memories of infantile amnesia, but not the rarity of memories of the period of childhood amnesia.
However, thanks to the recent development of neuroimaging methods, it was observed that maturation processes continued within the hippocampus during the period of childhood amnesia. The hippocampus is made up of several different subregions, all of which perform a specific function. These sub-regions are organized in circuits that serve to create and recall memories. Around the age of about 6 years, the most complex of these circuits reaches maturation: this corresponds to the end of childhood amnesia.
Therefore, there is a direct relationship between the major periods of hippocampal maturation, and the major periods of episodic memory development.
The three theories of early amnesia
Observing a relationship between hippocampal maturation and the development of memory skills shows the involvement of the hippocampus, but does not provide a direct explanation for the forgetting of early memories. What are the mechanisms underlying this phenomenon?
Three main theories have been proposed so far. The first may be called the developmental theory. According to it, during infantile amnesia, the hippocampus is too ‘immature’ (its internal circuits are not in place; it is not effectively connected to other brain regions; etc.) to allow for efficient formation of memories. Infantile amnesia is therefore simply explained: we do not have episodic memories before the age of two because we do not create them until that age.
A second theory is that of neurogenesis. Unlike most organs, the brain does not produce new cells (i.e., new neurons) during life. We are born with all the neurons we will use during our lives. The hippocampus is an exception. It is one of the only regions where there is a continuous creation of new neurons after birth. The creation of new neurons (neurogenesis) is particularly important in the hippocampus during early childhood. For the theory of neurogenesis, the hippocampus actively participates to memory formation from an early age. However, the massive creation of new neurons at this period ends up disrupting and replacing already existing neurons. Access to memories previously stored by these neurons may therefore be lost. These early memories may remain in the brain, but in a way that would make them inaccessible. It is a bit like being unable to open a software program after updating your OS (thanks Apple).
A third theory is that of critical periods, which can be seen as a form of synthesis of the first two. For this theory, early childhood constitutes for the hippocampus a critical period. A critical period is a developmental window during which the brain is particularly plastic, i.e. sensitive to the environment’s influence, allowing very rapid learning. For example, we know that early childhood is a critical period for language acquisition, because young children can quickly learn any language if they are exposed to it. According to this theory, the hippocampus learns progressively to create memories during early childhood, under the environment’s influence. Therefore, this theory agrees with the developmental theory that the hippocampus is too immature in early childhood to create long-lasting memories, as the hippocampus is still learning to memorize. However, it agrees with the neurogenesis theory that the hippocampus nevertheless actively participates in creating new memories. Even if they are forgotten, these early memories can remain in the brain in a latent form. They can even be reactivated following exposure to appropriate cues.
Infantile amnesia, and then childhood amnesia, can therefore be explained by a progressive learning process of the hippocampus, reconfiguring its internal and external connections under the influence of the environment, in order to learn how to memorize efficiently.
(Generally speaking, when two convincing theories oppose each other, the truth is often somewhere in the middle).
This theory thus provides an explanation for the paradox of early amnesia. If certain early events can have a considerable influence on later development in the absence of that event’s memory, it is because: 1) emotional memory, dependent on the amygdala (another brain region), matures before episodic memory. Therefore, early traumatic events can have a lasting influence on later development via an emotional memory trace that is not accompanied by an episodic memory trace. 2) An episodic memory trace can nevertheless remain latent in the brain and influence later development. 3) A critical period is a developmental window in which a brain region has particularly high plasticity under the influence of the environment. Hence, an early traumatic event can exert a long-term impact, by modifying the “normal” developmental trajectory of the brain given this plasticity. The earlier the event occurs, the greater the potentially deleterious effects, because the affected developmental range (the development that remains to occur) is greater.
If early memories remain in the brain, even in a latent or degraded form, would it be possible to retrieve some of them? Recent techniques, still in the experimental stage, make it possible to bring forgotten memories to the surface by reactivating the neurons that store them. On paper, it is therefore not impossible.
Note
The boundaries of infantile amnesia (0–2 years old) and childhood amnesia (2–6 years old) are not clearly delineated or set in stone; these are approximations. Some authors define infantile amnesia as a period covering the first 3 or 4 years of life; others extend childhood amnesia to the age of 7 or 8. Here, we used these age limits mainly because they arguably directly relate to marked transitions in hippocampal maturation. See references below for further reading, especially Newcombe, Lloyd & Ratliff 2007, Mullaly & Maguire 2014 , and Gomez & Edgin 2016.
References
Alberini, C. M., & Travaglia, A. (2017). Infantile amnesia: a critical period of learning to learn and remember. Journal of Neuroscience, 37(24), 5783–5795.
Bouyeure, A., & Noulhiane, M. (2020). Memory: Normative development of memory systems. In Handbook of Clinical Neurology (Vol. 173, pp. 201–213). Elsevier.
Gómez, R. L., & Edgin, J. O. (2016). The extended trajectory of hippocampal development: Implications for early memory development and disorder. Developmental cognitive neuroscience, 18, 57–69.
Josselyn, S. A., & Frankland, P. W. (2012). Infantile amnesia: a neurogenic hypothesis. Learning & Memory, 19(9), 423–433.
Li, S., Callaghan, B. L., & Richardson, R. (2014). Infantile amnesia: forgotten but not gone. Learning & Memory, 21(3), 135–139.
Mullally, S. L., & Maguire, E. A. (2014). Learning to remember: The early ontogeny of episodic memory. Developmental cognitive neuroscience, 9, 12–29.
Newcombe, N. S., Lloyd, M. E., & Ratliff, K. R. (2007). Development of episodic and autobiographical memory: A cognitive neuroscience perspective. In R. V. Kail (Ed.), Advances in child development and behavior: Vol. 35. Advances in child development and behavior (p. 37–85). Elsevier Academic Press.
Stiles, J., & Jernigan, T. L. (2010). The basics of brain development. Neuropsychology review, 20(4), 327–348.
Travaglia A, Bisaz R, Sweet ES, Blitzer RD, Alberini CM. Infantile amnesia reflects a developmental critical period for hippocampal learning. Nat Neurosci. 2016 Sep;19(9):1225–33.
Tulving, E., & Markowitsch, H. J. (1998). Episodic and declarative memory: role of the hippocampus. Hippocampus, 8(3), 198–204.
