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I'm drawing a blank Infantile amnesia occurs despite babies showing memory activity It looks like humans actively suppress our earliest memories. John Timmer Mar 21, 2025 3:41 pm | 10 Credit: Plume creative Credit: Plume creative Story textSizeSmallStandardLargeWidth *StandardWideLinksStandardOrange* Subscribers only Learn moreFor many of us, memories of our childhood have become a bit hazy, if not vanishing entirely. But nobody really remembers much before the age of 4, because nearly all humans experience what's termed "infantile amnesia," in which memories that might have formed before that age seemingly vanish as we move through adolescence. And it's not just us; the phenomenon appears to occur in a number of our fellow mammals.The simplest explanation for this would be that the systems that form long-term memories are simply immature and don't start working effectively until children hit the age of 4. But a recent animal experiment suggests that the situation in mice is more complex: the memories are there, they're just not normally accessible, although they can be re-activated. Now, a study that put human infants in an MRI tube suggests that memory activity starts by the age of 1, suggesting that the results in mice may apply to us.Less than total recallMice are one of the species that we know experience infantile amnesia. And, thanks to over a century of research on mice, we have some sophisticated genetic tools that allow us to explore what's actually involved in the apparent absence of the animals' earliest memories.A paper that came out last year describes a series of experiments that start by having very young mice learn to associate seeing a light come on with receiving a mild shock. If nothing else is done with those mice, that association will apparently be forgotten later in life due to infantile amnesia.But in this case, the researchers could do something. Neural activity normally results in the activation of a set of genes. In these mice, the researchers engineered it so one of the genes that gets activated encodes a protein that can modify DNA. When this protein is made, it results in permanent changes to a second gene that was inserted in the animal's DNA. Once activated through this process, the gene leads to the production of a light-activated ion channel.In practical terms, it means that if any neurons are activated in the area of the brain that stores memories of locations, they will make copies of a protein that allows ions to cross the cell membrane when exposed to light of the right wavelength. Since the flow of ions across the membrane is the primary component of a nerve impulse, this allows light exposure to trigger nerve impulses. (This sort of experimental manipulation is generically termed "optogenetics.")In these experiments, the young mice would start making the ion channel specifically in those cells that were activated as it learned its way around the maze. If exposed to the right light weeks or months later, those cells would start sending nerve impulses again, just as they would if they were re-activating the memory. In short, if the mice were forming memories as infants, the researchers should be able to replay those memories later in life simply by exposing the right cells to light.It worked. If you activated this memory in the mice after they matured, they once again behaved as if the light coming on is associated with a shock. The memory was still there, it just wasn't normally accessible to the mice.Dont shock the babyObviously, genetically manipulating human infants and giving them shocks wouldn't fly with an ethics review board. So, the new work relied on a standard test used for memory in infants: if an image is familiar to them, they tend to look at it longer. So, the researchers put the babies in an MRI tube with video screens and monitored activity in the hippocampus, the area of the brain that handles these sorts of memories. The babies were shown a series of pictures, some of which repeated after a long enough lag to ensure that the infant couldn't track them via short-term working memory.If you did the analysis purely on whether the babies stared at images that were familiar, you'd come up empty, with any effect buried in the statistical noise. But there was a significant correlation between staring longer and activity in the hippocampus, suggesting that the kids were more likely to stare at something that had triggered the memory formation process during their first viewing.There was a lot of noise in the data, but when broken down by age, it appeared that older infants were much more likely to form memories, with the ability starting roughly when they hit 1 year old. So, there does appear to be a period where the hippocampus hasn't matured enough to form long-term memories. It's just that this period ends a couple of years before infantile amnesia stops.It also suggests that humans may share this feature with mice: memories formed during this window between the onset of memory formation and the end of infantile amnesia are probably still there. We just don't have a way to access them unless something external to the brain manages to trigger them.The larger questions, however, remain unanswered. We don't know what mechanism suppresses these memories while letting those formed later operate normally, although having a well-described system in mice should help us start to address that. But the "why" will likely remain very difficult to answer. It's not obvious whether this selective amnesia is simply a necessary consequence of mammalian brain development, or if it actually provides us with some benefits.Science, 2025. DOI: 10.1126/science.adt7570 (About DOIs).John TimmerSenior Science EditorJohn TimmerSenior Science Editor John is Ars Technica's science editor. He has a Bachelor of Arts in Biochemistry from Columbia University, and a Ph.D. in Molecular and Cell Biology from the University of California, Berkeley. When physically separated from his keyboard, he tends to seek out a bicycle, or a scenic location for communing with his hiking boots. 10 Comments
