Babies of every species from mouse to human rapidly forget things that happen to them—an effect called infantile amnesia. A type of brain immune cell called microglia might control this type of forgetting in young mice, according to a study published January 20th in the open-access journal PLOS Biology by Erika Stewart, from Trinity College Dublin in Ireland, and colleagues.
Infants and young children are growing rapidly and taking in vast amounts of information as they grow. However, there is a lack of episodic memory from this early period of development —memory of past events such as a first birthday party or first day of preschool. To better understand how this infantile amnesia functions, the authors of this study inhibited the activity of microglia—the main immune cells of the brain—in very young mice and examined how well they could remember a fearful experience. They also examined microglia markers in two memory-related brain areas—the dentate gyrus of the hippocampus and the amygdala.
The researchers found that when microglia activity was suppressed, with less activity in the hippocampus and amygdala, young mice had better memories of their fearful experiences. The scientists also used glowing tags to identify engram cells—neurons whose activity is specifically associated with memory formation. When microglia were inhibited in infant mice, the engram cells were more activated, suggesting enhanced memory recall.
In previous work, the scientists found that mice born to mothers with activated immune systems do not have infantile amnesia. When the scientists inhibited microglia activity in those offspring without infantile amnesia, they were able to restore it — possibly reestablishing their normal memory access. While other cell types might also be involved, the authors suggest that microglia are required for infantile amnesia in mice and could help shape the networks that form memories in the brain.
Erika Stewart states, "Microglia, the resident immune cells of the central nervous system, can be considered as the 'memory managers' in the brain. Our paper highlights their role in infantile amnesia specifically, and indicates that common mechanisms may exist between infantile amnesia and other forms of forgetting – both in everyday life and in disease."
Coauthor Tomás Ryan notes, "Infantile amnesia is possibly the most ubiquitous form of memory loss in the human population. Most of us remember nothing from our early years of life, despite having so many novel experiences during these formative years. This is an overlooked topic in memory research, precisely because we all accept it as a fact of life.
Ryan adds, "But what if those memories are still present in the brain? Increasingly, the memory field views forgetting as a 'feature' of the brain rather than a 'bug'. It seems that the brain is filing away the neuronal units that store memory, the engrams, for later use. Microglia seem to be functioning in the brain to help organise how engrams are stored and expressed across the lifetime. The biology of infantile amnesia may give us insight into how forgetting happens in the brain in general. Furthermore, being able to manipulate infantile amnesia opens doors into new ways of imagining how learning, and forgetting, might work during the early years of life."
Ryan notes, "It will be interesting and important to identify humans that don't experience infantile amnesia. To learn how their brains work, and understand their experience of early childhood education."
In your coverage, please use this URL to provide access to the freely available paper in PLOS Biology: https://plos.io/4iiJGHn
Citation: Stewart E, Zielke LG, de Boer AR, Boulaire GG, Power SD, Ryan TJ (2026) Microglial activity during postnatal development is required for infantile amnesia in mice. PLoS Biol 24(1): e3003538. https://doi.org/10.1371/journal.pbio.3003538
Author countries: Ireland, Germany, Australia, Canada
Funding: This work was funded by the Lister Institute of Preventive Medicine ( https://lister-institute.org.uk/ , Fellowship to T.J.R.), European Research Council ( https://erc.europa.eu/ ; 715968 to T.J.R.), Irish Research Council ( https://research.ie/ ; GOIPG/2020/1294 to E.S.), Research Ireland ( https://www.researchireland.ie/ ; 15/YI/3187 and 24/FFP-A/13397 to T.J.R.), the Jacobs Foundation ( https://jacobsfoundation.org/ ; 2019-1356-2 to T.J.R.), the Canadian Institute for Advanced Research ( https://cifar.ca/) ; CF-0303 to T.J.R.), and the US National Institute of Health ( https://www.nih.gov/ ; 1R01NS121316 to T.J.R.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
