The first attempts at crawling, the taste of solid food, and the first embrace in a mother's arms can all be forgotten. This normal forgetting of early years is part of childhood development, with the brain selectively retaining only a fraction of the vast information absorbed during that period.
In a new research, published in Science Advances, from Trinity College Dublin researchers turn to mice models and found that brains retain these early memories. The study on mice models of autism spectrum disorder unveils the role of a mother's immune system in regulating access to early memories, explaining the phenomenon of infantile amnesia.
Mother's Immune System Link to Infantile Amnesia: New Study Reveals Insights into Autism Spectrum Disorder in Mice Models
Infantile Amnesia: Why People Can't Remember Their Earliest Memories?
Infantile amnesia refers to the inability of adults to remember episodic experiences from the first few years of life, typically 0-3 years, and the limited recollection of events before age 10. This phenomenon persists until around ages seven to ten, often referred to as childhood amnesia.
The precise cause of infantile amnesia remains a debated topic in neuroscience, with nearly all adults experiencing it. Exceptions are rare and often involve individuals with exceptional memory retention, including parallels observed in other mammals like rats.
The second aspect of concern is the impact of childhood memories on adult psychology, even though they can't be consciously recalled. Studies link events such as abuse, trauma, and neglect during the infantile amnesia period to psychopathologies like PTSD, borderline personality disorder, depression, and anxiety.
Neglected children commonly exhibit learning and cognitive function issues, some of which may improve with proper care, while others persist into adulthood. Researchers are actively investigating the brain processes during the prevalent period of infantile amnesia to unravel these questions and understand their influence on continued development.
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Mother's Immune System Affects Memories
Although people typically can't recall memories before the age of 2 or 3, research suggests infants can form memories, particularly related to external events. The findings focusing on immunological models of autism spectrum disorder (ASD) in mice indicate a surprising role of the mother's immune system in influencing infantile amnesia, potentially shedding light on why some individuals with ASD exhibit exceptional recall abilities.
Trinity College Dublin neuroscientist Tomás Ryan notes that despite the widespread relevance of infantile amnesia, the biological conditions and effects on memory-encoding engram cells remain poorly understood in society's perception.
The mental autobiography usually begins between the second and third birthday, even though the brain is capable of forming memories before this age. Researchers, assuming the vaults holding early experiences are inaccessible, explore the mechanisms behind this amnesia.
Previous clues from rat studies suggested that specific pharmaceuticals and corticosteroids could prevent infantile amnesia, implying an active role of biochemistry in eroding long-term memory pathways. Trinity College Dublin's study shifted focus to the mother's immune system, known to influence neurological conditions.
Young mice born to mothers with an immune response mid-pregnancy showed social behavior deficits and prolonged memory of fearful events, suggesting the influence of maternal immune activation on pathways associated with infantile amnesia.
Further investigations revealed crucial differences in the structure of memory neurons in the male offspring's hippocampus, implicating a small immune protein, cytokine IL-17a, in the process.
Neuroscientist Sarah Power, the study's lead author, emphasizes that early developmental trajectories impact memory storage and retrieval, and further research aims to explore the detailed relationship between development and childhood memory, with potential educational and medical implications. The study was published in Science Advances.
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