Neuroscientists have discovered a fascinating connection between the retention of early life memories and brain developmental trajectories associated with autism. 

The maternal immune response, sparked into life in response to infection during pregnancy, is known to contribute to the cause of autism in both humans and mice. The Trinity neuroscientists report for the first time that this altered brain state also prevents the usual loss of memories formed during infancy. 

Using a mouse model the team behind this discovery showed that exposure to maternal immune activation, where inflammation is artificially induced during pregnancy in the absence of infection in order to alter offspring brain development, acts as a safeguard against developmental memory loss in early life by impacting the way specialist memory cells (engrams) in the brain function.

Furthermore, the study revealed that memories normally forgotten from infancy can be permanently reinstated if the correct memory engrams are activated in adults (in these experiments they used an “optogenetics” approach, which uses light to trigger specific neural pathways linked to the memory engrams of interest). These findings imply that infantile amnesia stems from a retrieval deficiency, as early childhood memories are still stored in the adult brain but cannot normally be accessed through natural recall.