Proceedings of the Annual Meeting of the Cognitive Science Society

Early-life stress is a major risk factor for cognitive deficits, yet the circuit-level mechanisms remain unclear. We hypothesize that systemic stress hormones and localized neurotrophic deprivation during critical periods alter synaptic connectivity. To investigate, we developed a large-scale computational model (N = 100 paired seeds) simulating two developmental stages: an activity-independent growth phase where axons navigate a BDNF chemoattractant landscape, and a functional phase probed with a recurrent attractor model. The "trauma" condition modeled a "Double Hit": a transient cortisol pulse increasing stochastic axon diffusion, combined with localized BDNF deprivation that weakened synaptic efficacy. Trauma produced a significant rise in axon tortuosity (p < 0.001), yielding structurally inefficient networks with collapsed spectral radius. Functionally, recurrent gain loss impaired retention of clustered memory engrams (–ï41% deficit), while random patterns remained robust. Parameter sweeps confirmed this pathology arises non-linearly from guidance noise and trophic weakness, linking developmental stress to memory impairments.