When the Hexagons Fail: The Entorhinal–Hippocampal Origin of Autism's Social Disorder

When the Hexagons Fail: The Entorhinal–Hippocampal Origin of Autism’s Social Disorder This preprint proposes a unified neurocomputational hypothesis for autism’s social features. Rather than treating reduced joint attention, declarative pointing deficits, palm-reversed waving, and difficulties in self–other distinction as independent impairments, the paper argues that they may arise from a single upstream disturbance: distortion of the entorhinal–hippocampal grid-cell coordinate system. The proposed framework integrates evidence from studies of grid-cell coding, conceptual representation, social navigation, and temporoparietal junction (TPJ) function into a single mechanistic model. It further connects this hypothesis to a previously proposed cerebral energy-deficit framework, suggesting that metabolically demanding coordinate computations may be selectively vulnerable during neurodevelopment. This work is presented as a theoretical hypothesis and generates experimentally testable predictions regarding grid-like neural representations, TPJ function, and autism-related social cognition. Its aim is to stimulate further investigation and experimental testing of upstream mechanisms underlying autism’s social disorder.