Cross-modal temporal recalibration guarantees stable temporal perception across ever-changing environments. Yet, the mechanisms of cross-modal temporal recalibration remain unknown. Here, we conducted an experiment to measure how participants’ temporal perception was affected by exposure to audiovisual stimuli with constant temporal delays that we varied across sessions. Consistent with previous findings, recalibration effects plateaued with increasing audiovisual asynchrony (nonlinearity) and varied by which modality led during the exposure phase (asymmetry). We compared six observer models that differed in how they update the audiovisual temporal bias during the exposure phase and in whether they assume a modality-specific or modality-independent precision of arrival latency. The causal-inference observer shifts the audiovisual temporal bias to compensate for perceived asynchrony, which is inferred by considering two causal scenarios: when the audiovisual stimuli have a common cause or separate causes. The asynchrony-contingent observer updates the bias to achieve simultaneity of auditory and visual measurements, modulating the update rate by the likelihood of the audiovisual stimuli originating from a simultaneous event. In the asynchrony-correction model, the observer first assesses whether the sensory measurement is asynchronous; if so, she adjusts the bias proportionally to the magnitude of the measured asynchrony. Each model was paired with either modality-specific or modality-independent precision of arrival latency. A Bayesian model comparison revealed that both the causal-inference process and modality-specific precision in arrival latency are required to capture the nonlinearity and asymmetry observed in audiovisual temporal recalibration. Our findings support the hypothesis that audiovisual temporal recalibration relies on the same causal-inference processes that govern cross-modal perception.

As the world population ages, new molecular targets in aging and Alzheimer’s disease (AD) are needed to combat the expected influx of new AD cases. Until now, the role of RNA structure in aging and neurodegeneration has largely remained unexplored. In this study, we examined human hippocampal postmortem tissue for the formation of RNA G-quadruplexes (rG4s) in aging and AD. We found that rG4 immunostaining strongly increased in the hippocampus with both age and with AD severity. We further found that neurons with the accumulation of phospho-tau immunostaining contained rG4s, rG4 structure can drive tau aggregation, and rG4 staining density depended on APOE genotype in the human tissue examined. Combined with previous studies showing the dependence of rG4 structure on stress and the extreme power of rG4s at oligomerizing proteins, we propose a model of neurodegeneration in which chronic rG4 formation is linked to proteostasis collapse. These morphological findings suggest that further investigation of RNA structure in neurodegeneration is a critical avenue for future treatments and diagnoses.