bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.05.13.724907

Neural dynamics of updating social impressions during movie watching

Abstract

Updating impressions of others is essential to navigating social life. As we get to know an individual, we update our impressions of them in accordance with new information. How the brain dynamically revises impressions in real time under naturalistic conditions remains unclear. Here, we address this question using functional magnetic resonance imaging (fMRI) and natural language analysis in a naturalistic social cognition paradigm. Across 10 runs, participants viewed a character-driven TV episode, reported moments of insight, and described their impressions of the characters. Results reveal that impressions progressively evolved over time. Individuals with more similar existing impressions exhibit greater neural synchrony during movie-watching, which predicts convergence in post-movie impressions. Neural synchrony in the right superior temporal sulcus (STS) mediates the influence of initial similarity on later alignment. Insight moments accompany neural pattern shifts widespread across cortical regions, including the temporoparietal junction (TPJ), dorsomedial prefrontal cortex (dmPFC) and STS, and the magnitude of the shifts tracks the degree of impression updating. Specifically, distinct forms of insight selectively update complementary components of impressions: character insight updates person-centered representations, whereas non-character insight shapes social-event structure. Together, these findings show that people update their impressions of others through dynamic shifts in distributed brain activity patterns at moments of insight, providing a novel and ecologically grounded neural account of social cognition. Significance statementPeople do not simply form first impressions and keep them. As we learn new things about others, our judgments change--sometimes gradually, sometimes in a flash of insight. By tracking brain activity while people watched a TV show and described how their impressions of the characters evolved, we found that people who saw a character in more similar ways also show more similar brain responses when watching them onscreen, which in turn leads to convergence in subsequent impressions. Such updating is closely tied to "aha" moments, when a person is suddenly understood in a new way. These moments were marked by rapid shifts in the brain representational patterns, and larger shifts predicted greater changes in impressions. These findings offer a more naturalistic account of how the brain revises our understanding of other people in everyday life.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ke, J., Madhogarhia, R., Chun, M., Rosenberg, M. D., Leong, Y. C., Song, H.. 2026-05-18. Neural dynamics of updating social impressions during movie watching. https://doi.org/10.64898/2026.05.13.724907

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Neurodegeneration-inducing macromolecules exit the brain via nanovascular conduits formed by reticular fibroblasts

Accumulation of proteins such as amyloid beta (Abeta), hyperphosphorylated tau and alpha-synuclein within the brain alters neural information processing and causes neurodegeneration(1-3), but how toxic solutes are cleared from the brain remains highly controversial(4,5). Proposed exit routes include efflux across endothelial cells into the blood(6,7), and movement to the pial surface via vasomotion-induced pumping along spaces within arteriolar smooth muscle(8) or via outflow along the perivascular space of ascending venules promoted by water flux through astrocytes (the glymphatic system(9)). From the pial surface of the brain, drainage may continue to dural lymphatics, along the outer sheaths of exiting cranial nerves and across the cribriform plate(10-14). We now report the presence, in mice and humans, of 2 micron diameter conduits that remove fluorescently labelled tau and Abeta from the brain. These conduits form a spatially-organised mesh within the walls of penetrating arterioles and pial arteries, and around the surface of ascending venules and deep cerebral and pial veins. They course through the pial and arachnoid layers to span the CSF space, wrapping the brain and cranial nerves. They are formed of reticular fibroblasts, which label for VE-cadherin(15) and PDGFRalpha(16), the lymphatic markers(17) podoplanin, VEGFR3 and Prox1, and reticular fibroblast extracellular matrix components collagen I and VI(16,18-20). Parenchymal tau drains from the brain at a similar rate via arteriolar conduits and via conduits around venules, arguing against preferential removal by a glymphatic mechanism. In Alzheimer's disease model mice, Abeta is seen traversing these lymph node-like conduits. Modulation of molecular transfer via this route may accelerate or delay cognitive decline, and slowed transfer from arteriolar to pial-arachnoid conduits may initiate cerebral amyloid angiopathy.

neuroscience↗

Analysis of the influence of gradual changes in matrix sentence similarity on neural envelope tracking

Neural tracking of speech is a well-established phenomenon in neuroscience. However, for speech signals with a fixed structure, significant correlations between speech envelopes and neurophysiological representations occur even for unheard sentences. We exploit a structured speech-in-noise matrix hearing test (Oldenburger Sentence Test, OLSA) to systematically quantify the relationship between acoustic sentence similarity and neural tracking. Simultaneous magnetoencephalography (MEG) and 76-channel electroencephalography (EEG) data, including 16 channels positioned directly around the ears (ear-EEG), were recorded from 21 young adults with normal hearing during the presentation of clean-speech audiobooks and OLSA sentences at six signal-to-noise ratios. A linear decoder trained on audiobooks reconstructed OLSA sentence envelopes. Reconstruction accuracies were compared using a linear mixed model across heard (matched) and unheard (mismatched) sentences of varying acoustic similarity. Significant reconstruction accuracies were achieved across MEG, EEG, and ear-EEG for both matched and mismatched sentences. For mismatched sentences, these accuracies gradually increased with their acoustic similarity to the heard speech data. The high similarity between sentences, which is especially prominent in matrix tests, can cause significant spurious tracking for mismatched stimuli. This effect can reach levels comparable to those of matched sentences and can be mistaken for true neural tracking. Robust neural tracking across modalities further supported the established viability of ear-EEG compared to whole-head systems.

neuroscience↗

Seizures and tauopathy following neurotrauma are mediated by prion protein and metabotropic glutamate receptor 5

Traumatic brain injury (TBI) is one of the world's leading causes of death and disability and a major risk factor for dementias. The primary dementia associated with TBI is chronic traumatic encephalopathy (CTE), a neurodegenerative disease classified as a tauopathy, in which toxic tau molecules lead to disease pathologies and degeneration. The processes that lead to tauopathy and subsequent dementia after TBI remain unclear. Here, we built upon the finding that seizures after TBI may be a mechanism leading to tauopathy, by dissecting the functions of the metabotropic glutamate receptor 5 - cellular prion protein (mGluR5-PrPC) pathway. We delivered TBI to larval in a blast paradigm, and quantified aggregation of Tau via a genetically-encoded Tau-GFP fusion reporter. Zebrafish larvae lacking prp2 (homolog of mammalian cellular Prion Protein, PrPC) displayed a 168% increase in post-traumatic seizures activity after TBI. An mGluR5 agonist (CHPG) reduced post-traumatic seizures, whereas an mGluR5 antagonist (MPEP) increased post-traumatic seizures. Moreover, agonizing mGluR5 reduced tau aggregation and antagonizing mGluR5 increased tau burden. Larvae seizing from convulsants, rather than TBI, were treated with CHPG/MPEP and provided a similar pattern of outcomes, suggesting seizures may be a factor needed for mGluR5 activity to influence tau aggregation. The PrPC-mGluR5 pathway is proposed as one candidate pathomechanism linking TBI to subsequent seizures and tauopathy, and thus it warrants investigation as a target for prophylactic interventions.

neuroscience↗