In-group neural alignment serves as a biomarker of social identity In this study, we propose a perspective on neural synchronization. Beyond reflecting shared understanding between individuals, we suggest it serves as a biological marker of social homogeneity. We examined fMRI neural responses of 42 participants (21 religious, 21 secular) watching neutral and religion-relevant video narratives. While explicit measures of emotional response, agreement, and engagement showed no significant differences in within-group variance, religious participants—representing a tighter social structure—exhibited significantly higher in-group neural synchrony across all content types and brain networks. Remarkably, synchrony values predicted religious orientation with an accuracy of up to 92%. We conclude that a community’s homogeneous social structure drives pervasive neural alignment, positioning neural synchrony as a potential signature of group cohesion beyond explicit behavioral measures.
The resource elasticity of control The ability to determine how much the environment can be controlled through our actions has long been viewed as fundamental to adaptive behavior. While traditional accounts treat controllability as a fixed property of the environment, we argue that real-world controllability often depends on the effort, time, and money we are able and willing to invest. In such cases, controllability can be said to be elastic to invested resources. Here, we propose that inferring this elasticity is essential for efficient resource allocation, and thus, elasticity misestimations result in maladaptive behavior. To test this hypothesis, we developed a novel treasure hunt game where participants encountered environments with varying degrees of controllability and elasticity. Across two pre-registered studies (N=514), we first demonstrate that people infer elasticity and adapt their resource allocation accordingly. We then present a computational model that explains how people make this inference and identify individual elasticity biases that lead to suboptimal resource allocation. Finally, we show that overestimation of elasticity is associated with elevated psychopathology involving an impaired sense of control. These findings establish the elasticity of control as a distinct cognitive construct guiding adaptive behavior and a computational marker for control-related maladaptive behavior.
Brain-Derived Neurotrophic Factor (BDNF), Estrogen Receptors, and Mossy Cells Dentate gyrus (DG) function depends on the neurotrophin brain-derived neurotrophic factor (BDNF) which shows robust synthesis in the principal cells, the granule cells (GCs). However, BDNF protein is present in the inner molecular layer (IML), where most afferents to GCs are from hilar mossy cells (MCs). Therefore, we asked whether MCs express BDNF mRNA and protein. Using adult mice, we found that MC BDNF mRNA and protein were expressed in the majority of MC somata and few other hilar neurons. Interestingly, IML BDNF was significantly greater in the ventral compared to dorsal DG. Additionally, dorsal IML BDNF was significantly higher in females on proestrous morning, when serum levels of estrogen peak, relative to metestrous morning, when estrogen is lower. Consistent with this observation, ventral MC somata, which project to the dorsal IML, showed more BDNF mRNA on proestrous morning than metestrous morning. Next, we asked if strong IML BDNF protein expression on proestrous morning was due to estrogen action at estrogen receptors (ERs) because estrogen binding to ERs can increase BDNF synthesis. We found that MCs have high expression of all ERs: ERα, ERβ and GPER1 in both sexes. When sexes were pooled, the percent of MCs labeled by ERβ and GPER1 exceeded the percent of MCs expressing ERα. When proestrous females were examined, GPER1-labeled MCs were greater than MCs labeled by ERα. The results demonstrate robust MC somatic expression of BDNF, relatively high ventral IML expression of BDNF, and estrous cycle dependence. The results also highlight robust MC ER expression, especially ERβ and GPER1, making the hilus a previously underestimated site of estrogen and BDNF action.
Estradiol-Dependent Memory and Hippocampal Spine Remodeling Require Proteasomal Protein Degradation Although 17β-estradiol (E2) is a critical neuromodulator of hippocampus-dependent memory and synaptic plasticity, the molecular mechanisms underlying these effects remain incompletely understood. Previous studies showed that E2 enhances dorsal hippocampus (DH)-dependent memory consolidation by activating signaling pathways that promote protein synthesis and dendritic spine formation. However, these studies largely overlooked the contribution of protein degradation mediated by the ubiquitin proteasome system (UPS), despite extensive evidence implicating UPS activity in long-term memory and synaptic plasticity. Here, we combined temporally specific dorsal hippocampal infusions of the proteasome inhibitor β-lactone with three-dimensional spine morphometry to examine the role of UPS-mediated protein degradation in E2-induced memory consolidation and CA1 spinogenesis. Immediate post-training bilateral infusion of β-lactone into the DH of ovariectomized female mice blocked E2-induced enhancement of object recognition memory and attenuated E2-associated improvements in spatial memory. Arbor-wide Golgi-based analyses revealed robust E2-induced increases in spine number across the apical dendritic tree and smaller parallel effects within the basal arbor. Segment-level analyses showed that E2 produced the greatest structural changes on tertiary apical dendritic segments, increasing total, mushroom, and thin spine density and enhancing multiple morphometric features, including mushroom spine surface area and head-to-neck ratio. Secondary basal dendritic segments exhibited smaller, more variable changes. Many E2-associated structural effects were attenuated or abolished by β-lactone. Together, these findings provide the first evidence that proteasomal protein degradation contributes to estrogenic enhancement of hippocampus-dependent memory and CA1 dendritic spine remodeling, identifying UPS-mediated protein degradation as a previously unrecognized mechanism regulating estrogenic memory consolidation and structural plasticity.
Pre-sleep acute stress modulates sleep-dependent emotional memory Acute stress prior to bedtime significantly alters the subsequent sleep. Although sleep is crucial for consolidating newly acquired memories, the impact of pre-sleep stress remains unclear. This experimental study examined how acute stress induction before bedtime influences overnight consolidation of emotional and neutral memories.
Intuitive knowledge of object acoustics enables perceptual separation of physical variables from impact sounds Upon hearing objects collide, humans can estimate physical attributes such as material and mass. Although the physics of sound generation is well established, the inverse problem that listeners solve—of inferring physical parameters from sound—remains poorly understood. Classical accounts posit the use of acoustic cues that correlate with physical variables but do not explain how humans might distinguish multiple concurrent physical causes. To study this problem, we measured impulse responses from hundreds of everyday objects, extracted their resonances, and used statistics of the resonances to build a probabilistic generative model of impact sounds. We then used the model to synthesize and manipulate stimuli for experiments measuring judgments of physical variables. Humans accurately judged object properties from collision sounds. However, when both of the colliding objects varied, performance was impaired if the distribution of object resonances deviated from those measured in real-world objects. The results suggest that humans have internalized the statistical regularities of real-world object acoustics, and use this knowledge to separate the acoustic contributions of the distinct objects in the world that give rise to sounds.
Single-neuron encoding of rapidly learned visual information reshapes human perception Humans can swiftly learn to recognize visual objects after minimal exposure. Integrating new information with existing knowledge requires forming enduring neuronal representations to enable future recognition. Yet, the neuronal mechanisms in the human brain underlying such rapid perceptual changes remain unclear. Here we recorded single-neuron activity in occipital cortex (OC) and medial temporal lobe (MTL) regions as participants rapidly learned to recognize degraded images. OC and MTL neurons modulated their activity to encode newly learned visual information and reshape perception. Population decoding revealed that OC neurons required additional processing time to resolve the identity of learned images, with delayed neuronal responses in the MTL. Our findings suggest that OC supports recognition after rapid learning via extensive recurrent processing, potentially involving higher-order neocortical areas, without relying on feedback from MTL. These results provide mechanistic constraints for biologically plausible models of visual recognition and few-shot visual learning.
A functional connectome identifies vulnerability to cognitive decline and Alzheimer’s disease progression Identifying the neurobiological basis of cognitive vulnerability is essential for preventing Alzheimer’s disease (AD). We derived the Alzheimer’s Resilience-Vulnerability Connectome (ARC) by contrasting SuperAgers (SA), an extreme phenotype of preserved late-life memory, with AD using resting-state fMRI. ARC distinguished SA from AD in a discovery cohort (N = 290; AUC = 0.85) and replicated independently (N = 143), involving prefrontal, temporal, and insular networks and associating with brain age. Applied to cognitively unimpaired adults (discovery: N = 818; replication: N = 497), ARC-based subtyping revealed SA-like and AD-like subgroups with comparable baseline cognition but divergent longitudinal trajectories. AD-like individuals exhibited faster cognitive decline, greater amyloid-β accumulation, and higher AD conversion risk. Exploratory GWAS nominated CLYBL and FRMD6 as candidate novel loci associated with the subtype difference. These findings suggest that ARC captures a continuous connectomic dimension of cognitive aging spanning SA, cognitively typical aging, and AD, highlighting the potential of functional connectomic variation for early risk stratification in AD.