Adolescents at risk for depression show increased white matter microstructure with age across diffuse areas of the brain.

Maternal history of depression is a strong predictor of depression in offspring and linked to structural and functional alterations in the developing brain. However, very little work has examined differences in white matter in adolescents at familial risk for depression. In a sample aged 9-14 (n = 117), we used tract-based spatial statistics (TBSS) to examine differences in white matter microstructure between adolescents with (n = 42) and without (n = 75) maternal history of depression. Microstructure was indexed using fractional anisotropy (FA). Threshold-free cluster enhancement was applied and cluster maps were thresholded at whole-brain family-wise error < .05. There was no significant main effect of risk status on FA. However, there was a significant interaction between risk status and age, such that large and diffuse portions of the white matter skeleton showed relatively increased FA with age for youth with a maternal history of depression compared to those without. Most tracts identified by the interaction were robust to controlling for sex, youth internalizing, in-scanner motion, neighborhood SES, and intra-cranial volume, evidence that maternal depression is a unique predictor of white matter alterations in youth. Widespread increases in FA with age may correspond to a global pattern of accelerated brain maturation in youth at risk for depression.

Awake Hippocampal-Cortical Co-reactivation Is Associated with Forgetting.

Systems consolidation theories posit that consolidation occurs primarily through a coordinated communication between hippocampus and neocortex [Moscovitch, M., & Gilboa, A. Systems consolidation, transformation and reorganization: Multiple trace theory, trace transformation theory and their competitors. PsyArXiv, 2021; Kumaran, D., Hassabis, D., & McClelland, J. L. What learning systems do intelligent agents need? Complementary learning systems theory updated. Trends in Cognitive Sciences, 20, 512-534, 2016; McClelland, J. L., & O'Reilly, R. C. Why there are complementary learning systems in the hippocampus and neocortex: Insights from the successes and failures of connectionist models of learning and memory. Psychological Review, 102, 419-457, 1995]. Recent sleep studies in rodents have shown that hippocampus and visual cortex replay the same information at temporal proximity ("co-replay"; Lansink, C. S., Goltstein, P. M., Lankelma, J. V., McNaughton, B. L., & Pennartz, C. M. A. Hippocampus leads ventral striatum in replay of place-reward information. PLoS Biology, 7, e1000173, 2009; Peyrache, A., Khamassi, M., Benchenane, K., Wiener, S. I., & Battaglia, F. P. Replay of rule-learning related neural patterns in the prefrontal cortex during sleep. Nature Neuroscience, 12, 919-926, 2009; Wierzynski, C. M., Lubenov, E. V., Gu, M., & Siapas, A. G. State-dependent spike-timing relationships between hippocampal and prefrontal circuits during sleep. Neuron, 61, 587-596, 2009; Ji, D., & Wilson, M. A. Coordinated memory replay in the visual cortex and hippocampus during sleep. Nature Neuroscience, 10, 100-107, 2007). We developed a novel repetition time (TR)-based co-reactivation analysis method to study hippocampal-cortical co-replays in humans using fMRI. Thirty-six young adults completed an image (face or scene) and location paired associate encoding task in the scanner, which were preceded and followed by resting state scans. We identified post-encoding rest TRs (± 1) that showed neural reactivation of each image-location trials in both hippocampus (HPC) and category-selective cortex (fusiform face area [FFA]). This allowed us to characterize temporally proximal coordinated reactivations ("co-reactivations") between HPC and FFA. Moreover, we found that increased HPC-FFA co-reactivations were associated with incorrectly recognized trials after a 1-week delay (p = .004). Finally, we found that these HPC-FFA co-reactivations were also associated with trials that were initially correctly recognized immediately after encoding but were later forgotten in 1-day (p = .043) and 1-week delay period (p = .031). We discuss these results from a trace transformation perspective [Sekeres, M. J., Winocur, G., & Moscovitch, M. The hippocampus and related neocortical structures in memory transformation. Neuroscience Letters, 680, 39-53, 2018; Winocur, G., & Moscovitch, M. Memory transformation and systems consolidation. Journal of the International Neuropsychological Society, 17, 766-780, 2011] and speculate that HPC-FFA co-reactivations may be integrating related events, at the expense of disrupting event-specific details, hence leading to forgetting.

Little brain, little minds: The big role of the cerebellum in social development.

Seminal work in the 1990's found alterations in the cerebellum of individuals with social disorders including autism spectrum disorder and schizophrenia. In neurotypical populations, distinct portions of the posterior cerebellum are consistently activated in fMRI studies of social cognition and it has been hypothesized that the cerebellum plays an essential role in social cognition, particularly in theory of mind. Here we review the lesion literature and find that the effect of cerebellar damage on social cognition is strongly linked to the age of insult, with dramatic impairments observed after prenatal insult, strong deficits observed after childhood damage, and mild and inconsistent deficits observed following damage to the adult cerebellum. To explain the developmental gradient, we propose that early in life, the forward model dominates cerebellar computations. The forward model learns and uses errors to help build schemas of our interpersonal worlds. Subsequently, we argue that once these schemas have been built up, the inverse model, which is the foundation of automatic processing, becomes dominant. We provide suggestions for how to test this, and also outline directions for future research.

Building the perfect curse word: A psycholinguistic investigation of the form and meaning of taboo words.

Taboo words represent a potent subset of natural language. It has been hypothesized that "tabooness" reflects an emergent property of negative valence and high physiological arousal of word referents. Many taboo words (e.g., dick, shit) are indeed consistent with this claim. Nevertheless, American English is also rife with negatively valenced, highly arousing words the usage of which is not socially condemned (e.g., cancer, abortion, welfare). We evaluated prediction of tabooness of single words and novel taboo compound words from a combination of phonological, lexical, and semantic variables (e.g., semantic category, word length). For single words, physiological arousal and emotional valence strongly predicted tabooness with additional moderating contributions from form (phonology) and meaning (semantic category). In Experiment 2, raters judged plausibility for combinations of common nouns with taboo words to form novel taboo compounds (e.g., shitgibbon). A mixture of formal (e.g., ratio of stop consonants, length) and semantic variables (e.g., ± receptacle, ± profession) predicted the quality of novel taboo compounding. Together, these studies provide complementary evidence for interactions between word form and meaning and an algorithmic prediction of tabooness in American English. We discuss applications for models of taboo word representation.