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Neural Correlates of Semantic Interference and Phonological Facilitation in Picture Naming: A Systematic Review and Coordinate-Based Meta-analysis

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NEUROPSYCHOLOGY REVIEW 2025年第1期35卷 35-53页

作者： [Anonymous] PhD Program in Neuroscience School of Medicine and Surgery University of Milano-Bicocca Monza Italy Department of Psychology University of Milano-Bicocca Milan Italy Center for Mind/Brain Sciences (CIMeC) Neurocognitive Rehabilitation Center (CeRiN) University of Trento Rovereto Italy

Semantic interference (SI) and phonological facilitation (PF) effects occur when multiple representations are co-activated simultaneously in complex naming paradigms, manipulating the context in which word production is set. Although the behavioral consequences of these psycholinguistic effects are well-known, the involved brain structures are still controversial. This paper aims to provide a systematic review and a coordinate-based meta-analysis of the available functional neuroimaging studies investigating SI and PF in picture naming paradigms. The included studies were fMRI experiments on healthy subjects, employing paradigms in which co-activations of representations were obtained by manipulating the naming context using semantically or phonologically related items. We examined the principal methodological aspects of the included studies, emphasizing the existing commonalities and discrepancies across single investigations. We then performed an exploratory coordinate-based meta-analysis of the reported activation peaks of neural response related to SI and PF. Our results consolidated previous findings regarding the involvement of the left inferior frontal gyrus and the left middle temporal gyrus in SI and brought out the role of bilateral inferior parietal regions in PF.

关键词： Picture naming Semantic interference Phonological facilitation Meta-analysis fMRI

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Transspinal stimulation downregulates flexion reflex pathways during walking in healthy humans

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Journal of Neurophysiology 2025年第2期133卷 530-538页

作者： Knikou, Maria Sayed Ahmad, Abdullah M. Klab4Recovery SCI Research Program The City University of New York Staten Island NY United States Department of Physical Therapy College of Staten Island The City University of New York Staten Island NY United States PhD Program in Biology and Collaborative Neuroscience Program Graduate Center of The City University of New York College of Staten Island Staten Island NY United States

The phase-dependent modulation pattern of the tibialis anterior (TA) flexion reflex was characterized during treadmill walking while transspinal stimulation was delivered at 15, 30, and 50 Hz above and below paresthesia in healthy participants. The flexion reflex was elicited following medial arch foot stimulation with a 30 ms (300 Hz) pulse train. During treadmill walking, the flexion reflex was evoked in the right leg every 3–5 steps, and stimuli were randomly dispersed across the step cycle that was divided into 16 equal bins. For each participant, condition and bin of the step cycle, the flexion reflex was measured as the area of the linear EMG envelope starting 20 ms after the end of the pulse train up to 200 ms and was normalized to the maximum locomotor TA EMG activity. The unconditioned flexion reflex was modulated in a phase-dependent manner. Transspinal stimulation, regardless frequency, or intensity produced pronounced flexion reflex depression during walking that coincided with an unchanged slope and intercept, computed from the linear relationship between the flexion reflex and background EMG activity. These findings suggest that transspinal stimulation above and below paresthesia intensities at 15, 30, and 50 Hz downregulates the flexion reflex. Based on our recently reported absent effects on the soleus H-reflex under similar conditions and our current findings we propose that transspinal stimulation downregulates flexion and not extension reflex pathways. More research is needed to delineate whether similar neuromodulation effects are present in flexion and extension reflexes after spinal cord injury in humans. Copyright © 2025 the American Physiological Society.

关键词： flexion reflex phase-dependent modulation stimulation frequency - intensity transcutaneous spinal cord stimulation transspinal stimulation

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Why are threatening experiences remembered so well? Insights into memory strengthening from protocols of gradual aversive learning

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neuroscience and Biobehavioral Reviews 2025年 174卷 106145页

作者： Tezanos, Patricia Trejo, José Luis Instituto Cajal Consejo Superior de Investigaciones Científicas Madrid 28002 Spain PhD Program in Neuroscience Universidad Autónoma de Madrid-Instituto Cajal Madrid 28002 Spain

Aversive experiences often result in strong and persistent memory traces, which can sometimes lead to conditions such as Post-Traumatic Stress Disorder or phobias. Aversive stimulation tests are key tools in psychology and neuroscience for studying learning and memory. These tests typically use electric shocks as the unconditioned stimulus, allowing for precise control over the aversive content of the learning event. This feature has led to extensive research applying these tests with varying shock intensities to examine differences in learning, behavior, and memory formation between low- and high-aversive experiences. This line of research is particularly valuable for understanding the neurobiology underlying memory strengthening, but, to our knowledge, no review has yet compiled and organized the findings from this specific methodology. In this comprehensive review, we focus primarily on animal studies that have employed the same aversive test (i.e. Fear Conditioning, Passive Avoidance, Active Avoidance or Operant boxes) at different intensities. We will first outline and briefly describe the main aversive learning paradigms used in this field. Next, we will examine the relationship between aversiveness and memory strength. Finally, we will explore the neurobiological insights these studies have revealed over the years. Our aim is to gain a better understanding of how the nervous system gradually strengthens memory, while also addressing the remaining gaps and challenges in this area of research. © 2025 The Authors

关键词： Aversive intensity Electric shocks memory strengthening system redundancy temporal dynamics

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Beyond the heart: Mind-body connection from birth and the holistic intervention in cardiovascular care

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International Journal of Cardiology 2025年 432卷 133270-133270页

作者： Polese, Daniela PhD Program in Sensorineural Plasticity Department of Neuroscience Mental Health and Sensory Organs NESMOS Sapienza University of Rome Rome Italy UOD of Childhood Neuropsychiatry Sant'Andrea University Hospital Sapienza University of Rome Rome Italy

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Brain-derived neurotrophic factor in main neurodegenerative diseases

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Neural Regeneration Research 2023年第3期18卷 554-555页

作者： Serena Camuso Sonia Canterini Division of Neuroscience Department of PsychologyUniversity La SapienzaRomeItaly PhD Program in Behavioral Neuroscience Sapienza University of RomeRomeItaly

Discovered in pig brains in 1982,the brain-derived neurotrophic factor(BDNF)is one of the most studied and characterized neurotrophins in the central nervous *** recent years,BDNF has received considerable attention for its importance in the development and maintenance of normal brain *** is because BDNF plays an important role in crucial functions of the nervous system,such as the survival,differentiation,and maturation of neurons and glial cells as well as the actions of neuroprotection in adverse conditions,such as glutamatergic overstimulation,cerebral ischemia,hypoglycemia,and neurotoxicity(Kowiański et al.,2018).

关键词： stimulation diseases

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Genome-wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease

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Alzheimer's and Dementia 2025年第4期21卷 e70198页

作者： Hou, Xu Heckman, Michael G. Fiesel, Fabienne C. Koga, Shunsuke Soto-Beasley, Alexandra I. Watzlawik, Jens O. Zhao, Jing Valentino, Rebecca R. Johnson, Patrick W. White, Launia J. Quicksall, Zachary S. Reddy, Joseph S. Bras, Jose Guerreiro, Rita Zhao, Na Bu, Guojun Dickson, Dennis W. Ross, Owen A. Springer, Wolfdieter Department of Neuroscience Mayo Clinic Jacksonville FL United States Division of Clinical Trials and Biostatistics Mayo Clinic Jacksonville FL United States Neuroscience PhD Program Mayo Clinic Graduate School of Biomedical Sciences Jacksonville FL United States Department of Quantitative Health Sciences Mayo Clinic Jacksonville FL United States Department of Neurodegenerative Science Van Andel Institute Grand Rapids MI United States Division of Psychiatry and Behavioral Medicine Michigan State University College of Human Medicine Grand Rapids MI United States

INTRODUCTION: Phosphorylated ubiquitin (p-S65-Ub) is generated during PINK1-PRKN mitophagy as a specific marker of mitochondrial damage. Despite the widespread deposition of p-S65-Ub in aged and diseased human brain, the genetic contribution to its accumulation remains unclear. METHODS: To identify novel mitophagy regulators, we performed a genome-wide association study using p-S65-Ub level as a quantitative trait in 1012 autopsy-confirmed Lewy body disease (LBD) samples. RESULTS: We identified a significant genome-wide association with p-S65-Ub for rs429358 (apolipoprotein E ε4 [APOE4]) and a suggestive association for rs6480922 (ZMIZ1). APOE4 was associated with higher p-S65-Ub levels and greater neuropathological burden. Functional validation in mouse and human induced pluripotent stem cell (iPSC) models confirmed APOE4-mediated mitophagy alterations. Intriguingly, ZMIZ1 rs6480922 was associated with lower p-S65-Ub levels, reduced neuropathological load, and increased brain weight, indicating a potential protective role. DISCUSSION: Our findings underscore the importance of mitochondrial quality control in LBD pathogenesis and nominate regulators that may contribute to disease risk or resilience. Highlights: p-S65-Ub levels were used as a quantitative marker of mitochondrial damage. A GWAS identified two genetic variants that modify mitophagy in LBD autopsy brain. APOE4 was associated with increased p-S65-Ub accumulation and neuropathology. APOE4 altered mitophagy via pathology-dependent and pathology-independent mechanisms. ZMIZ1 was linked to reduced p-S65-Ub and neuropathology indicative of protection. © 2025 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.

关键词： autophagy GWAS mitochondria Parkin Parkinson's disease phosphorylated ubiquitin PINK1 PRKN ubiquitin ZMIZ1

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Neuroimmune signaling mediates astrocytic nucleocytoplasmic disruptions and stress granule formation associated with TDP-43 pathology

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Neurobiology of Disease 2025年 211卷 106939-106939页

作者： Zhou, Constance Hardin, Evelyn J. Zimmer, Till S. Jackvony, Stephanie Barnett, Daniel Khobrekar, Noopur Giacomelli, Elisa Studer, Lorenz Orr, Adam L. Orr, Anna G. Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program New York NY United States Helen and Robert Appel Alzheimer's Disease Research Institute New York NY United States Feil Family Brain and Mind Research Institute New York NY United States Neuroscience Graduate Program Weill Cornell Medicine New York NY United States The Center for Stem Cell Biology Sloan-Kettering Institute for Cancer Research New York NY United States Developmental Biology Program Sloan-Kettering Institute for Cancer Research New York NY United States

Alterations in transactivating response region DNA-binding protein 43 (TDP-43) are prevalent in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other neurological disorders. TDP-43 influences neuronal functions and might also affect glial cells. However, specific intracellular effects of TDP-43 alterations on glial cells and underlying mechanisms are not clear. We report that TDP-43 dysregulation in mouse and human cortical astrocytes causes nucleoporin mislocalization, nuclear envelope remodeling, and changes in nucleocytoplasmic protein transport. These effects are dependent on interleukin-1 (IL-1) receptor activity and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling and are associated with the formation of cytoplasmic stress granules. Stimulation of IL-1 receptors and NF-κB signaling are necessary and sufficient to induce astrocytic stress granules and rapid nucleocytoplasmic changes, which are broadly alleviated by inhibition of the integrated stress response. These findings establish that TDP-43 alterations and neuroimmune factors can induce nucleocytoplasmic changes through NF-κB signaling, revealing mechanistic convergence of proteinopathy and neuroimmune pathways onto glial nucleocytoplasmic disruptions that may occur in diverse neurological conditions. © 2025 The Author(s)

关键词： Astrocytes Integrated stress response Neurodegeneration Neuroimmune signaling Nuclear pore Stress granules TDP-43

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Multimodal identification of the mouse brain using simultaneous Ca²⁺ imaging and fMRI

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Communications Biology 2025年第1期8卷 1-14页

作者： Mandino, Francesca Horien, Corey Shen, Xilin Desrosiers-Grégoire, Gabriel Luo, Wendy Markicevic, Marija Constable, R. Todd Papademetris, Xenophon Chakravarty, Mallar M. Betzel, Richard F. Lake, Evelyn M. R. Department of Radiology and Biomedical Imaging Yale University School of Medicine New Haven CT United States Interdepartmental Neuroscience Program Yale University School of Medicine New Haven CT United States MD/PhD program Yale University School of Medicine New Haven CT United States Computational Brain Anatomy Laboratory Douglas Mental Health University Institute Montreal QC Canada Integrated Program in Neuroscience McGill University Montreal QC Canada Department of Biomedical Engineering Yale University School of Medicine New Haven CT United States Department of Neurosurgery Yale University School of Medicine New Haven CT United States Deparment of Biomedical Informatics and Data Science Yale University New Haven CT United States Department of Psychological and Brain Sciences Indiana University Bloomington IN United States Wu Tsai Institute Yale University New Haven CT United States

Individual differences in neuroimaging are of interest to clinical and cognitive neuroscientists based on their potential for guiding the personalized treatment of various heterogeneous neurological conditions and diseases. Despite many advantages, the prevailing modality in this field—blood-oxygen-level-dependent (BOLD) functional magnetic resonance imaging (fMRI)—suffers from low spatiotemporal resolution and specificity as well as a propensity for noise and spurious signal corruption. To better understand individual differences in BOLD-fMRI data, we can use animal models where fMRI, alongside complementary but more invasive contrasts, can be accessed. Here, we apply simultaneous wide-field fluorescence calcium imaging and BOLD-fMRI in mice to interrogate individual differences using a connectome-based identification framework adopted from the human fMRI literature. This approach yields high spatiotemporal resolution cell-type specific signals (here, from glia, excitatory, as well as inhibitory interneurons) from the whole cortex. We found mouse multimodal connectome-based identification to be successful and explored various features of these data. © The Author(s) 2025.

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Adjunctive pharmacotherapy for cognitive deficits in schizophrenia: meta-analytical investigation of efficacy (vol 203, pg 172, 2013)

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BRITISH JOURNAL OF PSYCHIATRY 2013年第5期203卷 392-392页

作者： Choi, K. H. Kee-Hong Choi PhD Department of Psychology Korea University Seoul South Korea Til Wykes PhD Institute of Psychiatry Kings College London UK Matthew M. Kurtz PhD Department of Psychology and Program in Neuroscience and Behavior Wesleyan University Middletown Connecticut USA

BackgroundA growing number of studies have investigated the efficacy of novel, adjunctive pharmacotherapies for treatment of cognitive deficits in schizophrenia with conflicting *** investigate the comparative efficacy of these agents on cognition and symptoms in schizophrenia, and to identify promising cognitive domains and candidate medications that can be incorporated in treatment trials combined with cognitive remediation to maximise treatment *** total of 26 double-blind, placebo-controlled studies investigating medications targeted at cholinergic, glutamatergic or serotonergic receptor classes and with participants with schizophrenia or schizoaffective disorder were *** targeted at the cholinergic receptor class produced marginal improvements in verbal learning and memory (d = 0.23, P = 0.06), and donepezil, a specific type of cholinergic agonist, produced a moderate effect (d = 0.58) on spatial learning and memory. Cholinergic and glutamatergic agents produced moderate effect-size improvements on negative symptoms (d = 0.54 and d = 0.62 respectively), and small effect-size improvements on general symptoms (d = 0.46 and d = 0.41 respectively). Serotonergic agents produced small effect-size improvements in positive symptoms (d = 0.33).ConclusionsCholinergic medications produced marginal improvement in verbal learning and memory and moderate improvements on spatial learning and memory, although there was no evidence to support the use of glutamatergic or serotonergic medications as a stand-alone treatment for improving cognitive function. Cholinergic and glutamatergic agents improved negative and general symptoms, whereas serotenergic medications improved positive symptoms.

关键词： Cognitive Decline Schizophrenia Drug Therapy

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Reward monitoring in the frontopolar cortex of macaques

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Scientific Reports 2025年第1期15卷 1-14页

作者： Ferrucci, Lorenzo Ceccarelli, Francesco Londei, Fabrizio Arena, Giulia Elyasizad, Leyla Nougaret, Simon Genovesio, Aldo Department of Physiology and Pharmacology Sapienza University of Rome Piazzale Aldo Moro 5 Rome 00185 Italy Institute of Biochemistry and Cell Biology (IBBC) National Research Council of Italy (CNR) Via Ramarini 32 Monterotondo Scalo Rome 00015 Italy Behavioral Neuroscience PhD Program Sapienza University Rome Italy Institut de Neurosciences de La Timone UMR 7289 Centre National de La Recherche Scientifique and Aix-Marseille Universite Marseille France Department of Pharmaceutical Sciences University of Piemonte Orientale Novara Italy

Reward processing involves several prefrontal cortex areas, enabling individuals to learn from behavioral outcomes and shape decisions. However, the role of the frontopolar cortex (FPC) in these processes remains unclear due to limited single-neuron research. In this study, we recorded neural activity from the FPC of two macaques performing a fast-learning task, the object-in-place reward task, which examined how reward size affects learning. Results showed that FPC feedback monitoring activity extends to the value of specific choices. Moreover, once the association between scenes and reward had been learned, FPC neural activity before choice reflected the future animal’s behavior to stay or to switch on their previous behavioral strategy, i.e., to choose the same target or the other one. These results suggest that FPC neurons integrated information for action monitoring and later reprocessed it to decide the best behavioral strategy to adopt, determining whether to maintain or change the action plan. © The Author(s) 2025.

关键词： Area 10 Explore-exploit Frontal pole Learning Monkey Reward

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