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Development and Developmental Disorders
Published in Andrei I. Holodny, Functional Neuroimaging, 2019
The most dynamic period of brain development occurs while in utero, but continues at a fast rate for the first two years after birth. At two years of age, a child’s brain mass is approximately 80% of the expected adult weight (14). Synapse formation follows a similar curve, with an overabundance of synaptic connections in the young child relative to the older child and adult. The process of synaptogenesis occurs in a region-specific fashion in humans. For example, in the auditory cortex, synaptic density peaks at three months of age, whereas in the middle frontal cortex, this occurs at 15 months of age (14).
Phthalates
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Even though detrimental effects of phthalates on the reproductive system have been extensively researched, there is increasing concern regarding the relatively poorly understood neurotoxic potential of phthalates. Exposure to toxicants during critical periods of development might lead to changes in brain structure, cell morphology, and connectivity.74 Acute exposure to DEHP during a critical period of hippocampal development negatively affects proper development in this brain region, including disrupted connectivity and decreased cell density.75 Additionally, DEHP exposure resulted in decreased synapse formation, suggesting decreased axonal innervation in the hippocampus. Again, this finding was only reported in male rats, with no differences noticed between the females exposed to DEHP and controls.
Bioscience indications for chronic disease management and neuromedical interventions following traumatic brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Mark J. Ashley, Grace S. Griesbach, David L. Ripley, Matthew J. Ashley
Microglia’s monitoring capabilities allow it to have an influence on experience-dependent plasticity through mechanisms such as synaptic stripping.152 This mechanism may occur during experience-dependent learning given that synapse formation and elimination is an integral component of learning processes.153 Although microglia-dependent synaptic pruning is most notable during brain development,154,155 it is also observed in the adult brain. For example, live imaging of visual cortex has shown microglial stripping of inactive synapses.156 Synaptic stripping may diminish energetic demands from weakened neurons that are metabolically compromised.
One size does not fit all: navigating the multi-dimensional space to optimize T-cell engaging protein therapeutics
Published in mAbs, 2021
Wei Chen, Fan Yang, Carole Wang, Jatin Narula, Edward Pascua, Irene Ni, Sheng Ding, Xiaodi Deng, Matthew Ling-Hon Chu, Amber Pham, Xiaoyue Jiang, Kevin C. Lindquist, Patrick J. Doonan, Tom Van Blarcom, Yik Andy Yeung, Javier Chaparro-Riggers
Previously, through building on our charge-steering Fc heterodimerization technology,14 we engineered a bispecific IgG2 platform for T-cell engagement and demonstrated its superior pharmacological activity and minimal nonspecific activation. In this study, we sought to take a deeper dive into how epitope, binding affinity, receptor density, and kinetics drive the activity of T-cell-engaging biologics. In light of the finding that geometric configurations may play critical roles in forming immunological synapses,9 we created a new bispecific diabody-Fc (DbFc) format, which adopts a much more compact configuration between the two paratopes. More specifically, the distance between the two antigen-recognition arms was estimated to be 3–6 nm15,16 and 9–15 nm17–19 (Figure 1) for our bispecific DbFc and previously described IgG-based molecules, respectively. This difference in distance between binding sites makes them ideal tools to study the effectiveness of synapse formation as a function of distance. By using B-cell maturation antigen (BCMA) as the TAA in our model system, we first generated a series of artificial antigen-expressing cell lines whereby BCMA, a relatively small glycoprotein, is tethered to the cell surface via increasing numbers of protein domains to gradually extend its distance from the membrane, or in another scenario, is anchored to the juxtamembrane region and masked by growing numbers of structural spacer units.
C. elegans MAGU-2/Mpp5 homolog regulates epidermal phagocytosis and synapse density
Published in Journal of Neurogenetics, 2020
Salvatore J. Cherra, Alexandr Goncharov, Daniela Boassa, Mark Ellisman, Yishi Jin
The regulation of synaptic connections plays an essential role in promoting circuit function and robust signaling. Cell-cell signaling is a common mechanism to modulate synapse formation and maintenance. In mammals, Drosophila, and C. elegans non-neuronal cells play essential roles in controlling synapse number through multiple mechanisms (Allen, 2013; Cherra & Jin, 2015; Corty & Freeman, 2013). Phagocytosis-mediated synapse pruning requires cell-cell interactions that enable glia or other non-neuronal cells to remove synapses (Cherra & Jin, 2016; Chung et al., 2013; MacDonald et al., 2006). Here, we have presented a new approach for investigating cellular interactions by electron microscopy, using genetically encoded miniSOG enzyme that enables the labeling of specific proteins or cellular compartments for electron microscopic analysis (Shu et al., 2011). miniSOG can be expressed in a tissue-specific or temporal manner to enable the analysis of discrete interactions, such as between the epidermis and neurons. This approach provides a complementary method for immuno-EM analysis of protein localization or cell-cell interactions, including the analysis of phagocytosis.
Association and epistatic analysis of white matter related genes across the continuum schizophrenia and autism spectrum disorders: The joint effect of NRG1-ErbB genes
Published in The World Journal of Biological Psychiatry, 2022
C. Prats, M. Fatjó-Vilas, M. J. Penzol, O. Kebir, L. Pina-Camacho, D. Demontis, B. Crespo-Facorro, V. Peralta, A. González-Pinto, E. Pomarol-Clotet, S. Papiol, M. Parellada, M. O. Krebs, L. Fañanás
Current evidence suggests that a phenotypic continuum links neurodevelopmental disorders, such as schizophrenia-spectrum disorders (SSD) and autism spectrum disorders (ASD). Although they are considered separate disease entities, emerging data has increasing recognition of these conditions overlap. Epidemiological studies have revealed the co-occurrence of these disorders in the same subject and different family members (Stahlberg et al. 2004; Daniels et al. 2008; Sullivan et al. 2012, 2013). Concerning clinical characteristics, both SSD and ASD present deficits in social interaction and communication and show impairments in similar cognitive domains (i.e. attention, memory, executive function, and social cognition) (Kerns et al. 2008; Sasson et al. 2011; Martinez et al. 2019). At a neurobiological level, subjects with SSD and ASD show microscopic and macroscopic evidence of brain disruption in overlapping areas (de Lacy and King 2013). For example, recent studies focussing on induced pluripotent stem cells-derived neural cells from SSD and ASD patients support common alterations in glutamatergic synapse formation and function in both disorders (Habela et al. 2016). Also, from neuroimaging approaches, different studies have reported WM alterations in SSD and ASD (Dennis and Thompson 2013; Wheeler and Voineskos 2014). The observed differences in both disorders as compared to healthy subjects include structural connectivity deficits regarding long-distance and interhemispheric bundles in the corpus callosum and the superior longitudinal, the inferior fronto-occipital, and the inferior longitudinal fasciculi (Ford et al. 2002; Mueller et al. 2012; Karlsgodt 2020; Katz et al. 2016).