{"title":"Astrocyte-Neuron Interactions Contributing to Amyotrophic Lateral Sclerosis Progression.","authors":"Brigid K Jensen","doi":"10.1007/978-3-031-64839-7_12","DOIUrl":"10.1007/978-3-031-64839-7_12","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a complex disease impacting motor neurons of the brain, brainstem, and spinal cord. Disease etiology is quite heterogeneous with over 40 genes causing the disease and a vast ~90% of patients having no prior family history. Astrocytes are major contributors to ALS, particularly through involvement in accelerating disease progression. Through study of genetic forms of disease including SOD1, TDP43, FUS, C9orf72, VCP, TBK1, and more recently patient-derived cells from sporadic individuals, many biological mechanisms have been identified to cause intrinsic or glial-mediated neurotoxicity to motor neurons. Overall, many of the normally supportive and beneficial roles that astrocytes contribute to neuronal health and survival instead switch to become deleterious and neurotoxic. While the exact pathways may differ based on disease-origin, altered astrocyte-neuron communication is a common feature of ALS. Within this chapter, distinct genetic forms are examined in detail, along with what is known from sporadic patient-derived cells. Overall, this chapter highlights the interplay between astrocytes and neurons in this complex disease and describes the key features underlying: astrocyte-mediated motor neuron toxicity, excitotoxicity, oxidative/nitrosative stress, protein dyshomeostasis, metabolic imbalance, inflammation, trophic factor withdrawal, blood-brain/blood-spinal cord barrier involvement, disease spreading, and the extracellular matrix/cell adhesion/TGF-β signaling pathways.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"39 ","pages":"285-318"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Homeostasis to Allostasis: Prefrontal Astrocyte Roles in Cognitive Flexibility and Stress Biology.","authors":"Bolati Wulaer, Mika A Holtz, Jun Nagai","doi":"10.1007/978-3-031-64839-7_6","DOIUrl":"10.1007/978-3-031-64839-7_6","url":null,"abstract":"<p><p>In the intricate landscape of neurophysiology, astrocytes have been traditionally cast as homeostatic cells; however, their mechanistic involvement in allostasis-particularly how they modulate the adaptive response to stress and its accumulative impact that disrupts cognitive functions and precipitates psychiatric disorders-is now starting to be unraveled. Here, we address the gap by positing astrocytes as crucial allostatic players whose molecular adaptations underlie cognitive flexibility in stress-related neuropsychiatric conditions. We review how astrocytes, responding to stress mediators such as glucocorticoid and epinephrine/norepinephrine, undergo morphological and functional transformations that parallel the maladaptive changes. Our synthesis of recent findings reveals that these glial changes, especially in the metabolically demanding prefrontal cortex, may underlie some of the neuropsychiatric mechanisms characterized by the disruption of energy metabolism and astrocytic networks, compromised glutamate clearance, and diminished synaptic support. We argue that astrocytes extend beyond their homeostatic role, actively participating in the brain's allostatic response, especially by modulating energy substrates critical for cognitive functions.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"39 ","pages":"137-163"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evaluation and Management of Traumatic Brain Injuries in the Pediatric Intensive Care Unit.","authors":"Michael Cronin","doi":"10.1007/978-3-031-69832-3_2","DOIUrl":"https://doi.org/10.1007/978-3-031-69832-3_2","url":null,"abstract":"<p><p>In this overview, intended for a multidisciplinary readership, we address the challenges in early management of children who have sustained mild, moderate, or severe traumatic brain injuries. Pediatric traumatic brain injuries (pTBIs) present unique diagnostic and management challenges as compared with adults. Proper management requires careful interpretation of data and strong clinical judgment. Children with injuries due to nonaccidental trauma present unique diagnostic and management challenges. In the pediatric intensive care unit, care is provided as part of a multidisciplinary, collaborative team, with medical and surgical interventions tailored to injury severity. Intensive care focuses on managing cerebral perfusion, temperature, mechanical ventilation, and continuous EEG monitoring to mitigate secondary brain injury. Long-term recovery emphasizes multidisciplinary rehabilitation and support to address physical, cognitive, and emotional challenges.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"42 ","pages":"21-32"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuroimaging Biomarkers in Parkinson's Disease.","authors":"Sophie Holmes, Sule Tinaz","doi":"10.1007/978-3-031-69491-2_21","DOIUrl":"https://doi.org/10.1007/978-3-031-69491-2_21","url":null,"abstract":"<p><p>Idiopathic Parkinson's disease (PD) is a neurodegenerative disorder that affects multiple systems in the body and is characterized by a variety of motor and non-motor (e.g., psychiatric, autonomic) symptoms. As the fastest growing neurological disorder expected to affect over 12 million people globally by 2040 (Dorsey, Bloem JAMA Neurol 75(1):9-10. https://doi.org/10.1001/jamaneurol.2017.3299 . PMID: 29131880, 2018), PD poses an enormous individual and public health burden. Currently, there are no therapies that can slow down the disease progression in PD, and existing therapies are limited to symptomatic treatment. Importantly, people in the prodromal phase who are at high risk of developing PD can now be identified, which makes disease prevention an achievable goal. An in-depth understanding of the pathological processes in PD is crucial for prevention and treatment development. Advanced multimodal neuroimaging techniques provide unique biomarkers that can further our understanding of PD at multiple levels ranging from neurotransmitters to neural networks. These neuroimaging biomarkers also have value in clinical application, for example, in the differential diagnosis of PD. As the field continues to advance, neuroimaging biomarkers are expected to become more specific, more widely accessible, and can be readily incorporated into translational research for treatment development in PD.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"40 ","pages":"617-663"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Biomarkers for Cognitive Control, Response Inhibition, Aggressivity, Impulsivity, and Violence.","authors":"Matthew J Hoptman, Ragy R Girgis, Daniel C Javitt","doi":"10.1007/978-3-031-69491-2_24","DOIUrl":"https://doi.org/10.1007/978-3-031-69491-2_24","url":null,"abstract":"<p><p>Deficits in cognitive control contribute to behavioral impairments across neuropsychiatric disorders. Cognitive control is captured as a construct in the Research Domain Construct (RDoC) matrix and incorporate subdomains of goal selection, response selection, and performance monitoring. Relevant tasks for these subdomains include the \"AX\" version of the continuous performance task (goal selection) and the Go/NoGo and Stop-Signal reaction time tasks (response selection). Underlying mechanisms for these domains have been investigated intensively using fMRI and event-related potential (ERP) approaches, which provide candidate biomarkers for translational research. In RDoC, impulsive behaviors are provisionally assigned to the cognitive control/response selection construct, but other factors may also contribute. Impulsivity has gained increased importance over recent years due to its link to aggression and suicidality, which is mediated especially through the constructs of urgency and frustrative nonreward. These constructs, in turn, may be captured through scales such as the Urgency, (Lack of) Premeditation, (Lack of) Perseverance, and Sensation Seeking (UPPS-P) impulsivity scale and the Point Subtraction Aggression Paradigm (PSAP), respectively. At present, no validated biomarkers exist for either urgency or aggressivity. Potential directions for the development of predictive biomarkers for both targets are discussed.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"40 ","pages":"725-756"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Spatial Omics: Navigating Neuroscience Research into the New Era.","authors":"Pengfei Guo, Yanxiang Deng","doi":"10.1007/978-3-031-69188-1_6","DOIUrl":"https://doi.org/10.1007/978-3-031-69188-1_6","url":null,"abstract":"<p><p>The human brain's complexity is underpinned by billions of neurons and trillions of synapses, necessitating coordinated activities across diverse cell types. Conventional techniques like in situ hybridization and immunohistochemistry, while valuable, face limitations in resolution and comprehensiveness when analyzing neuron types. Advances in spatial omics technologies, especially those integrating transcriptomics and proteomics, have revolutionized our understanding of brain tissue organization. These technologies, such as FISH-based, in situ sequencing-based (ISS), and next-generation sequencing (NGS)-based methods, provide detailed spatial context, overcoming previous limitations. FISH techniques, including smFISH and its variants like seqFISH and MERFISH, offer high-resolution spatial gene expression data. ISS approaches leverage padlock probes and rolling circle amplification to yield spatial transcriptome information. NGS-based methods, such as spatial transcriptomics and spatial-epigenomics, integrate spatial barcodes with single-cell sequencing, enabling comprehensive profiling of gene expression and epigenetic states in tissues. These innovations have propelled insights into neural development and disease, identifying cellular heterogeneity and molecular alterations in conditions like Alzheimer's and major depression. Despite challenges in cost, speed, and data analysis, spatial omics technologies continue to evolve, promising deeper insights into the molecular mechanisms of the brain and neurodegenerative diseases.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"41 ","pages":"133-149"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142714917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Endogenous Opioids in the Homeostatic Regulation of Hunger, Satiety, and Hedonic Eating: Neurobiological Foundations.","authors":"Marcela Rodriguez Flores, Sylvana Stephano Zúñiga","doi":"10.1007/978-3-031-45493-6_16","DOIUrl":"10.1007/978-3-031-45493-6_16","url":null,"abstract":"<p><p>This chapter (part one of a trilogy) summarizes the neurobiological foundations of endogenous opioids in the regulation of energy balance and eating behavior, dysregulation of which translates to maladaptive dietary responses in individuals with obesity and eating disorders, including anorexia, bulimia, and binge eating disorder. Knowledge of these neurobiological foundations is vital to researchers' and clinicians' understanding of pathophysiology as well as the science-based development of multidisciplinary diagnoses and treatments for obesity and eating disorders. We highlight mechanisms of endogenous opioids in both homeostatic and hedonic feeding behavior, review research on the dysregulation of food reward that plays a role in a wide array of obesity and disordered eating, and the clinical implications of neurobiological responses to food for current science-based treatments for obesity and eating disorders.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"35 ","pages":"315-327"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cognitive and Neural Representations of Fractals in Vision, Music, and Action.","authors":"Mauricio de Jesus Dias Martins","doi":"10.1007/978-3-031-47606-8_46","DOIUrl":"10.1007/978-3-031-47606-8_46","url":null,"abstract":"<p><p>The concept of fractal was popularized by Mandelbrot as a tool to tame the geometrical structure of objects with infinite hierarchical depth. The key aspect of fractals is the use of simple parsimonious rules and initial conditions, which when applied recursively can generate unbounded complexity. Fractals are structures ubiquitous in nature, being present in coast lines, bacteria colonies, trees, and physiological time series. However, within the field of cognitive science, the core question is not which phenomena can generate fractal structures, but whether human or animal minds can represent recursive processes, and if so in which domains. In this chapter, we will explore the cognitive and neural mechanisms underlying the representation of recursive hierarchical embedding. Language is the domain in which this capacity is best studied. Humans can generate an infinite array of hierarchically structured sentences, and this capacity distinguishes us from other species. However, recent research suggests that humans can represent similar structures in the domains of music, vision, and action and has provided additional cues as to how these capacities are cognitively implemented. Using a comparative approach, we will map the commonalities and differences across domains and offer a roadmap to understand the neurobiological implementation of fractal cognition.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"36 ","pages":"935-951"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jennilee M Davidson, Luduan Zhang, Guang H Yue, Antonio Di Ieva
{"title":"Fractal Dimension Studies of the Brain Shape in Aging and Neurodegenerative Diseases.","authors":"Jennilee M Davidson, Luduan Zhang, Guang H Yue, Antonio Di Ieva","doi":"10.1007/978-3-031-47606-8_17","DOIUrl":"10.1007/978-3-031-47606-8_17","url":null,"abstract":"<p><p>The fractal dimension is a morphometric measure that has been used to investigate the changes of brain shape complexity in aging and neurodegenerative diseases. This chapter reviews fractal dimension studies in aging and neurodegenerative disorders in the literature. Research has shown that the fractal dimension of the left cerebral hemisphere increases until adolescence and then decreases with aging, while the fractal dimension of the right hemisphere continues to increase until adulthood. Studies in neurodegenerative diseases demonstrated a decline in the fractal dimension of the gray matter and white matter in Alzheimer's disease, amyotrophic lateral sclerosis, and spinocerebellar ataxia. In multiple sclerosis, the white matter fractal dimension decreases, but conversely, the fractal dimension of the gray matter increases at specific stages of disease. There is also a decline in the gray matter fractal dimension in frontotemporal dementia and multiple system atrophy of the cerebellar type and in the white matter fractal dimension in epilepsy and stroke. Region-specific changes in fractal dimension have also been found in Huntington's disease and Parkinson's disease. Associations were found between the fractal dimension and clinical scores, showing the potential of the fractal dimension as a marker to monitor brain shape changes in normal or pathological processes and predict cognitive or motor function.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"36 ","pages":"329-363"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Richard P Taylor, Catherine Viengkham, Julian H Smith, Conor Rowland, Saba Moslehi, Sabrina Stadlober, Anastasija Lesjak, Martin Lesjak, Branka Spehar
{"title":"Fractal Fluency: Processing of Fractal Stimuli Across Sight, Sound, and Touch.","authors":"Richard P Taylor, Catherine Viengkham, Julian H Smith, Conor Rowland, Saba Moslehi, Sabrina Stadlober, Anastasija Lesjak, Martin Lesjak, Branka Spehar","doi":"10.1007/978-3-031-47606-8_45","DOIUrl":"10.1007/978-3-031-47606-8_45","url":null,"abstract":"<p><p>People are continually exposed to the rich complexity generated by the repetition of fractal patterns at different size scales. Fractals are prevalent in natural scenery and also in patterns generated by artists and mathematicians. In this chapter, we will investigate the powerful significance of fractals for the human senses. In particular, we propose that fractals with mid-range complexity play a unique role in our visual experiences because the visual system has adapted to these prevalent natural patterns. This adaptation is evident at multiple stages of the visual system, ranging from data acquisition by the eye to processing of this data in the higher visual areas of the brain. Based on these results, we will discuss a fluency model in which the visual system processes mid-complexity fractals with relative ease. This fluency optimizes the observer's capabilities (such as enhanced attention and pattern recognition) and generates an aesthetic experience accompanied by a reduction in the observer's physiological stress levels. In addition to reviewing people's responses to viewing fractals, we will compare these responses to recent research focused on fractal sounds and fractal surface textures. We will extend our fractal fluency model to allow for stimuli across multiple senses.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"36 ","pages":"907-934"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}