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Biology of Brain Disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453801 Year: Pages: 586 DOI: 10.3389/978-2-88945-380-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology --- Physiology --- Medicine (General)
Added to DOAB on : 2018-11-16 17:17:57
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Brain disorders, including neurological and neuropsychiatric conditions, represent a challenge for public health systems and society at large. The limited knowledge of their biology hampers the development of diagnostic tools and effective therapeutics. A clear understanding of the mechanisms that underlie the onset and progression of brain disorders is required in order to identify new avenues for therapeutic intervention.Overlapping genetic risk factors across different brain disorders suggest common linkages and pathophysiological mechanisms that underlie brain disorders. Methodological and technological advances are leading to new insights that go beyond traditional hypotheses. Taking account of underlying molecular, cellular and systems biology underlying brain function will play an important role in the classification of brain disorders in future.In this Research Topic, the latest advances in our understanding of biological mechanisms across different brain disorders are presented. The areas covered include developments in neurogenetics, epigenetics, plasticity, glial cell biology, neuroimmune interactions and new technologies associated with the study of brain function. Examples of how understanding of biological mechanisms are translating into research strategies that aim to advance diagnoses and treatment of brain disorders are discussed.

Motor Cortex Microcircuits (Frontiers in Brain Microcircuits Series)

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193899 Year: Pages: 133 DOI: 10.3389/978-2-88919-389-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2015-12-03 13:02:24
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How does the motor cortex enable mammals to generate accurate, complex, and purposeful movements? A cubic millimeter of motor cortex contains roughly ~10^5 cells, an amazing ~4 Km of axons and ~0.4 Km of dendrites, somehow wired together with ~10^9 synapses. Corticospinal neurons (a.k.a. Betz cells, upper motor neurons) are a key cell type, monosynaptically conveying the output of the cortical circuit to the spinal cord circuits and lower motor neurons. But corticospinal neurons are greatly outnumbered by all the other kinds of neurons in motor cortex, which presumably also contribute crucially to the computational operations carried out for planning, executing, and guiding actions. Determining the wiring patterns, the dynamics of signaling, and how these relate to movement at the level of specific excitatory and inhibitory cell types is critically important for a mechanistic understanding of the input-output organization of motor cortex. While there is a predictive microcircuit hypothesis that relates motor learning to the operation of the cerebellar cortex, we lack such a microcircuit understanding in motor cortex and we consider microcircuits as a central research topic in the field. This Research Topic covers any issues relating to the microcircuit-level analysis of motor cortex. Contributions are welcomed from neuroscientists at all levels of investigation, from in vivo physiology and imaging in humans and monkeys, to rodent models, in vitro anatomy, electrophysiology, electroanatomy, cellular imaging, molecular biology, disease models, computational modeling, and more.

Building the gateway to consciousness - about the development of the thalamus

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194704 Year: Pages: 107 DOI: 10.3389/978-2-88919-470-4 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Since years, patterning and function of some brain parts such as the cortex in the forebrain and the optical tectum or cerebellum in the midbrain/hindbrain region are under strong investigation. Interestingly the diencephalon located in the caudal forebrain has been ignored for decades. Consequently, the existing knowledge from the development of this region to function in the mature brain is very fragmented. The central part of the diencephalon is the thalamus. This central relay station plays a crucial role in distributing incoming sensory information to appropriate regions of the cortex. The thalamus develops in the posterior part of the embryonic forebrain, where early cell fate decisions are controlled by local signaling centers. In this Research Topic we discuss recent achievements elucidating thalamic neurogenesis - from neural progenitor cells to highly specialized neurons with cortical target cells in great distance. In parallel, we highlight developmental aspects leading from the early thalamic anlage to the late the organization of the complex relay station of the brain.

Cytokines as Players of Neuronal Plasticity and Sensitivity to Environment in Healthy and Pathological Brain

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197682 Year: Pages: 158 DOI: 10.3389/978-2-88919-768-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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It is now accepted that immune molecules are not only present within the brain during pathology but they exert physiological functions in the "healthy" brain as well. Increasing evidence points to a neuro-modulatory role of cytokines and chemokines (CHEMOtactic cytoKINES) in basal transmission and plasticity processes where signaling between peri-synaptic astrocytes, microglia and neurons plays an important role. Nevertheless, the exact mechanisms as to how cytokines, and in particular chemokines, participate in the molecular and cellular processes thought to subserve memory formation, plasticity processes and responsiveness to environmental stimuli remain to be clarified. Interestingly, in in vitro preparations, molecules like TNF-a, interleukin (IL)-1ß, IL-6, CX3CL1, CXCL12, CCL2 and CCL3 are implicated in synaptic formation and scaling, in modulation of glutamatergic transmission, in plasticity and neurogenesis, in particular in the hippocampus. The hippocampus is an extremely plastic structure, one of the main neurogenic niches in the adult brain, that exhibits a marked sensibility to environmental stimuli. Indeed exposure of mice to environmental enrichment (EE) modifies learning and memory abilities increasing neurogenesis and neuronal plasticity whether exposure to severe stressful experiences diminishes neurotrophic support, impairs neurogenesis, plasticity and cognition. In the hippocampus cytokines play a key role in mediating both positive as well as negative effects of the environment affecting neuronal plasticity also in stress related pathologies, such as depression. It has been reported that mice lacking type 1 receptor for IL-1 display impaired hippocampal memory and LTP that are restored by EE; moreover negative effects on neuronal plasticity (and thus behavior) induced by stress exposure can be prevented by blocking IL-1 activity. In addition, mice lacking IL-6 have improved cognitive functions whereas the absence of microglia-driven CX3CR1 signaling increases hippocampal plasticity and spatial memory occluding the potentiating effects of EE. However, the factors mediating the effect of environmental stimuli on behavior and plasticity has been only partially identified. Interestingly, it has been suggested that chemokines can play a key role in the flexibility of hippocampal structure and may modulate neuronal signaling during behavior. The question is how cytokines may translate environmental stimuli in plasticity and behavioral changes. This research topic is proposed to explore the role of cytokines, and more in particular chemokines, in the modulation of neuronal activity as a fundamental step for the correct brain wiring, function and susceptibility to environment. We encourage the submission of original research reports, review articles, commentaries, perspectives or short communications, in the following (but not limited to) topics:- Role of cytokines and chemokines in neuronal plasticity- Immune molecules and responsiveness to environment- Role of chemokine in the flexibility of hippocampal structure

Spiking Neural Network Connectivity and its Potential for Temporal Sensory Processing and Variable Binding

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192397 Year: Pages: 123 DOI: 10.3389/978-2-88919-239-7 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2015-11-16 15:44:59
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The most biologically-inspired artificial neurons are those of the third generation, and are termed spiking neurons, as individual pulses or spikes are the means by which stimuli are communicated. In essence, a spike is a short-term change in electrical potential and is the basis of communication between biological neurons. Unlike previous generations of artificial neurons, spiking neurons operate in the temporal domain, and exploit time as a resource in their computation. In 1952, Alan Lloyd Hodgkin and Andrew Huxley produced the first model of a spiking neuron; their model describes the complex electro-chemical process that enables spikes to propagate through, and hence be communicated by, spiking neurons. Since this time, improvements in experimental procedures in neurobiology, particularly with in vivo experiments, have provided an increasingly more complex understanding of biological neurons. For example, it is now well understood that the propagation of spikes between neurons requires neurotransmitter, which is typically of limited supply. When the supply is exhausted neurons become unresponsive. The morphology of neurons, number of receptor sites, amongst many other factors, means that neurons consume the supply of neurotransmitter at different rates. This in turn produces variations over time in the responsiveness of neurons, yielding various computational capabilities. Such improvements in the understanding of the biological neuron have culminated in a wide range of different neuron models, ranging from the computationally efficient to the biologically realistic. These models enable the modelling of neural circuits found in the brain. In recent years, much of the focus in neuron modelling has moved to the study of the connectivity of spiking neural networks. Spiking neural networks provide a vehicle to understand from a computational perspective, aspects of the brain's neural circuitry. This understanding can then be used to tackle some of the historically intractable issues with artificial neurons, such as scalability and lack of variable binding. Current knowledge of feed-forward, lateral, and recurrent connectivity of spiking neurons, and the interplay between excitatory and inhibitory neurons is beginning to shed light on these issues, by improved understanding of the temporal processing capabilities and synchronous behaviour of biological neurons. This research topic aims to amalgamate current research aimed at tackling these phenomena.

Plasticity of primary afferent neurons and sensory processing after spinal cord injury

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193967 Year: Pages: 221 DOI: 10.3389/978-2-88919-396-7 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2015-12-03 13:02:24
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Traumatic injury of the spinal cord affects the entire organism directly and indirectly. Primary injury destroys neurons and severs axons which participate in neural circuits. Secondary injuries and pathologies arise from numerous sources including systemic inflammation, consequential damage of cutaneous, muscular, and visceral tissues, and dysregulation of autonomic, endocrine and sensory- motor functions. Evidence is mounting that spinal cord injury (SCI) affects regions of the nervous system spatially remote from the injury site, as well as peripheral tissues, and alters some basic characteristics of primary afferent cell biology and physiology (cell number, size/frequency, electrophysiology, other). The degree of afferent input and processing above the lesion is generally intact, while that in the peri-lesion area is highly variable, though pathologies emerge in both regions, including a variety of pain syndromes. Primary afferent input to spinal regions below the injury and the processing of this information becomes even more important in the face of complete or partial loss of descending input because such spared sensory processing can lead to both adaptive and pathological outcomes. This issue hosts review and research articles considering mechanisms of plasticity of primary afferent neurons and sensory processing after SCI, and how such plasticity contributes to sparing and/or recovery of functions, as well as exacerbation of existing and/or emergent pathologies. A critical issue for the majority of the SCI community is chronic above-, peri-, and below-level neuropathic pain, much of which may arise, at least in part, from plasticity of afferent fibers and nociceptive circuitry. For example, autonomic dysreflexia is common hypertensive syndrome that often develops after SCI that is highly reliant on maladaptive nociceptive sensory input and processing below the lesion. Moreover, the loss of descending input leaves the reflexive components of bladder/bowel/sexual function uncoordinated and susceptible to a variety of effects through afferent fiber plasticity. Finally, proper afferent feedback is vital for the effectiveness of activity-dependent rehabilitative therapies, but aberrant nociceptive input may interfere with these approaches since they are often unchecked due to loss of descending modulation.

The Neural Underpinnings of Vicarious Experience

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192649 Year: Pages: 169 DOI: 10.3389/978-2-88919-264-9 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2015-12-03 13:02:24
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Everyday we vicariously experience a range of states that we observe in other people: we may "feel" embarrassed when witnessing another making a social faux pas, or we may feel sadness when we see a loved one upset. In some cases this process appears to be implicit. For instance, observing pain in others may activate pain-related neural processes but without generating an overt feeling of pain. In other cases, people report a more literal, conscious sharing of affective or somatic states and this has sometimes been described as representing an extreme form of empathy. By contrast, there appear to be some people who are limited in their ability to vicariously experience the states of others. This may be the case in several psychiatric, neurodevelopmental, and personality disorders where deficits in interpersonal understanding are observed, such as schizophrenia, autism, and psychopathy. In recent decades, neuroscientists have paid significant attention to the understanding of the “social brain,” and the way in which neural processes govern our understanding of other people. In this Research Topic, we wish to contribute towards this understanding and ask for the submission of manuscripts focusing broadly on the neural underpinnings of vicarious experience. This may include theoretical discussion, case studies, and empirical investigation using behavioural techniques, electrophysiology, brain stimulation, and neuroimaging in both healthy and clinical populations. Of specific interest will be the neural correlates of individual differences in traits such as empathy, how we distinguish between ourselves and other people, and the sensorimotor resonant mechanisms that may allow us to put ourselves in another's shoes.

Parkinson's Disease Cell Vulnerability and Disease Progression

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196760 Year: Pages: 194 DOI: 10.3389/978-2-88919-676-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Parkinson's disease is a neurodegenerative disorder that affects 1.5% of the global population over 65 years of age. The hallmark feature of this disease is the degeneration of dopamine neurons in the substantia nigra pars compacta and a consequent striatal dopamine deficiency. The pathogenesis of Parkinson's Disease remains unclear. Despite tremendous growth in recent years in our knowledge of the molecular basis of Parkinson's Disease and the molecular pathways of cell death important questions remain regarding why are substantia nigra cells especially vulnerable, which mechanisms underlie progressive cell loss or what do Lewy bodies or alpha-synuclein reveal about disease progression. Understanding the different vulnerability of the dopaminergic neurons from midbrain regions and the mechanisms whereby pathology becomes widespread are primary objectives of basic and clinical research in Parkinson's Disease.This e-Book discusses the etiopathogenesis of Parkinson's Disease, presenting a series of papers that provide up-to-date, state-of-the-art information on molecular and cellular mechanisms involved in the neurodegeneration process in the disease, the role of activation of functional anatomical organization of the basal ganglia and in particular habitual vs goal directed systems as a factor of neuronal vulnerability, the possibility that Parkinson's Disease coulb be a prion disease and how genetic factors linked to familial and sporadic forms of PD. We hope that this e-Book will stimulate the continuing efforts to understand the cell and physiological mechanisms underlying the origin of Parkinson's Disease.

Metals and neurodegeneration: Restoring the balance

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197392 Year: Pages: 132 DOI: 10.3389/978-2-88919-739-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Biometals such as copper, zinc and iron have key biological functions, however, aberrant metabolism can lead to detrimental effects on cell function and survival. These biometals have important roles in the brain, driving cellular respiration, antioxidant activity, intracellular signaling and many additional structural and enzymatic functions. There is now considerable evidence that abnormal biometal homeostasis is a key feature of many neurodegenerative diseases and may have an important role in the onset and progression of disorders such as Alzheimer’s, Parkinson’s, prion and motor neuron diseases. Recent studies also support biometal roles in a number of less common neurodegenerative disorders. The role of biometals in a growing list of brain disorders is supported by evidence from a wide range of sources including molecular genetics, biochemical studies and biometal imaging. These studies have spurred a growing interest in understanding the role of biometals in brain function and disease as well as the development of therapeutic approaches that may be able to restore the altered biometal chemistry of the brain. These approaches range from genetic manipulation of biometal transport to chelation of excess metals or delivery of metals where levels are deficient. A number of these approaches are offering promising results in cellular and animal models of neurodegeneration with successful translation to pre-clinical and clinical trials. At a time of aging populations and slow progress in development of neurotherapeutics to treat age-related neurodegenerative diseases, there is now a critical need to further our understanding of biometals in neurodegeneration. This issue covers a broad range of topics related to biometals and their role in neurodegeneration. It is hoped that this will inspire greater discussion and exchange of ideas in this crucial area of research and lead to positive outcomes for sufferers of these neurodegenerative diseases.

Chemokines and chemokine receptors in brain homeostasis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196166 Year: Pages: 124 DOI: 10.3389/978-2-88919-616-6 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-08-16 10:34:25
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Virtually involved in all pathologies that present an inflammatory component, it is now evident that, in the central nervous system, chemokines and chemokine receptors possess pleiotropic properties beyond chemotaxis: costitutive brain expression of chemokines and their receptors on endothelial cells, but also on neurons and glia, suggests a role for such molecules in mediating homeostatic cross-talk between cells of the brain perenchyma. Cross-talk between neurons and glia is determinant to the establishment and maintenance of a brain enviroment that ensure normal function, and in particular glial cells are active players that respond to enviromental changes and act for the survival, growth, differentiation and repair of the nervous tissue: in this regard brain endogenous chemokines represent key molecules that play a role in brain development, neurogenesis, neurotransmission and neuroprotection. As important regulators of peripheral immune response, chemokines are molecules of the immune system that play a central role in coordinating communication between the nervous and the immune systems, in the context of infections and brain injury. Indeed, in phatological processes resulting from infections, brain trauma, ischemia and chronic neurodegenerative diseases, chemokines represent important neuroinflammatory mediators that drive leucocytes trafficking into the central nervous system, facilitating an immune response by targeting cells of the innate and adaptive immune system. The third edition of the international conference "Chemokines and Chemokine Receptors in the Nervous System", hold in Rome in October 2013, represented an exciting platform to promote discussion among researchers in different disciplines to understand the role of chemokines in brain homoestasis. This Frontiers Research Topic arises from this conference, and wants to be an opportunity to further discuss and highlight the importance of brain chemokines as key molecules that, not only grant the interplay between the immune and the nervous systems, but in addition drive modulatory functions on brain homeoastasis orchestrating neurons, microglia, and astrocytes communication.

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