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Books on the topic 'Glial Function'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Matsas, Rebecca, and Marco Tsacopoulos, eds. The Functional Roles of Glial Cells in Health and Disease. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4685-6.

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2

1957-, Castellano Bernardo, and Nieto-Sampedro Manuel 1944-, eds. Glial cell function. Amsterdam: Elsevier, 2001.

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3

1957-, Castellano Bernardo, and Nieto-Sampedro Manuel 1944-, eds. Glial cell function. Amsterdam: Elsevier, 2003.

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4

B. Castellano López (Editor) and M. Nieto-Sampedro (Editor), eds. Glial Cell Function (Paperback) (Progress in Brain Research). Elsevier Science, 2003.

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5

J, Marangos Paul, Campbell Iain C, and Cohen Robert M, eds. Neuronal and glial proteins: Structure, function, and clinical application. San Diego: Academic Press, 1988.

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6

Ransom, Bruce R. Neuroglia. Edited by Helmut Kettenmann. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.001.0001.

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This resource is the long-awaited new revision of the most highly regarded reference volume on glial cells, and has been completely revised, greatly enlarged, and enhanced with full color figures throughout. Neglected in research for years, it is now evident that the brain only functions in a concerted action of all the cells, namely glia and neurons. Seventy one chapters comprehensively discuss virtually every aspect of normal glial cell anatomy, physiology, biochemistry and function, and consider the central roles of these cells in neurological diseases including stroke, Alzheimer disease, multiple sclerosis, Parkinson's disease, neuropathy, and psychiatric conditions. With more than 20 new chapters it addresses the massive growth of knowledge about the basic biology of glia and the sophisticated manner in which they partner with neurons in the course of normal brain function.

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7

Marangos, Paul J., and Iain C. Campbell. Neuronal and Glial Proteins: Structure, Function, and Clinical Application (Neurobiological Research). Academic Pr, 1988.

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8

Marangos, Paul J., and Iain C. Campbell. Neuronal and Glial Proteins: Structure, Function, and Clinical Application (Neurobiological Research). Academic Pr, 1988.

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9

Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.

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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.

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10

The Functional Roles of Glial Cells in Health and Disease: Dialogue between Glia and Neurons. Springer, 2011.

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11

Chess, Andrew, and Schahram Akbarian. The Human Brain and its Epigenomes. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0003.

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Conventional psychopharmacology elicits an insufficient therapeutic response in more than one half of patients diagnosed with schizophrenia, bipolar disorder, depression, anxiety, or related disorders. This underscores the need to further explore the neurobiology and molecular pathology of mental disorders in order to develop novel treatment strategies of higher efficacy. One promising avenue of research is epigenetics.Deeper understanding of genome organization and function in normal and diseased human brain will require comprehensive charting of neuronal and glial epigenomes. This includes DNA cytosine and adenine methylation, hundred(s) of residue-specific post-translational histone modifications and histone variants, transcription factor occupancies, and chromosomal conformations and loopings. Epigenome mappings provide an important avenue to assign function to many risk-associated DNA variants and mutations that do not affect protein-coding sequences. Powerful novel single cell technologies offer the opportunity to understand genome function in context of the vastly complex cellular heterogeneity and neuroanatomical diversity of the human brain.

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12

Mason, Peggy. Medical Neurobiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.001.0001.

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This textbook guides the medical student, regardless of background or intended specialty, through the anatomy and function of the human nervous system. In writing specifically for medical students, the author concentrates on the neural contributions to common diseases, whether neurological or not, and omits topics without clinical relevance. The two fundamental building blocks of the nervous system are neural communication and neuroanatomy. Foundations in both topics must be mastered. After learning the neurons and glial cells that comprise the nervous system, the book begins with a study of the anatomy of the nervous system before moving on to neural communication. With these basics of neurophysiology and neuroanatomy in hand, the reader is ready to tackle how the brain “works” by examining perception, voluntary movement, and homeostasis. The book is intended as a “travel guide” to the human brain, one that communicates to the reader the profound power and beauty of brain function while providing a memorable and enjoyable trip.

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13

Kaur, Charanjit. Glial Cells: Embryonic Development, Types / Functions and Role in Disease. Nova Science Publishers, Incorporated, 2013.

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14

(Editor), Rebecca Matsas, and Marco Tsacopoulos (Editor), eds. The Functional Roles of Glial Cells in Health and Disease: Dialogue between Glia and Neurons (Advances in Experimental Medicine and Biology). Springer, 1999.

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15

Roback, John D. Neurotrophin and neurotrophin receptor expression in neurons and glia from the developing brain. 1992.

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16

Molecular Signaling and Regulation in Glial Cells: A Key to Remyelination and Functional Repair. Springer-Verlag Telos, 1997.

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17

1950-, Jeserich G., ed. Molecular signaling and regulation in glial cells: A key to remyelination and functional repair. Berlin: Springer, 1997.

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18

Klute, Rudolf, and Gunnar Jeserich Hans H. Althaus. Molecular Signaling and Regulation in Glial Cells: A Key to Remyelination and Functional Repair. Springer, 2011.

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19

Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.

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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.

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20

Krizbai, Istvan, Imola Wilhelm, Hans-Christian Bauer, and Hannelore Bauer. The Role of Glia in the Formation and Function of the Blood-Brain Barrier. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0033.

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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...

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21

1937-, Levi Giulio, and International Society for Neurochemistry. Meeting, eds. Differentiation and functions of glial cells: Proceedings of a satellite meeting of the International Society for Neurochemistry held in Rome, Italy, April 19-21, 1989. New York: Wiley-Liss, 1990.

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22

Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.

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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.

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23

Sada, Nagisa, and Tsuyoshi Inoue. Lactate Dehydrogenase. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0029.

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Glucose is transported into neurons and used as an energy source. It is also transported into astrocytes, a type of glial cell, and converted to lactate, which is then released to neurons and used as another energy source. The latter is called the astrocyte-neuron lactate shuttle. Although the lactate shuttle is a metabolic pathway, it also plays important roles in neuronal activities and brain functions. We recently reported that this metabolic pathway is involved in the antiepileptic effects of the ketogenic diet. Lactate dehydrogenase (LDH) is a metabolic enzyme that mediates the lactate shuttle, and its inhibition hyperpolarizes neurons and suppresses seizures. This enzyme is also a molecular target of stiripentol, a clinically used antiepileptic drug for Dravet syndrome. This review provides an overview of electrical regulation by the astrocyte-neuron lactate shuttle, and then introduces LDH as a metabolic target against epilepsy.

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24

Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.

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Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.

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25

Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.

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