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Books on the topic 'Neurotrophins'

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Author: Grafiati

Published: 4 June 2021

Last updated: 23 February 2023

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1

Mocchetti, Italo. Neurobiology of the neurotrophins. Johnson City, TN: FP Graham Pub., 2001.

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2

Adams, Terri. Stable gradients of neurotrophins for guided neurite outgrowth. Ottawa: National Library of Canada, 2002.

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3

Rush, Robert A. Neurotrophin Protocols. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590608.

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4

Patrick, Aebischer, and Hefti Franz, eds. Neurotrophic factors. Berlin: Springer, 1999.

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5

Boulton, Alan A., Glen B. Baker, and Franz Hefti. Neurotrophic Factors. New Jersey: Humana Press, 1993. http://dx.doi.org/10.1385/0896032493.

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6

Skaper, Stephen D., ed. Neurotrophic Factors. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7.

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7

Hefti, Franz, ed. Neurotrophic Factors. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59920-0.

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8

Lewin, Gary R., and Bruce D. Carter, eds. Neurotrophic Factors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-45106-5.

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9

Skaper, Stephen D., ed. Neurotrophic Factors. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7571-6.

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10

Van de Water, Thomas R. and Koszer Samuel, eds. Clinical applications of neurotrophic factors. Philadelphia: Lippincott-Raven, 1997.

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11

Duarte, Carlos B., and Enrico Tongiorgi, eds. Brain-Derived Neurotrophic Factor (BDNF). New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8970-6.

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12

The synapse: Function, plasticity, and neurotrophism. Oxford: Oxford University Press, 1995.

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13

Troficheskai͡a funkt͡sii͡a nervnoĭ sistemy. Moskva: "Nauka", 1990.

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14

Hefti, Elisabeth. Commercializing the new biopharmaceutical: Growth factors, neurotrophic factors, and therapeutic monoclonal antibodies. Waltham, MA: Decision Resources, 1993.

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15

Khundakar, Ahmad Adam. The effect of antidepressant treatment on brain-derived neurotrophic factor expression in the rat hippocampus. Leicester: De Montfort University, 2004.

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16

Liadis, Nicole. The role of caspase-3 in regulating neurotrophic and NMDA-dependent PCD in the mammalian CNS in vivo. Ottawa: National Library of Canada, 2001.

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17

Katayama, Yusuke. Prolonged release of brain-derived neurotrophic factor from poly(lactide-co-glycolide) microspheres dispersed within a polyethylene glycol hydrogel. Ottawa: National Library of Canada, 2003.

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18

Satellite Symposium of the European Neurological Society (1988 Sanremo, Italy). Peripheral nerve development and regeneration: Recent advances and clinical applications. Padova: Liviana Press, 1989.

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19

Litwack, Gerald. Neurotrophins. Elsevier Science & Technology Books, 2017.

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20

Litwack, Gerald. Neurotrophins. Elsevier Science & Technology Books, 2017.

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21

Hayat, M. A. Neurotrophins and Their Receptors. University of Cambridge ESOL Examinations, 2002.

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22

Mocchetti, Italo. Neurobiology of the Neurotrophins. F P Graham Company, 2001.

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23

Maya, Sieber-Blum, ed. Neurotrophins and the neural crest. Boca Raton, Fla: CRC Press, 1999.

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24

Bradbury, Elizabeth J., and Nicholas D. James. Mapping of neurotrophin receptors on adult sensory neurons. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0022.

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The paper discussed in this chapter describes the first mapping of neurotrophin receptors in adult sensory neurons. Neurotrophins and their receptors were a particularly hot topic at the time, but the primary focus of interest had been in their role in development. In this paper, McMahon and colleagues characterized both mRNA and protein expression of the recently discovered trk receptors on defined populations of adult sensory neurons, correlating trk expression with other primary afferent projection neuron properties such as cell size and neuronal function. Furthermore, by showing clear correlations between the expression of different trk receptors and the physical and functional properties of defined primary afferent projections, the authors provided key evidence suggesting that nerve growth factor and neurotrophin-3 acted on functionally distinct populations of adult sensory neurons. This paper provided the basis for subsequent research on neurotrophin signalling and function in both the healthy and the diseased nervous system.

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25

Triaca, Viviana, Bruno Pietro Imbimbo, and Robert Nistico, eds. Neurotrophins Biodelivery to CNS: Innovative Approaches for Disease-Modifying Therapy. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-303-0.

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26

Heim, Christine, Katharina Schultebraucks, Charles R. Marmar, and Charles B. Nemeroff. Neurobiological Pathways Involved in Fear, Stress, and PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0019.

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This chapter examines current findings relating to the molecular neuropharmacology of posttraumatic stress disorder (PTSD). Studies consistently show that neurochemical alterations after trauma exposure are associated with the development of PTSD and reflect in part stress sensitization in PTSD. We also review neuroendocrine, neurotransmitter, neuropeptide, and related molecular features that reflect preexisting vulnerability factors for the development of PTSD. In this chapter, we provide an overview of recent neuroendocrine findings mainly with regard to the influence of the hypothalamic-pituitary-axis. We also review recent neurochemical findings including the influence of different neurotransmitters such as catecholamines, serotonin, amino acids, neuropeptides, neurotrophins, and lipids. We incorporate these new and established neurobiological findings into a proposed integrative model of the neurobiology of PTSD.

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27

Neurotrophin Protocols. Humana Press, 2001.

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28

Rush, Robert A. Neurotrophin Protocols. Humana Press, 2013.

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29

Chen, Michael C., and Ian H. Gotlib. Molecular Foundations of the Symptoms of Major Depressive Disorder. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.002.

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Major Depressive Disorder (MDD) is a prevalent and costly disorder with a broad range of cognitive, affective, and behavioral symptoms. Despite the absence of a clear final common molecular pathway in depression, many molecular systems have been implicated in MDD. In particular, disruptions in molecular systems like serotonin, dopamine, glutamate, and other neurotransmitters, as well as in stress hormones, cytokines, neurotrophins, and neuropeptides, may contribute to MDD. To link the symptoms of MDD with molecular dysfunction, this article examines these molecules in the context of three symptom clusters of MDD: cognitive/affective symptoms, volitional/behavioral symptoms, and homeostatic/vegetative symptoms. It examines how these molecules and their receptor, transport, and regulatory systems contribute to MDD and to the development of specific symptom clusters. It presents two possible frameworks of molecular dysfunction in MDD that encompass the interactions between vulnerability phenotypes and biochemical perturbations that may lead to the heterogeneous symptoms of this disorder.

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30

1922-, Tsukada Yasuz0̄, and Shooter Eric M, eds. Neurotrophic factors. Tokyo: Japan Scientific Societies Press, 1992.

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31

Boulton, Alan A., Glen B. Baker, and Franz Hefti. Neurotrophic Factors. Humana Press, 2013.

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32

Hefti, Franz. Neurotrophic Factors. Springer London, Limited, 2012.

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33

1947-, Baker Glen B., Boulton A. A, and Hefti Franz, eds. Neurotrophic factors. Totowa, N.J: Humana Press, 1993.

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34

E, Loughlin Sandra, and Fallon James H, eds. Neurotrophic factors. San Diego: Academic Press, 1993.

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35

Neurotrophic Factors. Elsevier, 1993. http://dx.doi.org/10.1016/c2009-0-03357-1.

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36

Hefti, Franz. Neurotrophic Factors. Springer London, Limited, 2011.

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37

Fallon, James H., and Sandra E. Loughlin. Neurotrophic Factors. Elsevier Science & Technology Books, 2012.

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38

Carter, Bruce D., and Gary R. Lewin. Neurotrophic Factors. Springer London, Limited, 2014.

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39

Carter, Bruce D., and Gary R. Lewin. Neurotrophic Factors. Springer, 2014.

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40

Carter, Bruce D., and Gary R. Lewin. Neurotrophic Factors. Springer, 2016.

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41

(Editor), Alan A. Boulton, Glen B. Baker (Editor), and Franz Hefti (Editor), eds. Neurotrophic Factors (Neuromethods). Humana Press, 1993.

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42

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

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43

Duman, Ronald S. Neurotrophic Mechanisms of Depression. 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/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.

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44

Kapczinski, Flávio, Michael Berk, and Pedro Vieira da Silva Magalhães, eds. Neuroprogression in Psychiatry. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198787143.001.0001.

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Psychiatric disorders are characterized by an overlapping set of pathophysiological pathways that include monoamines but also neurotrophins, apoptotic and mitochondrial pathways, epigenetics, and dysregulation of immunity and redox balance, counterbalanced by cellular resilience and defence pathways and the effects of treatment. These conspire in a subset of individuals to cause changes in brain function and, over time, the activity of these pathways in chronic psychiatric disorders can lead to cognitive sequelae and changes in brain structure. This can lead to differences between early and late stages of illness. These biological underpinnings could explain why late-stage patients are more prone to treatment refractoriness, progressive brain changes, and consequent cognitive and functioning impairment. This process is understood under the construct of neuroprogression, which refers to the pathological rewiring of the brain underlying the clinical and cognitive changes that underpin the staged progression of the illness, caused by activities of the aforementioned biological pathways. It is important to note that the brain can adapt to the challenges of the environment and respond to medications to ameliorate this process. Understanding the process of neuroprogression provides a window into the core biology of the disorder and opens the door to therapeutic approaches addressing these pathways. This book is an account of the state of the art in the field of neuroprogression in different psychiatric disorders.

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45

Kuno, Motoy. Synapse: Function, Plasticity, and Neurotrophism. Oxford University Press, USA, 1995.

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46

Skaper, Stephen D. Neurotrophic Factors: Methods and Protocols. Springer New York, 2018.

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47

Skaper, Stephen D. Neurotrophic Factors: Methods and Protocols. Springer New York, 2017.

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48

Duarte, Carlos B., and Enrico Tongiorgi. Brain-Derived Neurotrophic Factor (BDNF). Springer New York, 2019.

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49

Neurotrophic Factors Methods And Protocols. Humana Press, 2012.

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50

Skaper, Stephen D. Neurotrophic Factors: Methods and Protocols. Humana Press, 2016.

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