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Books on the topic 'Hypothalamic-pituitary-adrenal axis'

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Published: 4 June 2021
Last updated: 23 February 2023

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1

Print͡s︡ipy i mekhanizmy reguli͡a︡t͡s︡ii gipofizarno-adrenokortikalʹnoĭ sistemy. Leningrad: Izd-vo "Nauka," Leningradskoe otd-nie, 1987.

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2

Geer, Eliza B., ed. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45950-9.

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3

F, Schatzberg Alan, Nemeroff Charles B, and American College of Neuropsychopharmacology. Meeting, eds. The Hypothalamic-pituitary-adrenal axis: Physiology, pathophysiology, and psychiatric implications. New York: Raven Press, 1988.

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4

Arkadʹevich, Filaretov Anatoliĭ, Mezhdunarodnai͡a problemnai͡a komissii͡a "Intervist͡ser.", Institut fiziologii im. I.P. Pavlova., and Institut ėvoli͡ut͡sionnoĭ fiziologii i biokhimii im. I.M. Sechenova., eds. Mezhdunarodnyĭ simpozium Fiziologii͡a gipofizarno-adrenokortikalʹnoĭ sistemy, Leningrad, 1-4 okti͡abri͡a 1990 g.: Tezisy dokladov. Leningrad: Akademii͡a nauk SSSR, 1990.

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5

T, Podvigina T., and Filaretova L. P, eds. Adaptat͡s︡ii͡a︡ kak funkt͡s︡ii͡a︡ gipofizarno-adrenokortikalʹnoĭ sistemy. Sankt-Peterburg: "Nauka", 1994.

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6

C, Gaillard Rolf, ed. The ACTH axis: Pathogenesis, diagnosis, and treatment. Boston: Kluwer Academic Publishers, 2003.

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7

F, Ganong William, Dallman M. F, Roberts James Lewis 1951, Krieger Dorothy T, Herbert E. 1926-, and New York Academy of Sciences., eds. The Hypothalamic-pituitary-adrenal axis revisited: A symposium in honor of Dorothy Krieger and Edward Herbert. New York, N.Y: New York Academy of Sciences, 1987.

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8

Abebe, Getachew. The integrity of the hypothalamic-pituitary-adrenal axis in Boran (Bos indicus) cattle infected with Trypanosoma congolense. Uxbridge: Brunel University, 1991.

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9

de, Kloet E. R., Azmitia Efrain C, Landfield Philip W, and New York Academy of Sciences., eds. Brain corticosteroid receptors: Studies on the mechanism, function, and neurotoxicity of corticosteroid action. New York, N.Y: New York Academy of Sciences, 1994.

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10

Young, Allan H., and Mario F. Juruena. Hypothalamic–pituitary–adrenal axis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0006.

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Increased adrenocortical secretion of hormones, primarily cortisol in depression, is one of the most consistent findings in neuropsychiatry. The maintenance of the internal homeostatic state of an individual is facilitated by the ability to circulate glucocorticoids to exert negative feedback on the secretion of hypothalamic–pituitary–adrenal (HPA) hormones through binding to mineralocorticoid and glucocorticoid receptors, thus limiting the vulnerability to diseases related to psychological stress in genetically predisposed individuals. The HPA axis response to stress can be thought of as a crucial part of the organism’s response to stress: acute responses are generally adaptive, but excessive or prolonged responses can lead to deleterious effects. A spectrum of conditions may be associated with increased and prolonged activation of the HPA axis, including depression, poorly controlled diabetes mellitus, and metabolic syndrome. HPA axis dysregulation and hypercortisolaemia may further contribute to a hyperglycaemic or poorly controlled diabetic state.
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11

Hypothalamus-Pituitary-Adrenal Axis. Elsevier Science & Technology Books, 2008.

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12

Besedovsky, Hugo, Adriana Del Rey, and George Chrousos. Hypothalamus-Pituitary-Adrenal Axis. Elsevier Science & Technology Books, 2008.

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13

The Control of the hypothalamo-pituitary-adrenocortical axis. Madison, Conn: International Universities Press, 1989.

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14

Schatzberg, Alan F. The Hypothalamic-Pituitary-Adrenal Axis: Physiology, Pathophysiology, and Psychiatric Implications. Raven Pr, 1988.

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15

Geer, Eliza B. Hypothalamic-Pituitary-Adrenal Axis in Health and Disease: Cushing's Syndrome and Beyond. Springer, 2016.

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16

Gaillard, Rolf C. Acth Axis: Pathogenesis, Diagnosis and Treatment. Springer, 2013.

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17

Gaillard, Rolf C. Acth Axis: Pathogenesis, Diagnosis and Treatment. Springer London, Limited, 2012.

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18

McDonald, Sarah D. The effect of tobacco exposure on the fetal hypothalamic-pituitary-adrenal axis. 2006.

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19

McKerns, Kenneth W. Neuroendocrine Correlates of Stress. Springer, 2012.

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20

McKerns, Kenneth W. Neuroendocrine Correlates of Stress. Springer, 2012.

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21

Geer, Eliza B. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease: Cushing’s Syndrome and Beyond. Springer, 2018.

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22

Geer, Eliza B. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease: Cushing’s Syndrome and Beyond. Springer, 2016.

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23

Sikes, Carolyn R. Neuropsychological correlates of hypothalamic-pituitary-adrenocortical dysregulation in depression. 1988.

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24

Jeffray, Treena. The effects of cortisol on the development of the fetal hypothalamic-pituitary adrenal axis. 1999.

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25

Patisaul, Heather B., and Scott M. Belcher. The Neuroendocrine System and General Mechanisms of Endocrine Disruption. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0004.

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The neuroendocrine system is the interface between the endocrine and nervous systems. This chapter presents an overview of the neuroendocrine system and endogenous hormones, with a primary focus on the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid axis (HPT). The importance of impacts of exogenous compounds, both natural and man-made, on the neuroendocrine system is discussed, with a focus on endocrine-disruptive actions of plant-derived phytoestrogens and the role of the aryl hydrocarbon receptor as an environmental sensor. The impacts of EDCs on feed-forward and negative feedback regulation of neuroendocrine functions, including those mediated by estrogen, androgen, and thyroid pathways, as well as other less studied pathways of hormonal signaling that involve disruption of neurosteroids, peptide hormones, and adrenal hormone signaling are also presented.
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26

Ganong, William F., and Mary F. Dallman. Hypothalamic-Pituitary-Adrenal Axis Revisited: A Symposium in Honor of Dorothy Krieger and Edward Herbert (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1988.

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27

Effects of thymopentin on the responses of hypothalamic-pituitary-adrenal axis to a high intensity dynamic exercise protocol. 1993.

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28

Effects of thymopentin on the responses of hypothalamic-pituitary-adrenal axis to a high intensity dynamic exercise protocol. 1993.

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29

Effects of thymopentin on the responses of hypothalamic-pituitary-adrenal axis to a high intensity dynamic exercise protocol. 1993.

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30

Korpal, Manav. The impact of acute live-trapping stress on the hippocampal-hypothalamic-pituitary-adrenal axis of wild snowshoe hares (Lepus americanus). 2004.

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31

Lightman, Stafford. Can neurobiology explain the relationship between stress and disease? Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780198530343.003.0006.

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This chapter explores if neurobiology can explain the relationship between stress and disease. It considers if events that occurred early in life, perhaps during a period of prolonged stress, may affect biological processes, sometimes permanently, through changes in the midbrain neurotransmitter concentrations, the hypothalamic-pituitary-adrenal (HPA) axis, and the central nervous system (CNS). Animal models of stress are used to demonstrate these changes.
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32

(Editor), Efrain C. Azmitia, E. R. De Kloet (Editor), New York Academy of Sciences (Corporate Author), and Philip W. Landfield (Editor), eds. Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action (Annals of the New York Academy of). New York Academy of Sciences, 1995.

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33

K, Lüdecke Dieter, Chrousos George P, Tolis George, and International Symposium on Challenges of Hypersecretion: ACTH, Cushing's Syndrome, and Other Hypercortisolemic States (2nd : 1989 : Crete, Greece), eds. ACTH, Cushing's syndrome, and other hypercortisolemic states. New York: Raven Press, 1990.

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34

V, Everitt Arthur, and Walton Judie R. 1940-, eds. Regulation of neuroendocrine aging. Basel: Karger, 1988.

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35

Yang, James. Endocrine Disorders: Integrative Treatments of Hypothyroidism, Diabetes, and Adrenal Dysfunction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0014.

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Thyroid function, glucose metabolism, and an adaptive hypothalamic–pituitary–adrenal (HPA) axis are critical determinants of health and wellness. This chapter highlights the integrative physiology and interactions between these three systems and an integrative medicine approach to these conditions. Integrative medicine expands the evaluation of endocrine dysfunction through a person-centered approach. Patients’ overall symptoms and physiological function should be taken into account in evaluating thyroid function and planning treatment. Our approach to diabetes focuses on the importance of lifestyle changes and nutrition. Our perspective of the effects of chronic stress has been informed by current perspectives on neurobiology and neuroplasticity; chronic stress leaves its mark on the brain through changes in structure as well as its function in adapting to further stress. We present an integrative approach to manage and improve these three endocrine systems to address disease and improve patients’ energy and health.
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36

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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37

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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38

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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39

Pace-Schott, Edward F., and Samuel Gazecki. The Role of Stress in the Etiology of PTSD. Edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, and Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0012.

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This chapter reviews the biological features of stress and their correlation to symptoms of posttraumatic stress disorder (PTSD). Over the past 15 years, advances in understanding the neurobiology of stress and anxiety have revealed underlying neural abnormalities that might help explain why posttraumatic symptoms—intrusive memories or nightmares, avoidance of situations or stimuli associated with the event, persistent negativity of mood and cognition, and hyperarousal—persist in patients with PTSD. This chapter focuses on research that has discovered how abnormal hypothalamic-pituitary-adrenal axis activity, abnormalities of the catecholamingergic/autonomic system, and atypical physiologic and neural circuit responses during fear extinction recall may be important biological factors in the etiology and maintenance of PTSD symptoms.
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40

Murray-Close, Dianna, Nicole L. Breslend, and Leigh Ann Holterman. Psychophysiology Indicators of Relational Aggression. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190491826.003.0009.

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Mounting evidence implicates psychophysiological processes in the development of relational aggression. This review discusses the state of the field regarding associations between physiological stress systems—including the sympathetic nervous system, the parasympathetic nervous system, and the hypothalamic-pituitary-adrenal axis—and relational aggression. The theoretical significance of these processes is discussed, and potential moderators of associations, such as functions of relational aggression, contextual risk, and gender, are considered. Finally, critical next steps in this research area, including the incorporation of additional physiological indicators, are reviewed. This research has the potential to advance our understanding of many of the significant questions in relational aggression research, such as who engages in relational aggression and why, and whether these behaviors result in negative or positive developmental outcomes.
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41

Neyrinck, Arne P., Patrick Ferdinande, Dirk Van Raemdonck, and Marc Van de Velde. Donor organ management. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0034.

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Organ transplantation is the standard treatment modality for end-stage organ disease in selected cases. Two types of potential organ donors can be identified: the brain-dead ‘heart-beating donors’, referred to as DBD (donation after brain death), and the warm ischaemic ‘non-heart-beating donors’, referred to as DCD (donation after circulatory death). Brain death induces several physiological changes in the DBD donor. An autonomic storm is characterized by massive catecholamine release, followed by autonomic depletion during a vasoplegic phase. This is associated with several hormonal changes (suppression of vasopressin, the hypothalamic-pituitary-adrenal axis, and the hypothalamic-pituitary-thyroid axis) and an inflammatory response. These physiological changes form the basis of organ donor management, including cardiovascular stabilization and hormonal therapy (including vasopressin and analogues, thyroid hormone, and cortisol). Donor management is the continuation of critical care, with a shift towards individual organ stabilization. An aggressive approach to maximize organ yield is recommended; however, many treatment strategies need further investigation in large randomized trials. DCD donors have now evolved as a valid alternative to increase the potential donor pool and challenge the clinician with new questions. Optimal donor comfort therapy and end-of-life care are important to minimize the agonal phase. A strict approach towards the determination of death, based on cardiorespiratory criteria, is prerequisite. Novel strategies have been developed, using ex situ organ perfusion as a tool, to evaluate and recondition donor organs. They might become more important in the future to further optimize organ quality.
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42

Loewenstein, David A., Rosie E. Curiel, and Arlene Raffo. PTSD and Neurodegenerative Disorders. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0006.

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This chapter examines the potential effects of post-traumatic stress disorder (PTSD) on cognitive function, evaluates mechanisms that may mediate this relationship, determines the potential effects of PTSD on neurobiological systems such as the hypothalamic–pituitary–adrenal axis and different limbic and frontal lobe pathways, and discusses how this might be related to an increased risk for neurodegeneration. The chapter propose that associations and increased odds ratios associated with PTSD and dementia, while worthy of study, do not firmly establish a causative relationship between PTSD and dementia. The barriers to studying the associations between PTSD and dementia as they relate to causal mechanisms are also examined. Further research is needed, with more precise definitions, diagnostic rigor, and a focus on examining actual brain–behavior mechanisms that may shed light on potential causation.
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43

Greven, Corina U., Jennifer S. Richards, and Jan K. Buitelaar. Sex differences in ADHD. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198739258.003.0016.

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This chapter reviews sex differences in ADHD, focusing on differences in prevalence, comorbidity, and impairment, and discusses potential mechanisms underlying these differences. ADHD is more common in males than females (sex ratio ~3:1). Males with ADHD show greater comorbidity with comorbid externalizing (conduct) problems, while females with ADHD show internalizing problems. Females with ADHD may experience greater subjective impairment than males with ADHD. Referral and diagnostic issues, relating to sex-specific display of ADHD symptoms (more overt and disruptive in males, more subtle in females), underdiagnosis, or misdiagnosis in girls, as well as biases due to informant source, likely contribute to sex differences in ADHD. Potential biological mechanisms include endocrine factors (testosterone, glucocorticoids, and hypothalamic–pituitary–adrenal axis activation differences), aetiological sex differences (sex-chromosome genes), sex differences in neurocognitive functioning, and differences in brain structure and function. The chapter provides an outlook for future research and clinical implications.
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44

Post, Robert M. The Neurochemistry and Epigenetics of PTSD. Edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, and Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0014.

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This chapter reviews the neurochemistry and epigenetics of posttraumatic stress disorder (PTSD). Traditional views of the neurochemistry of PTSD focus on alterations in classical central nervous system neurotransmitters serotonin and norepinephrine and pathological reactivity in the hypothalamic-pituitary-adrenal axis, and these are only briefly noted here. Instead, the chapter emphasizes a series of new conceptualizations and neurochemical data that have recently been elucidated. One is the recognition of the symptoms and neurobiology of PTSD as a moving target, being very different in different stages of illness evolution. Differences are apparent in the neurochemistry involved in early life stressor-related vulnerabilities to PTSD, the acute stress reaction, compensation and resolution phases, or ongoing chronicity with sleep disturbance, nightmares, flashbacks, hyperarousal, and dulling and depression. The neurochemical abnormalities vary as a function of this temporal unfolding and the common acquisition and progression of comorbid syndromes of alcohol and substance abuse.
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45

Carvalho, André F., Gilberto S. Alves, Cristiano A. Köhler, and Roger S. McIntyre. Cognitive Enhancement in Major Depressive Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190214401.003.0010.

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Major depressive disorder (MDD) is a chronic and disabling illness often associated with elevated rates of non-recovery and substantial psychosocial burden. Cognitive impairment is a common residual manifestations of MDD. Overactivation of the hypothalamic–pituitary–adrenal axis, along with immune–inflammatory imbalances, a decrease in neurotrophin signaling, and an increase in oxidative and nitrosative stress, leads to neuroprogression and cognitive deterioration in MDD. “Cognitive remission” has been proposed as a novel treatment target for MDD. Cognitive remediation therapy has provided encouraging results for the management of cognitive deficits in MDD. The effects of standard antidepressant drugs on MDD-related cognitive dysfunction are often suboptimal, which calls for the development of novel agents with the potential to target cognitive impairments in MDD. The incorporation of biobehavioral strategies (e.g., exercise) and multimodal treatment approaches (e.g., cognitive training, antidepressant therapy, and neuromodulation) is more likely to generate therapeutic benefit.
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46

Mystakidou, Kyriaki, Irene Panagiotou, Efi Parpa, and Eleni Tsilika. Sleep disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0086.

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Sleep disturbances represent frequent distressing symptoms in the palliative care setting. The more common disorders include insomnia, excessive daytime sleepiness, and circadian rhythm sleep disorders. The most prevalent sleep disorder, insomnia, includes difficulty initiating and/or maintaining sleep, waking up too early, and non-restorative or poor quality sleep. Primary sleep disturbances are thought to be a disorder of hyperarousal, while a hypothalamic-pituitary-adrenal axis dysfunction has also been confirmed. Secondary sleep disorders have been associated with a large number of potential causes, both physical and psychological. Sleep disturbances in palliative care can be due to either the advanced disease and/or its treatment. Chronic medication use, neurological or psychiatric disorders, as well as environmental factors, can also present contributing factors. This chapter discusses the diagnosis and treatment of sleep disturbances, both pharmacological and non-pharmacological, including cognitive behavioural therapy, the cornerstone of non-pharmacological interventions.
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47

Yehuda, Rachel. Neuroendocrinology of PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0020.

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Initial studies on the neuroendocrine basis of post-traumatic stress disorder (PTSD) showed a biological dysregulation of stress response systems that appeared to be incompatible with the stress response theories that had prevailed when PTSD was first established as a diagnosis. Cortisol levels were found to be lower and catecholamine higher in patients with PTSD than in those with major depression and other psychiatric disorders. There was no explanation for why levels of two stress hormones that are generally correlated—cortisol and norepinephrine—would be different, and it was also not clear why cortisol levels would be on the low end of the normal spectrum, when the classic stress response paradigms suggested stress results in elevated cortisol. The study of neuroendocrinology and hypothalamic–pituitary–adrenal (HPA) axis alterations in PTSD provides an object lesson in how paradoxical observations might be pursued toward a better understanding of the pathophysiology of a disorder. This chapter reviews HPA findings in PTSD in cross-sectional and prospective longitudinal studies.
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48

Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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49

Jürimäe, Jaak. Hormones and training. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0033.

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Physical exercise regulates energy balance and is important to growth and maturation. These processes are regulated by the endocrine system. Endocrine mechanisms in the response to sport training include growth hormone-insulin-like growth factor-1 (GH-IGF-1), hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes, and peripheral markers of energy homeostasis. Physical performance is associated with anabolic adaptations of the GH-IGF-1 system in child athletes alongside spontaneous growth, while heavy training does not affect basal testosterone levels. In female adolescent athletes, the major factor altering reproductive hormone secretion is energy deficiency, rather than exercise stress or increase in exercise energy expenditure. Ghrelin is another indicator of energy imbalance across the menstrual cycle. Pubertal onset decreases ghrelin, and leptin levels are reduced and may remain unchanged between prepuberty and maturation in athletes. To better understand the influence of high training load on hormonal markers responsible for overall growth and energy homeostasis, growing athletes should be monitored often.
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Sloboda, Deborah M. The impact of prenatal glucocorticoid administration on the development and long term activity of the hypothalamic-pituitary-adrenal and metabolic axes. 2001.

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