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Książki na temat „Hypothalamic Pituitary Adrenal Axis (HPA)”

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Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

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

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2

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

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3

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

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4

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 Academy of Sciences, 1987.

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5

T, Podvigina T., та Filaretova L. P, ред. Adaptat͡s︡ii͡a︡ kak funkt͡s︡ii͡a︡ gipofizarno-adrenokortikalʹnoĭ sistemy. "Nauka", 1994.

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6

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

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7

Siller, Stefanie. Epigenetic modification of the hypothalamic-pituitary-adrenal axis during early life of the house sparrow (Passer domesticus). [publisher not identified], 2022.

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8

Banjanin, Sonja. Effects of repeated antenatal dexamethasone (dex) exposure on hypothalamic-pituitary-adrenal (HPA) function in mature adult guinea pigs (Cavis porcellus). National Library of Canada, 2003.

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9

Castro-Diehl, Olga Cecilia. Association of Sleep Duration and Quality with Activation of Two Neuroendocrine Systems: Hypothalamic-Pituitary-Adrenal Axis and Sympathetic Nervous System. The Multi-Ethnic Study of Atherosclerosis (MESA). [publisher not identified], 2016.

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10

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. Raven Press, 1990.

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11

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 cr

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12

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 environme

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13

Butler, Gary, and Jeremy Kirk. Adrenal gland disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199232222.003.0068.

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Physiology 236Adrenal insufficiency 238Adrenal steroid excess 246Further reading 247The adrenal cortex, which produces steroid hormones, is under the control of both the hypothalamo–pituitary–adrenal (HPA) endocrine axis, which regulates cortisol secretion, and the renin–angiotensin system, which regulates aldosterone secretion (Figs 8.1 and ...

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14

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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15

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 lif

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16

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 clea

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17

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

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18

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

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19

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 t

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20

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

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21

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

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22

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

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23

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

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24

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

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25

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

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26

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

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27

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

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28

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

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29

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

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30

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

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31

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

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32

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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33

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

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34

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

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35

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

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36

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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37

(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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38

Meaney, Michael J., and Rachel Yehuda. Epigenetic Mechanisms and the Risk for PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0017.

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This chapter discusses the epigenetic mechanisms involved in individual variation in and persistence of post-traumatic stress disorder (PTSD). Such mechanisms make it possible to trace vulnerability for PTSD to effects that predate development of PTSD. While some may be genetic in origin, others may involve parental stress occurring pre-conception, in utero changes in the maternal environment contributing to developmental programming, and childhood adversity, resulting in modifications of genes’ contribution to PTSD risk. The chapter discusses epigenetic alterations implicated in hypothalamic–

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39

Hodgkiss, Andrew. Psychiatric consequences of particular cancers. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0004.

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Certain tumour types can cause psychopathology through direct biological mechanisms such as metastatic spread to the brain, release of onconeuronal antibodies, ectopic hormone secretion, or release of pro-inflammatory cytokines. Lung cancers, adenocarcinoma of the pancreas, brain tumours, and ovarian tumours are considered in detail. Confusional states due to brain metastases, syndrome of inappropriate ADH secretion, hypercalcaemia of malignancy, and anti-Hu encephalitis are found in lung cancers. Severe depression, due to interleukin-6 release and its actions on the HPA axis and tryptophan me

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40

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 allocat

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41

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 allocat

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42

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 allocat

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43

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-adrena

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44

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 are

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45

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 (

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46

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

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47

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

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48

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 differ

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49

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 enc

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50

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 potenti

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