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  1. Article ; Online: Post-COVID dysautonomias: what we know and (mainly) what we don't know.

    Goldstein, David S

    Nature reviews. Neurology

    2024  Volume 20, Issue 2, Page(s) 99–113

    Abstract: Following on from the COVID-19 pandemic is another worldwide public health challenge that is referred to variously as long COVID, post-COVID syndrome or post-acute sequelae of SARS-CoV-2 infection (PASC). PASC comes in many forms and affects all body ... ...

    Abstract Following on from the COVID-19 pandemic is another worldwide public health challenge that is referred to variously as long COVID, post-COVID syndrome or post-acute sequelae of SARS-CoV-2 infection (PASC). PASC comes in many forms and affects all body organs. This heterogeneous presentation suggests involvement of the autonomic nervous system (ANS), which has numerous roles in the maintenance of homeostasis and coordination of responses to various stressors. Thus far, studies of ANS dysregulation in people with PASC have been largely observational and descriptive, based on symptom inventories or objective but indirect measures of cardiovascular function, and have paid little attention to the adrenomedullary, hormonal and enteric nervous components of the ANS. Such investigations do not consider the syndromic nature of autonomic dysfunction. This Review provides an update on the literature relating to ANS abnormalities in people with post-COVID syndrome and presents a theoretical perspective on how the ANS might participate in common features of PASC.
    MeSH term(s) Humans ; Post-Acute COVID-19 Syndrome ; Pandemics ; COVID-19 ; SARS-CoV-2 ; Autonomic Nervous System Diseases ; Disease Progression
    Language English
    Publishing date 2024-01-11
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Intramural
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-023-00917-9
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  2. Article: Linking the Extended Autonomic System with the Homeostat Theory: New Perspectives about Dysautonomias.

    Goldstein, David S

    Journal of personalized medicine

    2024  Volume 14, Issue 1

    Abstract: Dysautonomias are conditions in which altered functions of one or more components of the autonomic nervous system (ANS) adversely affect health. This essay is about how elucidating mechanisms of dysautonomias may rationalize personalized treatments. ... ...

    Abstract Dysautonomias are conditions in which altered functions of one or more components of the autonomic nervous system (ANS) adversely affect health. This essay is about how elucidating mechanisms of dysautonomias may rationalize personalized treatments. Emphasized here are two relatively new ideas-the "extended" autonomic system (EAS) and the "homeostat" theory as applied to the pathophysiology and potential treatments of dysautonomias. The recently promulgated concept of the EAS updates Langley's ANS to include neuroendocrine, immune/inflammatory, and central components. The homeostat theory builds on Cannon's theory of homeostasis by proposing the existence of comparators (e.g., a thermostat, glucostat, carbistat, barostat) that receive information about regulated variables (e.g., core temperature, blood glucose, blood gases, delivery of blood to the brain). Homeostats sense discrepancies between the information and response algorithms. The presentation links the EAS with the homeostat theory to understand pathophysiological mechanisms of dysautonomias. Feed-forward anticipatory processes shift input-output curves and maintain plateau levels of regulated variables within different bounds of values-"allostasis". Sustained allostatic processes increase long-term wear-and-tear on effectors and organs-allostatic load. They decreaseing thresholds for destabilizing and potentially fatal positive feedback loops. The homeostat theory enables mathematical models that define stress, allostasis, and allostatic load. The present discussion applies the EAS and homeostat concepts to specific examples of pediatric, adolescent/adult, and geriatric dysautonomias-familial dysautonomia, chronic orthostatic intolerance, and Lewy body diseases. Computer modeling has the potential to take into account the complexity and dynamics of allostatic processes and may yield testable predictions about individualized treatments and outcomes.
    Language English
    Publishing date 2024-01-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662248-8
    ISSN 2075-4426
    ISSN 2075-4426
    DOI 10.3390/jpm14010123
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  3. Article ; Online: Stress and the autonomic nervous system.

    Goldstein, David S

    Autonomic neuroscience : basic & clinical

    2023  Volume 247, Page(s) 103096

    MeSH term(s) Autonomic Nervous System/physiology ; Stress, Psychological ; Allostasis/physiology ; Stress, Physiological/physiology
    Language English
    Publishing date 2023-05-10
    Publishing country Netherlands
    Document type Editorial ; Research Support, N.I.H., Intramural
    ZDB-ID 2020105-9
    ISSN 1872-7484 ; 1566-0702
    ISSN (online) 1872-7484
    ISSN 1566-0702
    DOI 10.1016/j.autneu.2023.103096
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  4. Article ; Online: Extra-cranial cholinergic lesions in dementia with Lewy bodies.

    Goldstein, David S

    Brain : a journal of neurology

    2023  Volume 147, Issue 1, Page(s) 10–11

    MeSH term(s) Humans ; Lewy Body Disease/pathology ; Lewy Bodies/pathology ; Pancreas/pathology ; Cholinergic Agents ; Colon/pathology
    Chemical Substances Cholinergic Agents
    Language English
    Publishing date 2023-12-07
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awad408
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  5. Article ; Online: Is postural tachycardia syndrome a psychogenic disorder?

    Goldstein, David S

    Brain : a journal of neurology

    2022  Volume 145, Issue 11, Page(s) e105–e106

    MeSH term(s) Humans ; Postural Orthostatic Tachycardia Syndrome/diagnosis ; Somatoform Disorders ; Fear
    Language English
    Publishing date 2022-09-21
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awac345
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  6. Article ; Online: Correction to: Baroreflex‑sympathoneural dysfunction characterizes at‑risk individuals with preclinical central Lewy body diseases.

    Goldstein, David S / Sharabi, Yehonatan

    Clinical autonomic research : official journal of the Clinical Autonomic Research Society

    2023  Volume 33, Issue 1, Page(s) 79

    Language English
    Publishing date 2023-02-01
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 1080007-4
    ISSN 1619-1560 ; 0959-9851
    ISSN (online) 1619-1560
    ISSN 0959-9851
    DOI 10.1007/s10286-022-00917-7
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  7. Article ; Online: Stress and the "extended" autonomic system.

    Goldstein, David S

    Autonomic neuroscience : basic & clinical

    2021  Volume 236, Page(s) 102889

    Abstract: This review updates three key concepts of autonomic neuroscience-stress, the autonomic nervous system (ANS), and homeostasis. Hans Selye popularized stress as a scientific idea. He defined stress variously as a stereotyped response pattern, a state that ... ...

    Abstract This review updates three key concepts of autonomic neuroscience-stress, the autonomic nervous system (ANS), and homeostasis. Hans Selye popularized stress as a scientific idea. He defined stress variously as a stereotyped response pattern, a state that evokes this pattern, or a stimulus that evokes the state. According to the "homeostat" theory stress is a condition where a comparator senses a discrepancy between sensed afferent input and a response algorithm, the integrated error signal eliciting specific patterns of altered effector outflows. Scientific advances since Langley's definition of the ANS have incited the proposal here of the "extended autonomic system," or EAS, for three reasons. (1) Several neuroendocrine systems are bound inextricably to Langley's ANS. The first to be described, by Cannon in the early 1900s, involves the hormone adrenaline, the main effector chemical of the sympathetic adrenergic system. Other neuroendocrine systems are the hypothalamic-pituitary-adrenocortical system, the arginine vasopressin system, and the renin-angiotensin-aldosterone system. (2) An evolving body of research links the ANS complexly with inflammatory/immune systems, including vagal anti-inflammatory and catecholamine-related inflammasomal components. (3) A hierarchical network of brain centers (the central autonomic network, CAN) regulates ANS outflows. Embedded within the CAN is the central stress system conceptualized by Chrousos and Gold. According to the allostasis concept, homeostatic input-output curves can be altered in an anticipatory, feed-forward manner; and prolonged or inappropriate allostatic adjustments increase wear-and-tear (allostatic load), resulting in chronic, stress-related, multi-system disorders. This review concludes with sections on clinical and therapeutic implications of the updated concepts offered here.
    MeSH term(s) Allostasis ; Autonomic Nervous System ; Homeostasis ; Humans ; Male ; Stress, Physiological ; Vagus Nerve
    Language English
    Publishing date 2021-10-02
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 2020105-9
    ISSN 1872-7484 ; 1566-0702
    ISSN (online) 1872-7484
    ISSN 1566-0702
    DOI 10.1016/j.autneu.2021.102889
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  8. Article ; Online: The Catecholaldehyde Hypothesis for the Pathogenesis of Catecholaminergic Neurodegeneration: What We Know and What We Do Not Know.

    Goldstein, David S

    International journal of molecular sciences

    2021  Volume 22, Issue 11

    Abstract: 3,4-Dihydroxyphenylacetaldehyde (DOPAL) is the focus of the catecholaldehyde hypothesis for the pathogenesis of Parkinson's disease and other Lewy body diseases. The catecholaldehyde is produced via oxidative deamination catalyzed by monoamine oxidase ( ... ...

    Abstract 3,4-Dihydroxyphenylacetaldehyde (DOPAL) is the focus of the catecholaldehyde hypothesis for the pathogenesis of Parkinson's disease and other Lewy body diseases. The catecholaldehyde is produced via oxidative deamination catalyzed by monoamine oxidase (MAO) acting on cytoplasmic dopamine. DOPAL is autotoxic, in that it can harm the same cells in which it is produced. Normally, DOPAL is detoxified by aldehyde dehydrogenase (ALDH)-mediated conversion to 3,4-dihydroxyphenylacetic acid (DOPAC), which rapidly exits the neurons. Genetic, environmental, or drug-induced manipulations of ALDH that build up DOPAL promote catecholaminergic neurodegeneration. A concept derived from the catecholaldehyde hypothesis imputes deleterious interactions between DOPAL and the protein alpha-synuclein (αS), a major component of Lewy bodies. DOPAL potently oligomerizes αS, and αS oligomers impede vesicular and mitochondrial functions, shifting the fate of cytoplasmic dopamine toward the MAO-catalyzed formation of DOPAL-destabilizing vicious cycles. Direct and indirect effects of DOPAL and of DOPAL-induced misfolded proteins could "freeze" intraneuronal reactions, plasticity of which is required for neuronal homeostasis. The extent to which DOPAL toxicity is mediated by interactions with αS, and vice versa, is poorly understood. Because of numerous secondary effects such as augmented spontaneous oxidation of dopamine by MAO inhibition, there has been insufficient testing of the catecholaldehyde hypothesis in animal models. The clinical pathophysiological significance of genetics, emotional stress, environmental agents, and interactions with numerous proteins relevant to the catecholaldehyde hypothesis are matters for future research. The imposing complexity of intraneuronal catecholamine metabolism seems to require a computational modeling approach to elucidate clinical pathogenetic mechanisms and devise pathophysiology-based, individualized treatments.
    MeSH term(s) Aldehyde Dehydrogenase/genetics ; Aldehydes/metabolism ; Animals ; Catechols/metabolism ; Dopamine/metabolism ; Humans ; Monoamine Oxidase/genetics ; Monoamine Oxidase/metabolism ; Monoamine Oxidase Inhibitors/therapeutic use ; Nerve Degeneration/genetics ; Nerve Degeneration/pathology ; Neurons/metabolism ; Neurons/pathology ; Oxidation-Reduction ; PC12 Cells ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Rats ; alpha-Synuclein/genetics
    Chemical Substances Aldehydes ; Catechols ; Monoamine Oxidase Inhibitors ; alpha-Synuclein ; Aldehyde Dehydrogenase (EC 1.2.1.3) ; Monoamine Oxidase (EC 1.4.3.4) ; catechol (LF3AJ089DQ) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2021-06-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22115999
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  9. Article ; Online: The possible association between COVID-19 and postural tachycardia syndrome.

    Goldstein, David S

    Heart rhythm

    2020  Volume 18, Issue 4, Page(s) 508–509

    MeSH term(s) Baroreflex ; COVID-19 ; Heart Rate ; Humans ; Postural Orthostatic Tachycardia Syndrome/diagnosis ; SARS-CoV-2
    Language English
    Publishing date 2020-12-11
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2020.12.007
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  10. Book: Adrenaline and the inner world

    Goldstein, David S.

    an introduction to scientific integrative medicine

    2006  

    Author's details David S. Goldstein
    Keywords Epinephrine / physiology ; Autonomic Nervous System / physiology ; Stress / physiopathology ; Autonomic Nervous System Diseases
    Language English
    Size XIV, 309 S. : Ill., graph. Darst.
    Publisher Johns Hopkins Univ. Press
    Publishing place Baltimore
    Publishing country United States
    Document type Book
    HBZ-ID HT014704735
    ISBN 0-8018-8289-3 ; 0-8018-8288-5 ; 978-0-8018-8289-0 ; 978-0-8018-8288-3
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2006 A 3027 order for loan Magazin

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