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Biological Mechanisms Linking Stress and Anhedonia.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Biological Mechanisms Linking Stress and Anhedonia./
Author:	Stanton, Colin Ho-Ming.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
Description:	183 p.
Notes:	Source: Dissertations Abstracts International, Volume: 83-08, Section: B.
Contained By:	Dissertations Abstracts International83-08B.
Subject:	Clinical psychology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28720703
ISBN:	9798790635410

Biological Mechanisms Linking Stress and Anhedonia.
Stanton, Colin Ho-Ming.

Biological Mechanisms Linking Stress and Anhedonia. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 183 p.

Source: Dissertations Abstracts International, Volume: 83-08, Section: B.

Thesis (Ph.D.)--Yale University, 2021.

This item must not be sold to any third party vendors.

Evidence from research across species suggests that stress exposure is linked with anhedonia (loss of pleasure and/or decreased motivation). However, the mechanisms through which stress might impact anhedonia remain unclear. Chapters 1 and 2 of this dissertation review putative etiological pathways from stress to anhedonia and discuss stressor characteristics that could inform experimental models of stress-induced anhedonia. Chapter 3 describes an attempt to identify which types of stress are most associated with anhedonia using stress interview data from multiple datasets. Unexpectedly, we found no credible effects on anhedonic symptoms for stressor chronicity, severity, dependence on behavior, or interpersonal focus. Instead, number of stressors endorsed was the best predictor of anhedonic symptoms. Next, Chapters 4 and 5 report on two studies that tested possible biological mediators of the stress-anhedonia link. Chapter 4 describes an analysis of the UK Biobank dataset aimed at evaluating frontostriatal functional connectivity as a mechanism of stress-induced anhedonia. Although stress exposure predicted anhedonia, analyses uncovered no stable relation between frontostriatal connectivity and anhedonia, and no support for the proposed mediation model. Chapter 5 details a study that implemented a laboratory-based stressor to assess its potential impact on motivated behavior (thought to be a key component of anhedonia), and whether any such effects might be mediated by inflammatory responding. Low concentrations of salivary cytokines suggested questionable validity of inflammatory assessment, and no effect of stress on inflammatory responding was observed. Additionally, stress produced no measurable changes in motivated behavior. Thus, analyses revealed no evidence consistent with inflammation as a mechanism of stress-induced anhedonia. Finally, Chapter 6 discusses conclusions and implications of the current findings, and provides ideas for future directions.

ISBN: 9798790635410Subjects--Topical Terms:

524863
Clinical psychology.
Subjects--Index Terms:

Biological mechanism

Biological Mechanisms Linking Stress and Anhedonia.
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300 $a 183 p.
500 $a Source: Dissertations Abstracts International, Volume: 83-08, Section: B.
500 $a Advisor: Joormann, Jutta.
502 $a Thesis (Ph.D.)--Yale University, 2021.
506 $a This item must not be sold to any third party vendors.
520 $a Evidence from research across species suggests that stress exposure is linked with anhedonia (loss of pleasure and/or decreased motivation). However, the mechanisms through which stress might impact anhedonia remain unclear. Chapters 1 and 2 of this dissertation review putative etiological pathways from stress to anhedonia and discuss stressor characteristics that could inform experimental models of stress-induced anhedonia. Chapter 3 describes an attempt to identify which types of stress are most associated with anhedonia using stress interview data from multiple datasets. Unexpectedly, we found no credible effects on anhedonic symptoms for stressor chronicity, severity, dependence on behavior, or interpersonal focus. Instead, number of stressors endorsed was the best predictor of anhedonic symptoms. Next, Chapters 4 and 5 report on two studies that tested possible biological mediators of the stress-anhedonia link. Chapter 4 describes an analysis of the UK Biobank dataset aimed at evaluating frontostriatal functional connectivity as a mechanism of stress-induced anhedonia. Although stress exposure predicted anhedonia, analyses uncovered no stable relation between frontostriatal connectivity and anhedonia, and no support for the proposed mediation model. Chapter 5 details a study that implemented a laboratory-based stressor to assess its potential impact on motivated behavior (thought to be a key component of anhedonia), and whether any such effects might be mediated by inflammatory responding. Low concentrations of salivary cytokines suggested questionable validity of inflammatory assessment, and no effect of stress on inflammatory responding was observed. Additionally, stress produced no measurable changes in motivated behavior. Thus, analyses revealed no evidence consistent with inflammation as a mechanism of stress-induced anhedonia. Finally, Chapter 6 discusses conclusions and implications of the current findings, and provides ideas for future directions.
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