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An Integrated Assessment of Changes in Brain Structure and Function among Older Adults with Major Depressive Disorder or Mild Cognitive Impairment.

Record Type:	Electronic resources : Monograph/item
Title/Author:	An Integrated Assessment of Changes in Brain Structure and Function among Older Adults with Major Depressive Disorder or Mild Cognitive Impairment./
Author:	Rashidi-Ranjbar, Neda.
Description:	1 online resource (233 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 84-06, Section: B.
Contained By:	Dissertations Abstracts International84-06B.
Subject:	Neurosciences. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29212497click for full text (PQDT)
ISBN:	9798357553331

An Integrated Assessment of Changes in Brain Structure and Function among Older Adults with Major Depressive Disorder or Mild Cognitive Impairment.
Rashidi-Ranjbar, Neda.

An Integrated Assessment of Changes in Brain Structure and Function among Older Adults with Major Depressive Disorder or Mild Cognitive Impairment. - 1 online resource (233 pages)

Source: Dissertations Abstracts International, Volume: 84-06, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2022.

Includes bibliographical references

Major Depressive Disorder (MDD) has been associated with an increased risk of developing dementia. In 2008 Butters et al. proposed a mechanistic model by which late-life depression (LLD) may increase the risk for Alzheimer's disease (AD) consisting of: I) a vascular hypothesis, i.e., structural damage to frontal-executive circuit, II) an inflammation hypothesis, i.e., a high level of stress hormones in depression can lead to hippocampal volume loss (i.e., corticolimbic circuit).In study 1, we conducted a systematic review between 2008 and October 2018 to evaluate the evidence for the conceptual mechanistic model, focusing on frontal-executive and corticolimbic circuits in LLD. Findings from this study revealed inconsistent evidence of alterations in these circuits in LLD (compared to healthy controls; HC). In study 2 and study 3, we assessed structural and functional brain alterations of frontal-executive (i.e., ECN) and corticolimbic (i.e., DMN) circuits in five groups of older adults putatively at-risk for developing dementia: remitted depression with normal cognition (MDD-NC), non-amnestic MCI (naMCI), remitted MDD+naMCI, amnestic MCI (aMCI), and remitted MDD+aMCI. We also examined non-psychiatric HC and individuals with AD. We hypothesized that structural (via T1-weighted imaging & diffusion-weighted imaging) and functional (via resting-state-fMRI) alterations of frontal-executive (i.e., ECN) and corticolimbic (i.e., DMN) circuits would be present among these seven groups of older individuals, with the degree of alterations ranked according to the expected degree of risk for AD. Findings from these studies were contrary to our hypotheses: older individuals with remitted MDD did not show early signs of structural or functional neural alterations in the frontal-executive (i.e., ECN) or corticolimbic (i.e., DMN) circuits associated with preclinical AD. Therefore, remission from depression may protect from the risk of developing AD conferred by depressionTaken together, our findings did not fully support the mechanistic 'multiple pathways model' linking depression and dementia. In contrast, our findings suggested that treating depression to remission in older adults could potentially reduce the likelihood of developing AD. Future large longitudinal studies should investigate differences in age of onset of depression, treatment-responsiveness, and the effects of antidepressant treatment in relation to risk of developing AD or dementia.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2023

Mode of access: World Wide Web

ISBN: 9798357553331Subjects--Topical Terms:

588700
Neurosciences.
Subjects--Index Terms:

Alzheimer's diseaseIndex Terms--Genre/Form:

542853
Electronic books.

An Integrated Assessment of Changes in Brain Structure and Function among Older Adults with Major Depressive Disorder or Mild Cognitive Impairment.
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500 $a Advisor: Voineskos, Aristotle.
502 $a Thesis (Ph.D.)--University of Toronto (Canada), 2022.
504 $a Includes bibliographical references
520 $a Major Depressive Disorder (MDD) has been associated with an increased risk of developing dementia. In 2008 Butters et al. proposed a mechanistic model by which late-life depression (LLD) may increase the risk for Alzheimer's disease (AD) consisting of: I) a vascular hypothesis, i.e., structural damage to frontal-executive circuit, II) an inflammation hypothesis, i.e., a high level of stress hormones in depression can lead to hippocampal volume loss (i.e., corticolimbic circuit).In study 1, we conducted a systematic review between 2008 and October 2018 to evaluate the evidence for the conceptual mechanistic model, focusing on frontal-executive and corticolimbic circuits in LLD. Findings from this study revealed inconsistent evidence of alterations in these circuits in LLD (compared to healthy controls; HC). In study 2 and study 3, we assessed structural and functional brain alterations of frontal-executive (i.e., ECN) and corticolimbic (i.e., DMN) circuits in five groups of older adults putatively at-risk for developing dementia: remitted depression with normal cognition (MDD-NC), non-amnestic MCI (naMCI), remitted MDD+naMCI, amnestic MCI (aMCI), and remitted MDD+aMCI. We also examined non-psychiatric HC and individuals with AD. We hypothesized that structural (via T1-weighted imaging & diffusion-weighted imaging) and functional (via resting-state-fMRI) alterations of frontal-executive (i.e., ECN) and corticolimbic (i.e., DMN) circuits would be present among these seven groups of older individuals, with the degree of alterations ranked according to the expected degree of risk for AD. Findings from these studies were contrary to our hypotheses: older individuals with remitted MDD did not show early signs of structural or functional neural alterations in the frontal-executive (i.e., ECN) or corticolimbic (i.e., DMN) circuits associated with preclinical AD. Therefore, remission from depression may protect from the risk of developing AD conferred by depressionTaken together, our findings did not fully support the mechanistic 'multiple pathways model' linking depression and dementia. In contrast, our findings suggested that treating depression to remission in older adults could potentially reduce the likelihood of developing AD. Future large longitudinal studies should investigate differences in age of onset of depression, treatment-responsiveness, and the effects of antidepressant treatment in relation to risk of developing AD or dementia.
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