Prognosis of Depression in Old Age Compared to Middle Age: A Systematic Review of Comparative Studies

Mitchell, Alex J.; Subramaniam, Hari

doi:10.1176/appi.ajp.162.9.1588

Cited by 279 publications

(174 citation statements)

References 76 publications

(80 reference statements)

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“…22 Successful diagnosis and treatment of LLD improves depressive symptoms and decreases suicide rates. 23 Despite the demonstrated effectiveness of treatment, many obstacles remain.…”

Section: Late-life Depression: Definition Extent Burden and Hopementioning

confidence: 99%

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

McKinney

Sibille

2013

The American Journal of Geriatric Psychiatry

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The phenomenological diagnosis of depression is successful in increasing diagnostic reliability, but it is a classification scheme without biological bases. One subtype of depression for which evidence suggests a unique biological basis is late-life depression (LLD), with first onset of symptoms after the age of 65. LLD is common and poses a significant burden on affected individuals, caretakers, and society. The pathophysiology of LLD includes disruptions of the neural network underlying mood, which can be conceptualized as the result of dysfunction in multiple underlying biological processes. Here, we briefly review current LLD hypotheses and then describe the characteristics of molecular brain aging and their overlap with disease processes. Further, we propose a new hypothesis for LLD, the Age-by-Disease Interaction hypothesis, which posits that the clinical presentation of LLD is the integrated output of specific biological processes that are pushed in LLD-promoting directions by changes in gene expression naturally occurring during brain aging, hence leading the brain to a physiological state that is more susceptible to LLD, since additional pushes by genetic, environmental and biochemical factors may now be sufficient to generate dysfunctional states that produce depressive symptoms. We put our propositions together into a decanalization model to aid in illustrating how age-related biological changes of the brain can shift the repertoire of available functional states in a pro-depression direction, and how additional factors can readily lead the system into distinct and stable maladaptive phenotypes, including LLD. This model brings together basic research on neuropsychiatric and neurodegenerative diseases more closely with the investigation of normal aging. Specifically, identifying biological processes affected during normal aging may inform the development of new interventions for the prevention and treatment of LLD.

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“…22 Successful diagnosis and treatment of LLD improves depressive symptoms and decreases suicide rates. 23 Despite the demonstrated effectiveness of treatment, many obstacles remain.…”

Section: Late-life Depression: Definition Extent Burden and Hopementioning

confidence: 99%

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

McKinney

Sibille

2013

The American Journal of Geriatric Psychiatry

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“…Once recovered from depressive symptoms, older people have a high risk of recurrence, with rates ranging between 15 and 50% (Hinrichsen and Hernandez, 1993;Little et al, 1996;Flint and Rifat, 1997;Kivela et al, 2000;Beekman et al, 2002). Recent studies revealed that older depressives have a higher risk of recurrence after recovery compared to younger adults (Mueller et al, 2004;Mitchell and Subramaniam, 2005). These prognosis data demonstrate the need to identify characteristics of older persons who are at high risk for recurrence.…”

Section: Introductionmentioning

confidence: 97%

“…The long-term prognosis for depression in later life has generally been considered mixed with only one quarter to one third of the patients robustly well at 1-3 years of follow-up (Murphy, 1983;Post et al, 1992;Cole et al, 1999;Beekman et al, 2002; for a review see Mitchell and Subramaniam, 2005). Once recovered from depressive symptoms, older people have a high risk of recurrence, with rates ranging between 15 and 50% (Hinrichsen and Hernandez, 1993;Little et al, 1996;Flint and Rifat, 1997;Kivela et al, 2000;Beekman et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Evidence for an association of the big five personality factors with recurrence of depressive symptoms in later life

Steunenberg

Braam

Beekman

et al. 2009

Int J Geriat Psychiatry

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SUMMARYObjectives Although it is well known that recurrence of late-life depression is very common, little is known about the characteristics of older people who are vulnerable for recurrence. In order to identify characteristics of those who are at risk, the present study aimed to investigate the strength of the associations of the big five personality factors with recurrence in later life. Secondly, we studied whether there are gender and age differences in the strength of these associations. Methods Using data from the longitudinal aging study Amsterdam (LASA) a subsample with clinically relevant depressive symptoms at one or more of the first three LASA-cycles, but who had recovered at the fourth cycle, was approached to participate in a fifth cycle to determine recurrence (n ¼ 92). Respondents completed self-report questionnaires on personality (NEO-FFI) and depression (CES-D). By means of logistic regression analyses the associations between the Big Five and recurrence of depression at fifth cycle was investigated. Results 58 (63%) had a recurrence of depressive symptoms. A high level of neuroticism was significantly associated with recurrence. No gender differences or age-related differences in strength of the associations of personality with recurrence were found. Conclusion In later life, neuroticism still is associated with the recurrence of depression. Efforts to prevent recurrence of late-life depression should focus on those with high levels of neuroticism and future research should aim at further unravelling the association between depression and personality in later life.

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“…While these psychotherapies have been shown to be effective in the treatment of LLD, as with medication treatments, a significant portion of individuals receiving treatment do not respond to these interventions (14, 23). Given the cognitive demands of psychotherapy and known associations between cognitive deficits and cortical atrophy in older adults (25, 26), as well as the impact of cortical atrophy on antidepressant treatment response (18, 27), there is compelling evidence to suggest that cortical atrophy may have a deleterious impact on psychotherapy treatment outcomes. Further, given recent findings of prominent reductions in right hemisphere cortical thickness associated with familial risk of depression; indices of cortical thickness may be a particularly sensitive phenotypic marker of psychotherapy treatment response in older adults.…”

Section: Introductionmentioning

confidence: 99%

Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

Mackin

Tosun

Mueller

et al. 2013

The American Journal of Geriatric Psychiatry

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Objective Cortical atrophy has been associated with late life depression (LLD) and recent findings suggest that reduced right hemisphere cortical thickness is associated with familial risk for major depressive disorder but cortical thickness abnormalities in LLD have not been explored. Further, cortical atrophy has been posited as a contributor to poor antidepressant treatment response in LLD but the impact of cortical thickness on psychotherapy response is unknown. This study was conducted to evaluate patterns of cortical thickness in LLD and in relation to psychotherapy treatment outcomes. Methods Participants included 22 individuals with LLD and 12 age matched comparison subjects. LLD participants completed 12 weeks of psychotherapy and treatment response was defined as a 50% reduction in depressive symptoms. All participants participated in Magnetic Resonance Imaging (MRI) of the brain and cortical mapping of grey matter tissue thickness was calculated. Results LLD individuals demonstrated thinner cortex than controls prominently in the right frontal, parietal, and temporal brain regions. Eleven participants (50%) exhibited positive psychotherapy response after 12 weeks of treatment. Psychotherapy non-responders demonstrated thinner cortex in bilateral posterior cingulate and parahippocampal cortices, left paracentral, precuneus, cuneus, and insular cortices, and the right medial orbito-frontal and lateral occipital cortices relative to treatment responders. Conclusions Our findings suggest more distributed right hemisphere cortical abnormalities in LLD than have been previously reported. Additionally, our findings suggest that reduced bilateral cortical thickness may be an important phenotypic marker of individuals at higher risk for poor response to psychotherapy.

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Prognosis of Depression in Old Age Compared to Middle Age: A Systematic Review of Comparative Studies

Cited by 279 publications

References 76 publications

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

Evidence for an association of the big five personality factors with recurrence of depressive symptoms in later life

Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

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