Is late onset depression a prodrome to dementia?

Schweitzer, Isaac; Tuckwell, Virginia; O’Brien, John T.; Ames, David

doi:10.1002/gps.525

Cited by 138 publications

(102 citation statements)

References 70 publications

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“…In addition, late-onset depression has been associated with more pronounced temporal lobe atrophy (Greenwald et al, 1997;Kumar et al, 1998) and hippocampal volume reductions (Steffens et al, 2000;Hickie et al, 2005), with specific genotypes possibly mediating this effect (Taylor et al, 2005). If these previous investigations are interpreted to be signs of different causes or risk factors for depression based on age at onset, greater splenium thinning in late-than early-onset depression might indeed point to more prominent atrophic or neurodegenerative processes in temporal connections, possibly reflecting higher risk for cognitive impairment and dementia conversion in the future (Geda et al, 2006;Salloway et al, 1996;Schweitzer et al, 2002;van Ojen et al, 1995). Indeed, regionally specific posterior callosal atrophy has been reported in mild Alzheimer's disease (Lyoo et al, 1997;Wang et al, 2006;Yamauchi et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…This subgroup, frequently referred to as having late-onset depression, exhibits certain unique clinical, biological, and neuroimaging characteristics (Burvill et al, 1989;Heun et al, 2000;Krishnan et al, 1995Krishnan et al, , 1997Schweitzer et al, 2002), implying that late-onset depression may represent a distinct subtype of depression in the elderly. Along with observations of greater cognitive deficits (Salloway et al, 1996) and an increased risk of dementia conversion (Geda et al, 2006;Schweitzer et al, 2002), there is some evidence that patients with late-onset depression may have more pronounced atrophy in cortical and subcortical regions implicated in the pathophysiology of elderly depression (Almeida et al, 2002;Hickie et al, 2005;Steffens et al, 2000). Using traditional volumetric region of interest analyses and computational cortical mapping methods, we previously found complex structural changes in frontal and temporo-parietal brain regions, which may point to differential patterns of atrophic or neurodegenerative processes that may be influenced by age at illness onset (Ballmaier et al, 2004a, b, c).…”

Section: Introductionmentioning

confidence: 99%

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Mapping Callosal Morphology in Early- and Late-Onset Elderly Depression: An Index of Distinct Changes in Cortical Connectivity

Ballmaier

Kumar

Elderkin‐Thompson

et al. 2007

Neuropsychopharmacol

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There is some evidence of corpus callosum abnormalities in elderly depression, but it is not known whether these deficits are regionspecific or differ based on age at onset of depression. Twenty-four patients with early-onset depression (mean age ¼ 68.00, SD75.83), 22 patients with late-onset depression (mean age ¼ 74.50, SD78.09) and 34 elderly control subjects (mean age ¼ 72.38; SD76.93) were studied. Using 3D MRI data, novel mesh-based geometrical modeling methods were applied to compare the midsagittal thickness of the corpus callosum at high spatial resolution between groups. Neuropsychological correlates of midsagittal callosal area differences were additionally investigated in a subsample of subjects. Depressed patients exhibited significant callosal thinning in the genu and splenium compared to controls. Significant callosal thinning was restricted to the genu in early-onset patients, but patients with late-onset depression exhibited significant callosal thinning in both the genu and splenium relative to controls. The splenium of the corpus callosum was also significantly thinner in subjects with late-vs early-onset depression. Genu and splenium midsagittal areas significantly correlated with memory and attention functioning among late-onset depressed patients, but not early-onset depressed patients or controls. Circumscribed structural alterations in callosal morphology may distinguish late-from early-onset depression in the elderly. These findings suggest distinct abnormalities of cortical connectivity in late-and early-onset elderly depression with possible influence on the course of illness. Patients with a late onset of depression may be at higher risk of illness progression and eventually dementia conversion than earlyonset depression, with potentially important implications for research and therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mapping Callosal Morphology in Early- and Late-Onset Elderly Depression: An Index of Distinct Changes in Cortical Connectivity

Ballmaier

Kumar

Elderkin‐Thompson

et al. 2007

Neuropsychopharmacol

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“…Além disso, na depressão de início tardio há maior prevalência de transtornos demenciais 12,13 , presença de atrofia cortical e/ou lesões profundas em substância branca, maior aumento dos ventrículos cerebrais bilaterais 14 e menor resposta terapêutica a antidepressivo 15 . Em anos recentes, tem começado a ficar clara também a associação entre fatores de risco cardiovascular e desenvolvimento de depressão e déficit cognitivo 12,16,17 .…”

Section: Depressão De Início Tardio Versus Depressão De Início Precoceunclassified

Depressão e infarto agudo do miocárdio

Alves¹,

Fráguas²,

Wajngarten³

2009

Rev. psiquiatr. clín.

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ResumoA associação entre transtorno depressivo maior e doenças cardiovasculares, em particular infarto agudo do miocár-dio, é frequente, levando a pior prognóstico tanto da depressão como da doença cardiovascular, com maiores taxas de reinfarto e maior morbidade e mortalidade. Os autores discutem as evidências na literatura que demonstram essa associação entre infarto agudo do miocárdio e quadros depressivos, com enfoque nos avanços em fisiopatologia e terapêutica psiquiátrica. Vários estudos têm mostrado que o tratamento da depressão associada a quadros cardíacos é eficaz, melhora a qualidade de vida e pode ser feito com segurança. Embora o tratamento da depressão tenha sido associado à melhora de alguns parâmetros cardiovasculares, ainda não existem, entretanto, evidências de associação entre tratamento da depressão e melhora da morbidade e mortalidade cardiovascular.Alves TCTF, et al. / Rev Psiq Clín. 2009;36(3):88-92 Palavras-chave: Depressão, infarto agudo do miocárdio, fisiopatologia, prognóstico. AbstractThe association between major depressive disorder and cardiovascular diseases, particularly myocardial infarction, is frequently observed, leading to worse prognosis both on the depressive disorder as well as cardiovascular disease, with increased rates of re-infarction and both morbidity and mortality. The authors review and discuss the evidence in the literature that supports the relationship between depressive disorder and cardiovascular disease, with focus on the advances on the physiopathology and the psychiatric management. Various studies have shown that treatment of depression is efficacious, improves quality of life and can be safely conducted. Although, treatment of depression has been associated with improvement on some cardiovascular parameters, there is no evidence so far that treatment of depression is associated with decrease of cardiovascular morbidity and mortality.Alves TCTF, et al. / Rev Psiq Clín. 2009;36(3):88-92

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“…Dementia in together with major depression may not completely reverse as the depression subsides [12]. Patients with late onset major depression with cognitive impairment are especially at risk of developing Alzheimer"s disease(AD), with as many as 40% developing dementia within three to five years [13,14]. Among other neurological disorders the incidence of major depression is highest among stroke patients (20-25%) and intermediate among those with Parkinson"s disease (15-20%) compared to 10-15% among those with AD [15,16].…”

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confidence: 99%