Persistence of Neuropsychologic Deficits in the Remitted State of Late-Life Depression

Bhalla, Rishi K.; Butters, Meryl A.; Mulsant, Benoit H.; Begley, Amy; Zmuda, Michelle; Schoderbek, Beth; Pollock, Bruce G.; Reynolds, Charles F.; Becker, James T.

doi:10.1097/01.jgp.0000203130.45421.69

Cited by 250 publications

(203 citation statements)

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“…or very mild impairment in MCDs (which may or may not include memory). In studies by Butters et al 19 and Bhalla et al,20 approximately one half of elderly depression patients (regardless of whether they were depressed or in remission) met cognitive criteria for MCI, with most of them exhibiting the MCI-MCD subtype. The National Alzheimer's Coordinating Center Uniform Data Set very recently implemented a new diagnostic system for use by Alzheimer Disease Research Centers, which contains 4 MCI subtypes that maximize the distinction between those who do and those who do not, have a deficit in episodic memory: (1) amnestic MCI-memory impairment only, (2) amnestic MCI-impairment in memory plus 1 or more other domains, (3) nonamnestic MCI-impairment in a single nonmemory domain, and (4) nonamnestic MCIimpairment in multiple nonmemory domains.…”

mentioning

confidence: 99%

Imaging Alzheimer Pathology in Late-Life Depression With PET and Pittsburgh Compound-B

Butters

Klunk²,

Mathis³

et al. 2008

Alzheimer Disease &Amp; Associated Disorders

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122

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There is increasing evidence for an empiric link between late-life depression and Alzheimer disease (AD). The neuropathology of AD, previously only confirmed at autopsy, may now be detectable in vivo using selective imaging ligands for β-amyloid. Positron emission tomography (PET) with [ 11 C] 6-OH-BTA-1 [Pittsburgh Compound-B (PiB)] has shown high tracer retention in cortical areas in patients with clinical diagnoses of probable AD and low retention in age-matched controls. We also previously reported variable PiB retention in patients with mild cognitive impairment (MCI). In this study, we used PiB-PET to evaluate whether amyloid is present in elders with treated major depression, many of whom have persistent cognitive impairment. We evaluated 9 subjects with remitted major depression [3M: 6F, mean (SD) age=71.8(5.7) y]. Seven of the 9 depressed subjects also met criteria for the diagnosis of MCI. PiB-PET data from healthy elders [n=8; mean (SD) age=71.5(3.0) y] were used for comparison. PET was acquired with arterial sampling and PiB retention was quantified using magnetic resonance imaging-guided cortical regions and graphical analysis of time-activity data; arterial line failure led to exclusion of 1 depressed subject. The data demonstrated variably elevated PiB retention. PiB retention in the 2 depressed subjects with normal cognitive ability was in the range of nondepressed cognitively normal subjects. PiB retention in 3 of the 6 depressed subjects with MCI fell in the range of subjects with AD. PiB retention in the remaining Reprints: Meryl A. Butters, PhD, Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, 3811 O'Hara St., Pittsburgh, PA 15213 (e-mail: buttersma@upmc.edu). Dr Reynolds receives research support (pharmaceutical supplies) from Glaxo Smith-Kline, Forest, Pfizer, Lilly, and Bristol Myers Squibb.GE Healthcare holds a license agreement with the University of Pittsburgh based on the technology described in this manuscript. Drs Klunk and Mathis are co-inventors of PiB and, as such, have a financial interest in this license agreement. GE Healthcare provided no grant support for this study and had no role in the design or interpretation of results or preparation of this manuscript. All other authors have no conflicts of interest with this work. Drs Butters, Meltzer, Klunk, Mathis, Price, and DeKosky as well as Mr Ziolko had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. The current study will extend these findings to perform the first in vivo human investigation of whether amyloid neuropathology is present in elders with major depression. NIH Public Access METHODS AND MATERIALS Subject SelectionWe studied a total of 9 subjects over age 65 with treated late-life major depression [3 men, 6 women; mean (SD) age=71.8 (5.7) y] ( Table 1). All of these subjects presented to a late-life depression clinic and remitted with escitalopram as part of a...

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mentioning

confidence: 99%

Imaging Alzheimer Pathology in Late-Life Depression With PET and Pittsburgh Compound-B

Butters

Klunk²,

Mathis³

et al. 2008

Alzheimer Disease &Amp; Associated Disorders

Self Cite

122

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“…Bhalla y colaboradores evaluaron prospectivamente 56 pacientes con depresión sin demencia, y luego al año, después del tratamiento cuando estuvieron en remisión. Ellos demostraron, que después de un año las áreas que permanecieron más frecuente y severamente afectadas fueron velocidad en el proceso de la informacion, función visuo-espacial y memoria retrasada (12). Sin embargo los estudios de comunidad no comparten los mismos hallazgos.…”

Section: Los Sintomas Cognitivos De Depresión De La Tercera Edadunclassified

Depresión en la tercera edad como factor de riesgo y su posible rol como pródromo de demencia

Custodio¹,

Herrera-Pérez²,

Lira³

et al. 2014

Rev Neuropsiquiatr

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Depresión y demencia, sobre todo enfermedad de Alzheimer (EA) son entidades críticas en la salud mental de la tercera edad. Ambas condiciones disminuyen la calidad de vida e incrementan el deterioro de actividades de vida diaria de individuos de la tercera edad. EA tiene pobre pronóstico al ser una enfermedad neurodegenerativa; mientras que la depresión es básicamente reversible. Los estudios de seguimiento longitudinal y de caso-control reportan una estrecha asociación entre depresión de inicio tardío y deterioro cognitivo progresivo, pues se ha demostrado riesgo de incremento en 2 a 5 veces para desarrollar demencia en pacientes con depresión de inicio tardío. Por otro lado, la depresión de inicio precoz ha demostrado en forma consistente ser también un factor de riesgo para demencia, y escasas probabilidades de ser pródromo de demencia.La naturaleza de la asociación (si depresión es un pródromo o consecuencia de demencia, o un factor de riesgo para desarrollar demencia) permanece aún sin ser esclarecida. Independiente de ello, las estrategias para tratar depresión podrían alterar el riesgo de desarrollar demencia.

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“…Furthermore, we predicted that (B) attention/processing speed would show the greatest degree of impairment, relative to scores for never-depressed control participants. Finally, based on previous work by our group demonstrating that executive functioning among older adults with depression improves after antidepressant treatment [13], we predicted that (C) participants in the depressed-euthymic group would perform better than participants in the currently depressed group on measures of executive functioning, but that (D) both depressed groups would perform worse on tests of executive functioning than never-depressed control participants [11].…”

Section: Introductionmentioning

confidence: 99%

“…In one study, 45% of individuals with LLD were cognitively impaired after one year of follow-up, and 94% of individuals with cognitive impairment at study baseline remained impaired one year later, despite reaching depression remission [13]. Others have similarly noted persistent cognitive impairment following treatment and/or remission of depressive symptoms [11,12,16,18,19], with certain risk factors, including lower baseline cognitive function, older age, later age of depression onset, and greater vascular burden associated with less improvement in specific cognitive domains [20].…”

Section: Introductionmentioning

confidence: 99%

“…The comparison of neuropsychological functioning in individuals during and after resolution of a major depressive episode suggests that a subset of LLD patients may exhibit an improvement in cognition following antidepressant treatment [12], but a significant proportion will continue to experience cognitive impairment following resolution of their depressive symptoms [11,[13][14][15][16][17]. In one study, 45% of individuals with LLD were cognitively impaired after one year of follow-up, and 94% of individuals with cognitive impairment at study baseline remained impaired one year later, despite reaching depression remission [13].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuropsychological Functioning in the Acute and Remitted States of Late-Life Depression

Koenig

DeLozier

Zmuda

et al. 2015

The American Journal of Geriatric Psychiatry

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Persistence of Neuropsychologic Deficits in the Remitted State of Late-Life Depression

Cited by 250 publications

References 56 publications

Imaging Alzheimer Pathology in Late-Life Depression With PET and Pittsburgh Compound-B

Imaging Alzheimer Pathology in Late-Life Depression With PET and Pittsburgh Compound-B

Depresión en la tercera edad como factor de riesgo y su posible rol como pródromo de demencia

Neuropsychological Functioning in the Acute and Remitted States of Late-Life Depression

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