Cognitive Impairment In Late-life Depression Research Articles

Chemosensory anhedonia facilitates depressive symptoms and cognitive impairment in late-life depression.

Chemosensory anhedonia refers to the lack of hedonic ability to experience pleasure through the senses of smell and taste, which reduces the pleasure and comfort of food, and increases the risk of nutritional and immune deficiencies. However, there is no direct scientific evidence regarding chemosensory anhedonia in patients with late-life depression (LLD). The aim of this study was to investigate chemosensory anhedonia in patients with LLD, and its potential association with depressive symptoms and cognitive function. A total of 114 patients with LLD and 92 normal controls were included in this study. They experienced clinical assessment, Chemosensory Pleasure Scale assessment, 17-item Hamilton Depression Rating Scale assessment and cognitive assessments, which contain the Verbal Fluency Test. The associations between chemosensory pleasure and depressive symptoms or cognitive function in patients with LLD were explored using partial correlation analysis and mediation analysis. The Chemosensory Pleasure Scale scores were lower in the LLD group than in the normal control group, and were negatively correlated with the total scores and factors' scores (retardation, cognitive bias and anxiety/somatization) of the 17-item Hamilton Depression Rating Scale, and positively correlated with the Verbal Fluency Test scores. The scores for the Food and Imagination dimensions of the Chemosensory Pleasure Scale showed partial mediating effects on the differences in Cognitive bias (a factor of the 17-item Hamilton Depression Rating Scale) between patients with LLD and normal controls. Patients with LLD showed significant chemosensory anhedonia, and both depressive symptoms and cognitive impairment were associated with the severity of chemosensory anhedonia. Enhancing chemosensory pleasure in patients with LLD could potentially ameliorate their depressive symptoms. Geriatr Gerontol Int 2024; ••: ••-••.

23 Cognitive Reserve Moderates Cognitive Functioning in Late-Life Depression

Objective:The concept of cognitive reserve (CR) explains why individuals with higher education, intelligence, or occupational attainment exhibit less severe cognitive changes in the presence of age-related or neurodegenerative pathology. CR may be a useful construct in understanding the cognitive performance of patients with late life depression (LLD), a cohort who are twice as likely to later receive a clinical diagnosis of dementia. It follows that depressed older adults with low CR may be at greater risk of cognitive decline compared to non-depressed older adults matched for CR. However, the literature on CR and LLD is limited to cross-sectional studies with mixed findings as to whether proxies of CR moderate cognitive outcomes in LLD. For example, both higher and lower education levels in LLD are associated with greater cognitive impairment in LLD compared to similarly educated non-depressed older adults. Longitudinal studies may help disentangle the association between CR and cognitive outcomes in LLD. The current study investigated the interaction between proxies of CR (e.g., education) and depression status on cognitive functioning over three years. We hypothesized that depressed older adults with low CR would demonstrate greater cognitive impairment and decline compared to depressed elders with high CR and non-depressed older adults with comparable CR.Participants and Methods:Older adults with LLD and non-depressed older adults age 59+ participated. All participants were free of dementia at baseline. We divided both patients and non-depressed participants into low (<16) and high (>=16) education groups based upon the median years of education (16) of the entire sample. All participants underwent detailed neuropsychological testing. Composite measures of episodic memory (CERAD Wordlist and recall, LM I and LM II, BVRT), processing speed-executive functioning (SDMT and Trail Making Part B), working memory (forward, reverse, ascending Digit Span), and verbal fluency (Animal Naming and COWA) were calculated based on the non-depressed older adults.Results:The baseline sample included 210 non-depressed older adults and 465 older adults with major depression (LLD). 150 non-depressed older adults and 235 LLD patients provided three-year follow-up data. Separate ANOVAs revealed a statistically significant interaction between education and depression status at baseline on the composite score of executive functioning F (1, 668) = 8.74, p <.003. Consistent with our hypothesis, LLD with low education performed significantly worse compared to non-depressed with low education (z-score difference -1.35) and this effect was significantly greater than the difference between LLD patients and non-depressed with high education (z-score difference -0.36). No other interactions were found at baseline. Longitudinal analyses also revealed significant interactions between education and depression on memory over time, although sensitivity analyses did not suggest findings consistent with our hypothesis.Conclusions:Cognitive reserve contribute to group differences between LLD and non-depressed older adults in cognitive performance but may not alter cognitive trajectories over time. Future studies should further explore structural and functional brain changes associated with CR in LLD.

Cognitive Impairment in Late-Life Depression: A Comparative Study of Healthy Older People, Late-Life Depression, and Mild Alzheimer's Disease Using Multivariate Base Rates of Low Scores.

Late-Life Depression (LLD) is often associated with cognitive impairment. However, distinction between cognitive impairment due to LLD and those due to normal aging or mild Alzheimer's Disease (AD) remain difficult. The aim of this study was to present and compare the multivariate base rates of low scores in LLD, mild AD, and healthy control groups on a battery of neuropsychological tests. Participants (ages 60–89) were 352 older healthy adults, 390 patients with LLD, and 234 patients with mild AD (i.e., MMSE ≥ 20). Multivariate base rates of low scores (i.e., ≤ 5th percentile) were calculated for each participant group within different cognitive domains (verbal episodic memory, executive skills, mental processing speed, constructional praxis, and language/semantic memory). Obtaining at least one low score was relatively common in healthy older people controls (from 9.4 to 17.6%), and may thus result in a large number of false positives. By contrast, having at least two low scores was unusual (from 0.3 to 4.6%) and seems to be a more reliable criterion for identifying cognitive impairment in LLD. Having at least three low memory scores was poorly associated with LLD (5.9%) compared to mild AD (76.1%) and may provide a useful way to differentiate between these two conditions [ = 329.8, p < 0.001; Odds Ratio = 50.7, 95% CI = 38.2–77.5]. The multivariate base rate information about low scores in healthy older people and mild AD may help clinicians to identify cognitive impairments in LLD patients, improve the clinical decision-making, and target those who require regular cognitive and clinical follow-up.

Be Fit, Be Sharp, Be Well: The Case for Exercise as a Treatment for Cognitive Impairment in Late-life Depression.

To lay out the argument that exercise impacts neurobiological targets common to both mood and cognitive functioning, and thus more research should be conducted on its use as an alternative or adjunctive treatment for cognitive impairment in late-life depression (LLD). This narrative review summarizes the literature on cognitive impairment in LLD, describes the structural and functional brain changes and neurochemical changes that are linked to both cognitive impairment and mood disruption, and explains how exercise targets these same neurobiological changes and can thus provide an alternative or adjunctive treatment for cognitive impairment in LLD. Cognitive impairment is common in LLD and predicts recurrence of depression, poor response to antidepressant treatment, and overall disability. Traditional depression treatment with medication, psychotherapy, or both, is not effective in fully reversing cognitive impairment for most depressed older adults. Physical exercise is an ideal treatment candidate based on evidence that it 1) is an effective treatment for depression, 2) enhances cognitive functioning in normal aging and in other patient populations, and 3) targets many of the neurobiological mechanisms that underlie mood and cognitive functioning. Results of the limited existing clinical trials of exercise for cognitive impairment in depression are mixed but overall support this contention. Although limited, existing evidence suggests exercise may be a viable alternative or adjunctive treatment to address cognitive impairment in LLD, and thus more research in this area is warranted. Moving forward, additional research is needed in large, diverse samples to translate the growing research findings into clinical practice.

The treatment of cognitive impairment in late-life depression: neurobiological predictors of treatment response.

The treatment of cognitive impairment in late-life depression: neurobiological predictors of treatment response.

The Impact of Amyloid Burden and APOE on Rates of Cognitive Impairment in Late Life Depression.

Cognitive impairment (CI) is a key feature of late life depression (LLD), but the contribution of underlying neurodegenerative pathology remains unclear. To evaluate cognitive dysfunction in LLD relative to a sample of nondepressed (ND) older adults with matched levels of memory impairment and amyloid-β (Aβ) burden. Participants included 120 LLD and 240 ND older adults matched on age, education, sex, Mini-Mental State Exam, mild cognitive impairment diagnosis, and PET Aβ burden. LLD showed higher rates of impairment relative to ND with 54.6% of the LLD sample demonstrating impairment in at least one cognitive domain compared to 42.9% of controls (H = 7.13, p = 0.008). LLD had poorer performance and higher rates of impairment on Rey Auditory Verbal Learning Test learning and memory compared to controls. In the overall sample, Aβ positivity was associated with worse performance on Logical Memory I (p = 0.044), Logical Memory II (p = 0.011), and Trail Making Test -B (p = 0.032), and APOEɛ4 genotype was associated with worse performance on Logical Memory I (p = 0.022); these relationships did not differ between LLD and ND. LLD showed higher rates of CI driven by focal deficits in verbal learning and memory. Alzheimer's disease (AD) biomarkers were associated with worse performance on timed set-shifting and story learning and memory, and these relationships were not impacted by depression status. These findings suggest that AD may account for a portion of previously reported multi-domain CI in LLD and highlight the potential for AD to confound studies of cognition in LLD.

Exploring Language Learning as a Potential Tool against Cognitive Impairment in Late-Life Depression: Two Meta-Analyses and Suggestions for Future Research.

Late-life depression (LLD) affects about an eighth of community-dwelling seniors. LLD impacts well-being, with loneliness and small social networks being typical. It has also been linked to cognitive dysfunction and an increased risk of developing dementia. Safety and efficacy of pharmacological treatments for LLD have been debated, and cognitive dysfunction often persists even after remission. Various cognitive interventions have been proposed for LLD. Among these, one has received special attention: foreign language learning could serve as a social intervention that simultaneously targets brain structures affected in LLD. Lifelong bilingualism may significantly delay the onset of cognitive impairment symptoms by boosting cognitive reserve. Even late-life foreign language learning without lifelong bilingualism can train cognitive flexibility. It is then counterintuitive that the effects of language learning on LLD have never been examined. In order to create a theoretical basis for further interdisciplinary research, this paper presents a status quo of current work through two meta-analyses investigating cognitive functioning in LLD on the one hand and in senior bilinguals or seniors following a language course on the other hand. While LLD was consistently associated with cognitive dysfunction, inconsistent results were found for bilingualism and language learners. Possible reasons for this and suggestions for future research are subsequently discussed.

Cognitive impairment in remitted late-life depression is not associated with Alzheimer's disease-related CSF biomarkers

BackgroundCognitive impairment is a common feature of late-life depression (LLD). Early studies using Alzheimer's disease (AD) biomarkers inferred a biological link between AD pathology and LLD, but recent findings have challenged this association. The aim of this investigation was to determine a panel of AD-related cerebrospinal fluid (CSF) biomarkers in a cross-section of elders with mild cognitive impairment (MCI) with and without LLD. MethodsSubjects comprised 102 older adults: 27 with ‘pure' amnestic MCI (aMCI), 53 with major depression and cognitive impairment – encompassing 22 late-onset (LOD) and 31 early-onset depression (EOD), and 22 euthymic elders without cognitive impairment (controls). Participants underwent lumbar puncture for determination of CSF concentrations of Aβ1-42, T-tau, and P-tau. Cut-off scores for suspected AD were: Aβ1-42 < 416p g/mL, P-tau > 36.1 pg/mL and Aβ/P-tau ratio < 9.53 (O. V. Forlenza et al. 2015). Statistical analyses consisted of analyses of variance (ANOVA), analyses of covariance (ANCOVA), Bonferroni post-hoc tests, and Pearson's chi-squared tests. ResultsANCOVA (age and schooling as covariates) displayed statistically significant results with respect to CSF biomarkers’ profiles regardless of the socio-demographic divergencies previously identified by one-way ANOVA. Mean Aβ1-42 values (pg/mL) were: aMCI, 360.3 (p < 0.001); LOD, 486.6 (p < 0.001); EOD, 494.2 (p < 0.001); controls, 528.3 (p < 0.001); p< 0.05. Mean Aβ1-42/P-tau ratio: aMCI, 7.9 (p < 0.001); LOD 14.2 (p < 0.001); EOD, 15.3 (p < 0.001); controls, 17.1 (p < 0.001); p < 0.05. Post-hoc tests indicated that patients with aMCI showed significant differences in biomarker profile compatible with AD signature. LimitationThe main limitation is the relatively small sample. ConclusionOur findings suggest that, distinctively from aMCI, cognitive impairment in LLD is not associated with AD's CSF pathological signature.

RESULTS OF THE ADNI-DEPRESSION STUDY: Session 323

Results Of The ADNI-Depression Study. Overview: Late life depression (LLD) is one of the most common mental health disorders with which older patients are afflicted. LLD is complicated by the common co-occurrence of cognitive impairment (CI). Estimates suggest as many as 50-60% of older depressed patients may have mild cognitive deficits however the mechanisms contributing to CI are unclear. The ADNI-Depression (ADNI-D) Study is a 5-year two-site (University of California San Francisco and the University of Pittsburgh) NIMH sponsored study of late life depression. The study aims to characterize cognitive functioning patients with LLD and clarify neurobiological mechanisms contributing to cognitive impairment and accelerated cognitive decline in this patient population. The ADNI -D study partners with the Alzheimer's Disease Network Initiative (ADNI) and utilizes its core labs for data management, brain imaging, and biomarker assessments. The ADNI D study has been designed to focus on evaluating the impact of reduced cerebral blood flow, cortical atrophy, white matter disease, and amyloid deposition on cognitive impairment in LLD. The study is longitudinal; after an initial assessment subject are followed for 2 ½ years. ADNI-D is committed to rapid data sharing of the ADNI-D data. This session will present initial data from the ADNI-Depression Study baseline evaluation and will be organized into 4 topic areas. ADNI-D Methodology and Sample Characteristics (Nelson) The ADNI D sample is a well characterized sample of older adults with depression. The ADNI D methodology facilitates comparisons of this cohort of LLD participants with the larger ADNI study of non-depressed older adults with normal cognition, Mild Cognitive Impairment (MCI), and dementia in order to clarify neurobiological mechanisms contributing to cognitive impairment and accelerated cognitive decline. This session will be focused on describing the ADNI-D methodology for participant enrollment and data collection and to report ADNI D sample (n=121) characteristics for depression severity, lifetime history of depression and depression treatment, and functional impairment. Specifically, participant enrollment criteria and methods for the assessment of depression severity and lifetime history of depression and depression treatments will be summarized. Additionally, standardized methodology for collection of neuroimaging data, biomarkers, and data management will be presented. Cognitive Functioning in the ADNI Depression cohort (Morin). The clarification of types and severity of cognitive dysfunction in LLD remains a significant area of research. This session will focus on identifying the cognitive impairment rates of participants with LLD in the ADNI-D study at baseline, highlighting methodological considerations for matching subjects to ADNI participants on basis of cognitive functioning for biomarker analyses, and to assess the relationship of subjective cognitive complaints and ApoE status with objective measures cognitive performance. Association of Cortical Atrophy, White Matter Lesions, and Amyloid Accumulation with Cognition in Late Life Depression (Mackin) Cognitive impairment (CI) in LLD is often characterized by deficits of executive functioning (EF), memory, and language and LLD has been strongly linked to accelerated rates of cognitive decline in older adults. However, the causes of CI in LLD are not clear, in part due to limitations of previous work which have lacked comparisons to well characterized non-depressed older adults with CI caused by neurodegenerative diseases that are often concurrent with LLD, such as the early stages of Alzheimer's disease (AD) and cerebrovascular disease (CVD). The ADNI-D study will facilitate clarification of neurobiological mechanisms contributing to CI in LLD. This session will be focused on evaluating the impact of reduced cerebral blood flow (hypoperfusion), cortical atrophy, and amyloid deposition on CI in LLD in the context of previously documented relationships between CI and subcortical white matter abnormalities and genetic risk factors. Functional Network Level Pathophysiologic Abnormalities Associated with Late Life Depression (Tosun) Cognitive impairment, particularly in the domains of information processing speed, executive functioning, and memory, in LLD is consistent with neurobiological conceptualizations of LLD as being heavily mediated by extended neural networks comprised of the orbitofrontal, medial prefrontal, and cingulate cortices, and anatomical connections with the temporal and parietal lobes, and basal ganglia. By disturbing the normal function and dynamics of different brain networks, the pathophysiological mechanisms of LLD may generate different specific clinical symptoms. Therefore we examine the extent to which multimodal neuroimaging techniques can identify biomarkers reflecting key pathophysiologic processes in LLD and whether such biomarkers may act as predictors, moderators, and mediators of depressive symptoms. This might facilitate development of personalized treatments based on a better understanding of the pathophysiological mechanisms of late life depression.

Cardiovascular diseases and related risk factors accelerated cognitive deterioration in patients with late-life depression: a one-year prospective study.

Cognitive impairment in late-life depression is common and associated with a higher risk of all-cause dementia. Late-life depression patients with comorbid cardiovascular diseases (CVDs) or related risk factors may experience higher risks of cognitive deterioration in the short term. We aim to investigate the effect of CVDs and their related risk factors on the cognitive function of patients with late-life depression. A total of 148 participants were recruited (67 individuals with late-life depression and 81 normal controls). The presence of hypertension, coronary heart disease, diabetes mellitus, or hyperlipidemia was defined as the presence of comorbid CVDs or related risk factors. Global cognitive functions were assessed at baseline and after a one-year follow-up by the Mini-Mental State Examination (MMSE). Global cognitive deterioration was defined by the reliable change index (RCI) of the MMSE. Late-life depression patients with CVDs or related risk factors were associated with 6.8 times higher risk of global cognitive deterioration than those without any of these comorbidities at a one-year follow-up. This result remained robust after adjusting for age, gender, and changes in the Hamilton Depression Rating Scale (HAMD) scores. This study suggests that late-life depression patients with comorbid CVDs or their related risk factors showed a higher risk of cognitive deterioration in the short-term (one-year follow up). Given that CVDs and their related risk factors are currently modifiable, active treatment of these comorbidities may delay rapid cognitive deterioration in patients with late-life depression.

The association between urinary Alzheimer-associated neuronal thread protein and cognitive impairment in late-life depression: a controlled pilot study.

Accumulation of tau protein is associated with both Alzheimer's disease (AD) and late-life depression (LLD). Alzheimer-associated neuronal thread protein (AD7c-NTP), which is closely linked with the tau protein, is elevated in the cerebrospinal fluid and urine of AD patients. This study examined the association between urinary AD7c-NTP and late-life depression with cognitive impairment. One hundred and thirty-eight subjects were recruited into late-life depression with cognitive impairment (LLD-CI, n=52), late-life depression without cognitive impairment (LLD-NCI, n=29), AD (n=27), and healthy control (HC, n=30) groups. The level of urinary AD7c-NTP was measured using the enzyme-linked immunosorbent assay method. The Montreal Cognitive Assessment scale (MoCA), Hamilton Rating Scale for Depression (HRSD) and Hamilton Anxiety Rating Scale (HAMA) were used to assess cognitive functions and depressive and anxiety symptoms in the AD and LLD groups. Urinary levels of AD7c-NTP in the LLD-CI group (1.0±0.7ng/ml) were significantly higher than both the LLD-NCI (0.5±0.3ng/ml) and HC groups (0.5±0.3ng/ml), but lower than in the AD group (1.6±1.7 ng/ml). No significant associations were found in the level of urinary AD7c-NTP in relation to age, gender, education and MoCA in the LLD-CI group. The level of urinary AD7c-NTP appears to be associated with cognitive impairment in late-life depression and may be a potential biomarker for early identification of cognitive impairment in LLD.

Diagnosis and treatment of depression and cognitive impairment in late life.

Cognitive impairment in late-life depression is prevalent, disabling, and heterogeneous. Although mild cognitive impairment in depression does not usually progress to dementia, accurate assessment of cognition is vital to prognosis and treatment planning. For example, executive dysfunction often accompanies late-life depression, influences performance across cognitive domains, and is associated with poor antidepressant treatment outcomes. Here, we review how assessment can capture dysfunction across cognitive domains and discuss cognitive trajectories frequently observed in late-life depression in the context of the neurobiology of this disorder. We also review the efficacy of a sample of interventions tailored to specific cognitive profiles.

Depression and cognition in the elderly.

This review provides an overview of the relationship between depression and cognition in the elderly, with an emphasis on psychotherapies and nonpharmacologic approaches. We first review the clinical presentation of late-life depression and comorbid cognitive impairment, as well as the epidemiology and risk factors for cognitive impairment in late-life depression and the temporal relationship between depression and cognitive impairment. Next, we discuss the salient topic of elderly suicide and cognitive impairment. We then touch briefly on the neuropsychological deficits, biomarkers, and neuroimaging findings in late-life depression with comorbid cognitive impairment. We then focus most of this review on psychotherapies and nontraditional treatments for late-life depression with comorbid cognitive impairment and examine what evidence, if any, exists of the cognitive and functional benefits of these treatments. Finally, we examine the cognitive effects of pharmacologic treatments and brain stimulation therapies.

Plasma biosignature and brain pathology related to persistent cognitive impairment in late-life depression.

Cognitive impairment is highly prevalent among individuals with late-life depression (LLD) and tends to persist even after successful treatment. The biological mechanisms underlying cognitive impairment in LLD are complex and likely involve abnormalities in multiple pathways, or “cascades,” reflected in specific biomarkers. Our aim was to evaluate peripheral (blood-based) evidence for biological pathways associated with cognitive impairment in older adults with LLD. To this end, we used a data-driven comprehensive proteomic analysis (multiplex immunoassay including 242 proteins), along with measures of structural brain abnormalities (gray matter atrophy and white matter hyperintensity volume via MRI), and brain amyloid-β (Aβ) deposition (PiB-PET). We analyzed data from 80 older adults with remitted major depression (36 with Mild Cognitive Impairment (LLD+MCI) and 44 with normal cognitive function (LLD+NC)). LLD+MCI was associated with differential expression of 24 proteins (p <0.05 and q-value <0.30) related mainly to the regulation of immune-inflammatory activity, intracellular signaling, cell survival, and protein and lipid homeostasis. Individuals with LLD+MCI also showed greater white matter hyperintensity burden compared with LLD+NC (p=0.015). We observed no differences in gray matter volume or brain Aβ deposition between groups. Machine learning analysis showed that a group of three proteins (Apo AI, IL-12, and stem cell factor) yielded accuracy of 81.3%, sensitivity of 75%, and specificity of 86.4% in discriminating participants with MCI from those with normal cognitive function (with an averaged cross-validation accuracy of 76.3%, sensitivity of 69.4% and specificity of 81.8% with nested cross-validation considering the model selection bias). Cognitive impairment in LLD seems to be related to greater cerebrovascular disease along with abnormalities in immune-inflammatory control, cell survival, intracellular signaling, protein and lipid homeostasis, and clotting processes. These results suggest that individuals with LLD and cognitive impairment may be more vulnerable to accelerated brain aging and shed light on possible mediators of their elevated risk for progression to dementia.

Depression versus dementia: is this construct still relevant?

Cognitive impairment has long been identified as a component of late-life depression (LLD), and depressive symptoms are common in neurodegeneration. Depression may confer a greater risk of cognitive decline in a cognitively intact population and further cognitive decline in a mild cognitive impairment population compared with those without depression. Exploration of the link between cognitive impairment in LLD and the depressive features of neurodegeneration is an essential part of a diagnostic algorithm. In this review, we will discuss these links; we will address depressive symptoms as a risk factor for dementia and as a prodrome to dementia. We will review clinical subtypes and imaging markers as predictors of development of dementia in depressed patients and explore vascular etiologies. We will also explore LLD and dementia as a spectrum, rather than mutually exclusive diagnostic entities.

The pattern and course of cognitive impairment in late-life depression

Cognitive deficits persist despite clinical recovery in subjects with late-life depression, but more needs to be known about their longer-term outcome and factors affecting their course. To investigate this, we followed the pattern of cognitive impairments over time and examined the effects of current mood, remission status, age of depression onset and antidepressant (AD) treatment on these deficits. Sixty-seven subjects aged > or = 60 years with DSM-IV major depressive disorder and 36 healthy comparison subjects underwent tests of global cognition, memory, executive functioning and processing speed at baseline, 6 and 18 months, with some subjects tested again after 4 years. z scores were compared between groups, with analyses of clinical factors that may have influenced cognitive performance in depressed subjects. Half of the patients exhibited a generalized cognitive impairment (GCI) that persisted after 18 months. Patients performed worse across all cognitive domains at all time points, without substantial variability due to current mood, remission status or AD treatment. Late age of onset was associated significantly with decline in memory and executive functioning. Impaired processing speed may be a partial mediator of some deficits, but was insufficient to explain differences between patients and controls. Four-year follow-up data suggest impairments persist, but do not further decline. Cognitive deficits in late-life depression persist up to 4 years, affect multiple domains and are related to trait rather than state effects. Differences in severity and course between early and late onset depression suggest different pathogenic processes.

Late life depression with cognitive impairment: Evaluation and treatment

Older adults with depression often present with signs and symptoms indicative of functional or cognitive impairment. These somatic symptoms make evaluating and treating depression in older adults more complex. Late life depression (LLD), depression in adults over the age of 65, is more frequently associated with cognitive changes. Cognitive impairment in LLD may be a result of the depressive disorder or an underlying dementing condition. Memory complaints are also common in older adults with depression. There is a wide range of cognitive impairment in LLD including decreased central processing speed, executive dysfunction, and impaired short-term memory. The etiology of cognitive impairment in LLD may include cerebrovascular disease, a significant risk factor for LLD, which likely interrupts key pathways between frontal white matter and subcortical structures important in mood regulation. Because depressive symptoms often coexist with dementia, it is important to determine the temporal relationship between depressive symptoms and cognitive change. If depressive symptoms pre-date the cognitive impairment and cognitive symptoms are mild and temporary, LLD is the likely etiology of the cognitive impairment. If cognitive changes appear prior to depressive symptoms and persist after LLD is successfully treated, an underlying dementia is more likely. Clinicians should be exclude common conditions such as thyroid disease which can contribute to depressive symptoms and cognitive impairment prior to treating LLD. Both antidepressants and psychotherapy can be effective in treating LLD. Subsequent evaluations following treatment should also reassess cognition.

P2-236: Odor identification test as a predictor of mild cognitive impairment in late-life depression

P2-236: Odor identification test as a predictor of mild cognitive impairment in late-life depression

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

Cognitive impairment in late-life depression (LLD) is prevalent, disabling, and persists despite the remission of depressive symptoms. This article characterizes neuropsychologic functioning during remission in LLD. The authors examined longitudinal performance on a comprehensive neuropsychologic battery in 56 nondemented subjects age 60 or older who initially presented with an episode of nonpsychotic unipolar major depression and 40 nondemented, age- and education-equated comparison subjects with no history of depression. Subjects were assessed at baseline (in a depressed state) and one year later (when remitted). After one year, 45% of the LLD subjects were cognitively impaired despite remission of depression. Visuospatial ability, information-processing speed, and delayed memory were most frequently impaired; 94% of the patients who were impaired at baseline remained impaired one year later. Twenty-three percent of the patients who were cognitively normal while depressed developed impairment one year later. Most older individuals who are cognitively impaired during a depressive episode remain impaired when their depression remits. In addition, a substantial proportion of older depressed individuals who are cognitively intact when depressed are likely to be impaired one year later, although their depression has remitted.

Residual cognitive impairment in late-life depression after a 12-month period follow-up.

This study investigated cognitive impairment in late-life depression in a follow-up design. The main objective was to assess the most important cognitive domains implicated in late-life depression, in patients who underwent pharmacological treatment, in the acute phase and twelve months after. Neuropsychological and clinical data were used from the baseline of patients and controls, to determine the cognitive impairment in the acute phase. Patients repeated the neuropsychological assessment at twelve months. There were significant differences between patients and controls at baseline. But in the patients there was no change over twelve months. There were no differences between remitted and non-remitted patients on neuropsychological scores. The cognitive impairment seen in the elderly depressed patients seems to be a trait characteristic of this mental disease, even when the depressive episode has remitted.