Rate of Forgetting in Dementia and Depression

Journal of Consulting and Clinical Psychology (Impact Factor: 4.85). 03/1987; 55(1):101-5. DOI: 10.1037/0022-006X.55.1.101
Source: PubMed


Patients with mild dementia of the Alzheimer's type (DAT), patients with major depression, and normal control subjects were examined for rate of forgetting line drawings of common objects after the groups had been equated for acquisition by the variation of stimulus exposure time. Depressed and DAT patients demonstrated learning impairments, but only the DAT group showed rapid forgetting in the first 10 min after learning to criterion. This finding suggests that some form of deficient consolidation contributes to memory loss in DAT but not in depression and implicates the disruption of different psychobiological mechanisms in these disorders. The rate of forgetting paradigm may be clinically useful for distinguishing patients with early DAT from elderly depressed patients with memory deficits. (53 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)

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    • "Depression is the most frequently reported psychiatric symptom among patients with MCI [16], with one-fifth reporting moderate-to-high levels of depression [17] and depression increases risk for progression from MCI to AD [18]. Increasing levels of depression have been found to be significantly linked to poorer neuropsychological scores on tests of executive functioning, psychomotor speed, motor functioning, and memory [19–22] with comorbid depression and cognitive dysfunction being associated with greater impairment in activities of daily living as well as decreased quality of life [23–25]. However, this work has focused on global depressive diagnoses or screening instrument scores without any prior work explicitly identifying the specific subset of depressive symptoms that increase risk for MCI or AD. "
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    ABSTRACT: Alzheimer's disease (AD) is a devastating public health problem that affects over 5.4 million Americans. Depression increases the risk of Mild Cognitive Impairment (MCI) and AD. By understanding the influence of depression on cognition, the potential exists to identify subgroups of depressed elders at greater risk for cognitive decline and AD. The current study sought to: 1) clinically identify a sub group of geriatric patients who suffer from depression related cognitive impairment; 2) cross validate this depressive endophenotype of MCI/AD in an independent cohort. Data was analyzed from 519 participants of Project FRONTIER. Depression was assessed with the GDS30 and cognition was assessed using the EXIT 25 and RBANS. Five GDS items were used to create the Depressive endophenotype of MCI and AD (DepE). DepE was significantly negatively related to RBANS index scores of Immediate Memory (B=-2.22, SE=.37, p<0.001), visuospatial skills (B=-1.11, SE=0.26, p<0.001), Language (B=-1.03, SE=0.21, p<0.001), Attention (B=-2.56, SE=0.49, p<0.001), and Delayed Memory (B=-1.54, SE = 037, p<0.001), and higher DepE scores were related to poorer executive functioning (EXIT25; B=0.65, SE=0.19, p=0.001). DepE scores significantly increased risk for MCI diagnosis (odds ratio [OR] = 2.04; 95% CI=1.54-2.69). Data from 235 participants in the TARCC (Texas Alzheimer's Research & Care Consortium) were analyzed for cross-validation of findings in an independent cohort. The DepE was significantly related to poorer scores on all measures, and a significantly predicted of cognitive change over 12- and 24-months. The current findings suggest that a depressive endophenotype of MCI and AD exists and can be clinically identified using the GDS-30. Higher scores increased risk for MCI and was cross-validated by predicting AD in the TARCC. A key purpose for the search for distinct subgroups of individuals at risk for AD and MCI is to identify novel treatment and preventative opportunities.
    PLoS ONE 07/2013; 8(7):e68848. DOI:10.1371/journal.pone.0068848 · 3.23 Impact Factor
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    • "Among studies that have used a matched control group, several (Kramer-Ginsberg et al 1999; Hart et al 1987; Boone et al 1995) suggested the presence of disturbances across a range of cognitive domains in LLD. However, in recent work, Butters et al (2004) found that group differences between controls and individuals with LLD in a range of cognitive domains (e.g., executive function, episodic memory, language processing, and visual spatial function) were fully mediated by deficits in processing speed. "
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    ABSTRACT: A number of studies have examined clinical factors linked to worse neuropsychological performance in late life depression (LLD). To understand the influence of LLD on cognition, it is important to determine if deficits in a number of cognitive domains are relatively independent, or mediated by depression- related deficits in a basic domain such as processing speed. Patients who met DSM-IV criteria for major depression (n = 155) were administered a comprehensive neuropsychological battery of tasks grouped into episodic memory, language, working memory, executive function, and processing speed domains. Multiple regression analyses were conducted to determine contributions of predictor variables to cognitive domains. Age, depression severity, education, race and vascular risk factors all made significant and independent contributions to one or more domains of cognitive function, with all five making independent contributions to processing speed. Age of onset made no independent contribution, after accounting for age and vascular risk factors. Of the five cognitive domains investigated, changes in processing speed were found to most fully mediate the influence of predictor variables on all other cognitive domains. While slowed processing speed appears to be the most core cognitive deficit in LLD, it was closely followed by executive function as a core cognitive deficit. Future research is needed to help clarify mechanisms leading to LLD- related changes in processing speed, including the potential role of white matter abnormalities.
    Biological Psychiatry 08/2006; 60(1):58-65. DOI:10.1016/j.biopsych.2005.09.019 · 10.26 Impact Factor
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    • "The results showed early accelerated forgetting in AD patients after the first 10 min, while the forgetting profiles in the subsequent intervals (2 and 18 hours) was parallel in the two groups. On the basis of these data, Hart et al. (1987) argued that forgetting was accelerated in AD patients during the first minutes after acquisition of the information , but normal after longer delays. "
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    ABSTRACT: In this study we explored the rate of forgetting from long-term memory in Alzheimer's (AD) and multi-infarct (MID) dementia. For this purpose, we administered to 15 AD, 15 MID, and 22 control subjects two tasks exploring, respectively, long-term verbal and long-term visuo-spatial memory. The absolute rate of forgetting in both tasks was computed as the difference between immediate and delayed recall of memorandum. Since level of immediate recall was significantly different between groups, a proportional rate of forgetting (percentage of memorandum lost passing from immediate to delayed recall) was computed for each patient. In the verbal task (Rey's 15 words) AD patients displayed significantly larger absolute and proportional rates of forgetting than MID and control subjects. In the spatial task (Corsi block supraspan), the absolute rate of forgetting was only marginally different between groups. Nevertheless, AD patients demonstrated a larger proportional rate of forgetting than MID and normal subjects. These results point out an exalted decay of information from long-term memory store in AD patients. In the light of previous data (Corkin et al., 1984; Kopelman, 1985) we propose that long-term memory deficits in AD is due, at least in part, to an abnormal forgetting of information within the first few minutes following acquisition. Information still present in the subsequent period (10 min to several days) is retained normally. The normal rate of forgetting in MID patients, further, suggests different mechanisms underlying memory disorders in vascular and degenerative dementias.
    International Journal of Neuroscience 12/1993; 73(1-2):1-11. DOI:10.3109/00207459308987206 · 1.52 Impact Factor
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