Episodic memory functioning in a community-based sample of old adults with major depression: Utilization of cognitive support.

Bäckman, Lars; Forsell, Yvonne

doi:10.1037/0021-843x.103.2.361

Cited by 105 publications

(87 citation statements)

References 74 publications

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“…There are numerous reasons for exhibiting cognitive impairment in old age in addition to being in a preclinical phase of AD. These include psychiatric (e.g., Bäckman & Forsell, 1994), metabolic (e.g., Calvaresi & Bryan, 2001), immunological (e.g., C. J. Wilson, Finch, & Cohen, 2002), hormonal (e.g., Wahlin, Robins Wahlin, Small, & Bäckman, 1998, and circulatory (e.g., Fahlander et al, 2000) disturbances, all of which could potentially result in false negatives.…”

Section: Discussionmentioning

confidence: 99%

Cognitive impairment in preclinical Alzheimer's disease: A meta-analysis.

Bäckman¹,

Jones²,

Berger³

et al. 2005

Neuropsychology

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To determine the size of the impairment across different cognitive domains in preclinical Alzheimer's disease (AD), a meta-analysis based on 47 studies involving 9,097 controls and 1,207 preclinical AD cases was conducted. There were marked preclinical deficits in global cognitive ability, episodic memory, perceptual speed, and executive functioning; somewhat smaller deficits in verbal ability, visuospatial skill, and attention; and no preclinical impairment in primary memory. Younger age (Ͻ 75 years) and shorter follow-up intervals (Ͻ 3 years) were associated with larger effect sizes for both global cognitive ability and episodic memory. For global cognitive ability, studies that used population-based sampling yielded larger effect sizes; for episodic memory, larger differences were seen in studies that preidentified groups in terms of baseline cognitive impairment. Within episodic memory, delayed testing and recall-based assessment resulted in the largest effect sizes. The authors conclude that deficits in multiple cognitive domains are characteristic of AD several years before clinical diagnosis. The generalized nature of the deficit is consistent with recent observations that multiple brain structures and functions are affected long before the AD diagnosis.

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Section: Discussionmentioning

confidence: 99%

Cognitive impairment in preclinical Alzheimer's disease: A meta-analysis.

Bäckman¹,

Jones²,

Berger³

et al. 2005

Neuropsychology

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633

468

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“…The neuropsychological examination included the following tests: similarities, block design, digit symbol, digit span total score, digit span forwards, and digit span backwards from the Wechsler Adult Intelligence Scale-Revised (WAIS-R), 8 letter fluency (FAS), 9 TrailMaking Test, parts A and B (TMTA, TMTB; 10 number of correct responses and log-transformed time score), Luria clock-setting and clock-reading test, 11 Rey-Osterreith copying 12 and Rey-Osterreith memory, immediate reproduction, 10 Rey Auditory Verbal Learning Test (RAVLT; 10 total learning and 30-minute delayed recall), word recall (number of correct responses) and recognition (d-primeintegrated measure of current and false recognitions) from Stockholm Gerontology Research Center (SGRC), 13 and finger-tapping for dominant, nondominant, and alternating hands. 14 Six mutation carriers and 4 controls were tested in the late 1980s and early 1990s at the Department of Neurology of Oulu University Hospital.…”

Section: Neuropsychological Assessmentmentioning

confidence: 99%

Insidious Cognitive Decline in CADASIL

Amberla

Wäljas

Tuominen

et al. 2004

Stroke

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Background and Purpose-Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) causes repeated ischemic attacks leading to subcortical vascular dementia. The aim of this study was to characterize cognitive function in subjects with a C475T (R133C) mutation in the Notch3 gene, leading to CADASIL. Methods-Prestroke (nϭ13) and poststroke (nϭ13) mutation carriers and mutation carriers with dementia (nϭ8) were compared with healthy noncarriers from the same families using a comprehensive set of neuropsychological tests. Results-Changes in working memory and executive function were observed in the very early phase of the disease before transient ischemic attack (TIA) or stroke. Later, in the poststroke phase, the cognitive impairment concerned also mental speed and visuospatial ability. Finally, the subjects with dementia had multiple cognitive deficits, which engaged even verbal functions, verbal episodic memory, and motor speed. The 2 mutation carrier groups without dementia and the controls could be reliably distinguished using 3 tests that assessed working memory/attention, executive function, and mental speed. Episodic memory was relatively well-preserved late in the disease. Conclusion-A deterioration of working memory and executive function was already observed in the prestroke phase, which means that cognitive decline may start insidiously before the first onset of symptomatic ischemic episodes.

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“…It might also affect the use of memory strategies, which are generally effortful as in the use of mental imagery (Hart et al, 1987;Kindermann and Brown, 1997). In the study of Bä ckman and Forsell (1994), depressive participants gained less benefit than non-depressive ones from an increase in study time and the possibility of organizing words in a learning task. Similarly, research by Bä ckman et al (1996) with non-depressive participants and using a depression scale made it possible to separate participants according to their depressive symptoms, although they did not actually present a clinical state of depression.…”

Section: Introductionmentioning

confidence: 99%