Cognitive functioning in aging and dementia : the role of psychiatric and somatic factors
Author: Fahlander, Kjell
Date: 2002-06-14
Location: Finskt Äldrecentrums föreläsningssal, Sabbatsbergs Sjukhus, Olivercronas väg 14, Stockholm
Time: 9.30
Department: Institutionen för klinisk neurovetenskap, arbetsterapi och äldrevårdsforskning (NEUROTEC) / Department of Clinical Neuroscience, Occupational Therapy and Elderly Care Research (NEUROTEC)
Abstract
This doctorial thesis concerns the role of psychiatric and somatic factors in aging and dementia. Five studies are included, all based on data from the Kungsholmen Project, a population-based longitudinal study of aging and dementia that was conducted in Stockholm, Sweden during 1987-2000.
Of the five studies, all but one mainly dealt with cognitive functioning in groups of participants that were diagnosed with dementia, whereas one study focused on cognitive functioning in non-demented persons. Four different disorders or conditions were explored with respect to their effects on cognitive functioning: depression in combination with Alzheimer's disease (AD), low levels of vitamin B in combination with AD, cardiovascular signs (CVS) among non-demented participants, and the similarities/differences in the nature of cognitive deficits in vascular dementia (VaD) and AD.
In general, the additional impact on cognitive functioning from depression as well as of low vitamin B levels were found to be limited when participants were already diagnosed as demented, or, as in the vitamin B study, were in a preclinical phase of the dementing disease. Among non-demented persons, however, CVS were found to contribute significantly to the variation in cognitive performance, after controlling for other factors that have an impact on the results. In addition, the differences in patterns of cognitive functioning between persons with AD or VaD, respectively, were found to be small.
These results are discussed in terms of the expectation of aggravated cognitive deficiency when additional pathological conditions are added to dementia. Specifically, it is argued that when the cognitive performance is already seriously disturbed by a major cognitive disorder, such as AD, the contribution from other factors might not be expected to be additive. The main reason for this is that the differences in magnitude of impact from the studied disorders are too large, making it difficult to detect effects of the condition with the least dramatic influence on cognitive functioning.
The dementing disorder might have reduced the potential variability in cognitive functioning, resulting in conformity among persons with dementia, and as AD progresses, a "functional floor" may be reached, where systematic variability in cognitive performance approaches zero. As was indicated in one of the studies, the reduction of systematic variability in cognitive functioning might start early in the disease, even before the time of the dementia diagnosis.
Depression, low levels of vitamin B, and type of dementia are among those factors that have reduced importance for cognitive variability among older demented adults. However, among nondemented older adults, signs of cardiovascular deficiency are related to cognitive performance, and mediate a substantial proportion of the agerelated cognitive variability.
Of the five studies, all but one mainly dealt with cognitive functioning in groups of participants that were diagnosed with dementia, whereas one study focused on cognitive functioning in non-demented persons. Four different disorders or conditions were explored with respect to their effects on cognitive functioning: depression in combination with Alzheimer's disease (AD), low levels of vitamin B in combination with AD, cardiovascular signs (CVS) among non-demented participants, and the similarities/differences in the nature of cognitive deficits in vascular dementia (VaD) and AD.
In general, the additional impact on cognitive functioning from depression as well as of low vitamin B levels were found to be limited when participants were already diagnosed as demented, or, as in the vitamin B study, were in a preclinical phase of the dementing disease. Among non-demented persons, however, CVS were found to contribute significantly to the variation in cognitive performance, after controlling for other factors that have an impact on the results. In addition, the differences in patterns of cognitive functioning between persons with AD or VaD, respectively, were found to be small.
These results are discussed in terms of the expectation of aggravated cognitive deficiency when additional pathological conditions are added to dementia. Specifically, it is argued that when the cognitive performance is already seriously disturbed by a major cognitive disorder, such as AD, the contribution from other factors might not be expected to be additive. The main reason for this is that the differences in magnitude of impact from the studied disorders are too large, making it difficult to detect effects of the condition with the least dramatic influence on cognitive functioning.
The dementing disorder might have reduced the potential variability in cognitive functioning, resulting in conformity among persons with dementia, and as AD progresses, a "functional floor" may be reached, where systematic variability in cognitive performance approaches zero. As was indicated in one of the studies, the reduction of systematic variability in cognitive functioning might start early in the disease, even before the time of the dementia diagnosis.
Depression, low levels of vitamin B, and type of dementia are among those factors that have reduced importance for cognitive variability among older demented adults. However, among nondemented older adults, signs of cardiovascular deficiency are related to cognitive performance, and mediate a substantial proportion of the agerelated cognitive variability.
List of papers:
I. Fahlander K, Berger AK, Backman L, Wahlin A (1999). Depression does not aggravate the episodic memory deficits associated with Alzheimers disease. Neuropsychology. 13(4): 532-8.
Pubmed
II. Berger AK, Fahlander K, Wahlin A, Backman L (2002). Negligible effects of depression on verbal and spatial performance in Alzheimers disease. Dement Geriatr Cogn Disord. 13(1): 1-7.
Pubmed
III. Fahlander K, Wahlin A, Backman L (2002). The relationship between vitamin B status and cognitive performance in preclinical and clinical Alzheimers disease: Data from the Kungsholmen Project. [Manuscript]
IV. Fahlander K, Wahlin A, Fastbom J, Grut M, Forsell Y, Hill RD, Winblad B, Backman L (2000). The relationship between signs of cardiovascular deficiency and cognitive performance in old age: a population-based study. J Gerontol B Psychol Sci Soc Sci. 55(5): P259-65.
Pubmed
V. Fahlander K, Wahlin A, Almkvist O, Backman L (2002). Cognitive functioning in Alzheimers disease and vascular dementia: Further evidence for similar patterns of deficits. Journal of clinical and experimental neuropsychology.
I. Fahlander K, Berger AK, Backman L, Wahlin A (1999). Depression does not aggravate the episodic memory deficits associated with Alzheimers disease. Neuropsychology. 13(4): 532-8.
Pubmed
II. Berger AK, Fahlander K, Wahlin A, Backman L (2002). Negligible effects of depression on verbal and spatial performance in Alzheimers disease. Dement Geriatr Cogn Disord. 13(1): 1-7.
Pubmed
III. Fahlander K, Wahlin A, Backman L (2002). The relationship between vitamin B status and cognitive performance in preclinical and clinical Alzheimers disease: Data from the Kungsholmen Project. [Manuscript]
IV. Fahlander K, Wahlin A, Fastbom J, Grut M, Forsell Y, Hill RD, Winblad B, Backman L (2000). The relationship between signs of cardiovascular deficiency and cognitive performance in old age: a population-based study. J Gerontol B Psychol Sci Soc Sci. 55(5): P259-65.
Pubmed
V. Fahlander K, Wahlin A, Almkvist O, Backman L (2002). Cognitive functioning in Alzheimers disease and vascular dementia: Further evidence for similar patterns of deficits. Journal of clinical and experimental neuropsychology.
Issue date: 2002-05-24
Publication year: 2002
ISBN: 91-7349-246-9
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