The general aims of this thesis were to examine the occurrence of depressive symptoms three years before the diagnoses of depression and Alzheimer’s disease (AD), and to study the effects of depression on cognitive functioning in aging and AD. Five empirical studies were conducted. All data were taken from the Kungsholmen Project, a longitudinal populationbased study of aging and dementia targeting persons who are 75 years and older, living in the Kungsholmen district in Stockholm, Sweden. The specific objectives of Study I were to examine preclinical markers of depression, in terms of presence and severity of depressive symptoms, as well as to examine whether cognitive deficits were present during the preclinical period of old age depression. The chief aim of Study II was to investigate depressive symptomatology, with respect to mood- or motivation-related symptoms, in the preclinical phase of AD. In particular, Study 11 examined mood- and motivation-related symptoms in relation to subjective memory problems to elucidate whether depressive symptoms reflect insight into the dementing process, or is rather a part of the neurodegenerative process. Study III and IV investigated the influence of depression on AD-related deficits in various cognitive domains (e.g., episodic memory, shortterm memory, verbal abilities, visuospatial skill) in mild to moderate stages of AD, whereas Study V examined the influence of depression on global cognitive functioning longitudinally, from the preclinical stage of AD to the time of diagnosis. Study V also addressed whether a concurrent diagnosis of depression causes more rapid decline in global cognitive functioning over a 3-year interval among persons who were going to develop AD. Findings from Study I showed that depressive symptoms are elevated preclinically in old age depression. Persons who were to be depressed showed a greater number of depressive symptoms (i.e., dysphoria, appetite disturbance) and their symptoms were also more severe (i.e., dysphoria, appetite disturbance, lack of interest, psychomotor disturbances), compared to individuals who remained nondepressed. In addition, depressive symptoms were associated with somewhat poorer global cognitive functioning. These data suggest that there are preclinical markers for old age depression. Study II revealed that depressive symptoms are elevated in preclinical AD as well. There was a predominance of motivation-related (e.g., lack of interest, concentration difficulties, loss of energy) over mood-related (e.g., dysphoria, feelings of guilt, thoughts of death) symptoms. This pattern remained after controlling for subjective memory complaints, indicating that the elevation of depressive symptoms may not merely reflect self-perceived cognitive deficits. Thus, depressive symptoms may be a part of the pathological process of AD. The studies (III and IV) examining the effects of depression on AD-related cognitive deficits showed no impact of depression among mild to moderate cases of AD in episodic memory, verbal ability, and visuospatial skill. However, depressionrelated deficits in global cognitive functioning were observed in the preclinical phase of AD (Study V), although a diagnosis of depression did not result in greater decline over a 3-year follow-up interval. To summarize the findings of this thesis, depressive symptoms were found to be elevated preclinically in both depression and AD. However, different patterns of symptoms were present. Mood-related symptoms were more elevated in depression, whereas motivationrelated symptoms were dominating in AD. In terms of depression-related effects on cognitive functioning in AD, the results indicated that, already at a very early clinical stage of AD, the neurodegenerative process overshadows the impact of depression, although this condition is associated with cognitive deficits in normal aging.
© Anna-Karin Berger, 2004