Effects of between-person differences and within-person changes in symptoms of anxiety and depression on older age cognitive performance.

BACKGROUND: Anxiety and depression are both important correlates of cognitive function. However, longitudinal studies investigating how they covary with cognition within the same individual are scarce. We aimed to simultaneously estimate associations of between-person differences and within-person variability in anxiety and depression with cognitive performance in a sample of non-demented older people. METHODS: Participants in the Lothian Birth Cohort 1921 study, a population-based narrow-age sample (mean age at wave 1 = 79 years, n = 535), were examined on five occasions across 13 years. Anxiety and depression were measured with the Hospital Anxiety and Depression Scale (HADS) and cognitive performance was assessed with tests of reasoning, logical memory, and letter fluency. Data were analyzed using two-level linear mixed-effects models with within-person centering. RESULTS: Divergent patterns were observed for anxiety and depression. For anxiety, between-person differences were more influential; people who scored higher on HADS anxiety relative to other same-aged individuals demonstrated poorer cognitive performance on average. For depression, on the other hand, time-varying within-person differences were more important; scoring higher than usual on HADS depression was associated with poorer cognitive performance relative to the average level for that participant. Adjusting for gender, childhood mental ability, emotional stability, and disease burden attenuated these associations. CONCLUSIONS: The results from this study highlight the importance of addressing both between- and within-person effects of negative mood and suggest that anxiety and depression affect cognitive function in different ways. The current findings have implications for assessment and treatment of older age cognitive deficits.

Cognitive deficits in unipolar old-age depression: a population-based study.

BACKGROUND: There is substantial variability in the degree of cognitive impairment among older depressed persons. Inconsistencies in previous findings may be due to differences in clinical and demographic characteristics across study samples. We assessed the influence of unipolar depression and severity of depression on cognitive performance in a population-based sample of elderly persons aged ⩾60 years. METHOD: Eighty-nine persons fulfilled ICD-10 criteria for unipolar depression (mild, n = 48; moderate, n = 38; severe, n = 3) after thorough screening for dementia (DSM-IV criteria), psychiatric co-morbidities and antidepressant pharmacotherapy. Participants (n = 2486) were administered an extensive cognitive test battery. RESULTS: Moderate/severe unipolar depression was associated with poorer performance on tasks assessing processing speed, attention, executive function, verbal fluency, episodic memory and vocabulary. Mild depression was associated with poorer performance in processing speed, and few differences between mild and moderate/severe depression were observed. No association between depression and short-term memory, general knowledge or spatial ability was observed. Increasing age did not exacerbate the depression-related cognitive deficits, and the deficits remained largely unchanged after excluding persons in a preclinical phase of dementia. Furthermore, depression-related cognitive deficits were not associated with other pharmacological treatments that may affect cognitive performance. CONCLUSIONS: Cognitive deficits in unipolar old-age depression involve a range of domains and the cognitive deficits seem to follow the spectrum of depression severity. The finding that mild depression was also associated with poorer cognitive functioning underscores the importance of detecting mild depression in elderly persons.

The influence of vascular disease on cognitive performance in the preclinical and early phases of Alzheimer's disease.

BACKGROUND/AIM: Alzheimer's disease (AD) is one of the most important causes of old-age cognitive impairment. We aimed to examine the influence of history of vascular disease on cognition in preclinical and early AD. METHODS: Participants from a population-based study were assessed twice with a test of global cognition. The study sample was nondemented at baseline. Three years later, 138 persons were diagnosed with AD and 783 persons remained nondemented. History of vascular disease (heart disease, cerebrovascular disease) was assessed at both occasions. RESULTS: Analyses of covariance revealed significant main effects of group (AD; comparison group) and vascular disease (present; absent) at baseline and follow-up (p < 0.01). At follow-up, a significant interaction indicated that the AD group was more negatively affected by vascular disease (p < 0.01). The fastest rate of cognitive decline was observed for those persons with preclinical AD who had new recordings of vascular disease. CONCLUSIONS: History of vascular disease has a negative impact on cognition in old age. This effect is most pronounced in persons in the earliest clinical phases of AD. Treatment of vascular risk factors in early AD might postpone time of diagnosis and slow down dementia progression.

Contrasting cognitive trajectories of impending death and preclinical dementia in the very old.

BACKGROUND: Both impending death and preclinical dementia are associated with cognitive impairment in old age, although their effects on cognitive functioning have rarely been examined within the same study. METHODS: Participants (n = 1,200, aged 75+ years) from a community-based study completed a measure of global cognitive performance (the Mini-Mental State Examination [MMSE]) at 3-year intervals over an 11-year period. Level and change of MMSE performance were compared for three groups: persons in close proximity to death, persons in a preclinical phase of dementia, and persons who remained alive and nondemented throughout the study. RESULTS: There were significant group differences in MMSE performance 3 years before each outcome (death, dementia, or end of study). Those with preclinical dementia performed the poorest and declined twice as fast on the MMSE relative to the other groups. Although persons in close proximity to death declined faster in general, no accelerated decline was observed for the impending death group after persons with dementia or preclinical dementia had been excluded. Group differences were attenuated for the oldest-old (81+ years) compared to the old-old (75 to 80 years). CONCLUSIONS: The lack of accelerated decline in proximity to death after excluding persons with dementia or preclinical dementia suggests that part of the terminal decline effect demonstrated in previous investigations may reflect preclinical dementia deficits. Further, accelerated cognitive decline might be a more reliable indicator of preclinical dementia than a low cognitive score due to confounds associated with cross-sectional cognitive performance.

Multiple cognitive deficits during the transition to Alzheimer's disease.

The literature on cognitive markers in preclinical AD is reviewed. The findings demonstrate that impairment in multiple cognitive domains is typically observed several years before clinical diagnosis. Measures of executive functioning, episodic memory and perceptual speed appear to be most effective at identifying at-risk individuals. The fact that these cognitive domains are most implicated in normal cognitive aging suggests that the cognitive deficit observed preclinically is not qualitatively different from that observed in normal aging. The degree of cognitive impairment prior to the diagnosis of Alzheimer's disease (AD) appears to generalize relatively well across major study characteristics, including sample ascertainment procedures, age and cognitive status of participants, as well as time to diagnosis of dementia. In episodic memory, there is evidence that the size of the preclinical deficit increases with increasing cognitive demands. The global cognitive impairment observed is highly consistent with observations that multiple brain structures and functions are affected long before the diagnosis of AD. However, there is substantial overlap in the distribution of cognitive scores between those who will and those who will not be diagnosed with AD, hence limiting the clinical utility of cognitive markers for early identification of cases. Future research should consider combining cognitive indicators with other types of markers (i.e. social, somatic, genetic, brain-based) in order to increase prediction accuracy.