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There is increasing evidence of an association between depressive symptoms and mild cognitive impairment (MCI) in cross-sectional studies, but the longitudinal association between depressive symptoms and risk of MCI onset is less clear. The authors investigated whether baseline symptom severity of depression was predictive of time to onset of symptoms of MCI.
These analyses included 300 participants from the BIOCARD study, a cohort of individuals who were cognitively normal at baseline (mean age = 57.4 years) and followed for up to 20 years (mean follow-up = 2.5 years). Depression symptom severity was measured using the Hamilton Depression Scale (HAM-D). The authors assessed the association between dichotomous and continuous HAM-D and time to onset of MCI within 7 years versus after 7 years from baseline (reflecting the mean time from baseline to onset of clinical symptoms in the cohort) using Cox regression models adjusted for gender, age, and education.
At baseline, subjects had a mean HAM-D score of 2.2 (SD = 2.8). Higher baseline HAM-D scores were associated with an increased risk of progression from normal cognition to clinical symptom onset ≤ 7 years from baseline (p = 0.043), but not with progression > 7 years from baseline (p = 0.194). These findings remained significant after adjustment for baseline cognition.
These results suggest that low levels of depressive symptoms may be predictive of clinical symptom onset within approximately 7 years among cognitively normal individuals and may be useful in identifying persons at risk for MCI due to Alzheimer’s disease.
This study examines the relationship of unmet dementia-related care needs of community-dwelling persons, and their caregivers (CGs), to measures of caregiver burden.
Cross-sectional baseline data were analyzed from participants in a dementia care coordination trial of community-residing persons with dementia (PWD) (n = 254) and their caregivers (n = 246). Participants were recruited from Northwest Baltimore, Maryland. The Zarit Burden Inventory (ZBI) was used to measure subjective caregiver burden. Objective burden was measured by estimating the total hours per week spent doing things for the PWD and/or how many hours CGs missed paid work in the prior month due to caregiving responsibilities. The Johns Hopkins Dementia Care Needs Assessment was used to identify unmet dementia-related care needs. Bivariate and multivariate linear regressions examined the relationship of unmet needs, demographic, clinical, or functional characteristics with caregiver burden measures.
In adjusted multivariable models, patient neuropsychiatric symptoms and caregiver unmet emotional needs explained 22% of the variance in ZBI scores. In adjusted multivariable models, caregiver need for respite, patient functional dependency, and caregiver unmet specialty medical needs explained 26% of the variance in the hours per week spent caregiving. PWD's level of functional dependency was the sole correlate of missed time at work, explaining 11% of the variance.
Addressing potentially modifiable unmet caregiver needs may reduce subjective and objective caregiver burden.
The prevalence of both type II diabetes mellitus (DM) and cognitive impairment is high and increasing in older adults. We examined the extent to which DM diagnosis was associated with poorer cognitive performance and dementia diagnosis in a population-based cohort of US older adults.
We studied 7,606 participants in the National Health and Aging Trends Study, a nationally representative cohort of Medicare beneficiaries aged 65 years and older. DM and dementia diagnosis were based on self-report from participants or proxy respondents, and participants completed a word-list memory test, the Clock Drawing Test, and gave a subjective assessment of their own memory.
In unadjusted analyses, self-reported DM diagnosis was associated with poorer immediate and delayed word recall, worse performance on the Clock Drawing Test, and poorer self-rated memory. After adjusting for demographic characteristics, body mass index, depression and anxiety symptoms, and medical conditions, DM was associated with poorer immediate and delayed word recall and poorer self-rated memory, but not with the Clock Drawing Test performance or self-reported dementia diagnosis. After excluding participants with a history of stroke, DM diagnosis was associated with poorer immediate and delayed word recall and the Clock Drawing Test performance, and poorer self-rated memory, but not with self-reported dementia diagnosis.
In this recent representative sample of older Medicare enrollees, self-reported DM was associated with poorer cognitive test performance. Findings provide further support for DM as a potential risk factor for poor cognitive outcomes. Studies are needed that investigate whether DM treatment prevents cognitive decline.
Overview
It is now widely understood that the number of persons living into old age increased dramatically during the last century. In 1900, the average life expectancy at birth was 47 years. By 1950, this had increased to 68 years. In the year 2000, the average life expectancy for males was estimated at slightly over 74 years, and for females it was almost 80 years of age. There is thus increasing interest in understanding the normal changes that occur with age. Along with this has come an interest in developing ways to maintain function at its maximum. This chapter will describe epidemiological aspects of aging, cognitive and motor changes that are associated with aging, the underlying neurobiologic alterations that are thought to be responsible for age-related changes in cognitive and motor function, and the implications of these alterations for the clinical evaluation of an older person.
Epidemiologic aspects of aging
The numbers of persons living to an old age has risen dramatically, and this is expected to continue until at least 2050, as noted above. During the first half of the twentieth century, the increase in life expectancy was largely the result of decreased mortality early in life. The continued expansion of life expectancy during the last half of the twentieth century was largely the result of increased survival during middle and old age. At the same time, virtually all developed countries experienced decreases in the birth rate.
Not too many years ago, the concept by both physicians and the general public was that your brain deteriorated as you got older. It was believed that, with aging, the brain shrank, there was significant drop out of nerve cells throughout the brain, and that once lost, those cells could not be replaced. In addition, at a subcellular level, data suggested that synaptic contacts markedly decreased. Moreover, it was thought that these changes began among individuals in young adulthood and progressed inexorably across the adult life span. As we will emphasize, among individuals who are optimally healthy these previously held concepts are wrong. The information that allows us to draw this conclusion is based on modern technologies for studying postmortem tissue, imaging the living brain, careful cognitive evaluations, and the innovative use of animal models.
Methodologic and technical issues
Focus on optimally healthy older individuals
One of the major changes to occur in the study of brain–behaviour relationships in aging is the focus on optimally healthy participants. This permits one to differentiate changes related to disease from those related to age. Among human subjects, this requires careful exclusion of subjects in the early stages of dementia. However, many medical diseases are common in older individuals (e.g. hypertension, respiratory or cardiac disease, vitamin deficiency), all of which may impair intellectual function. Ideally, if one wants to study healthy individuals, these disorders should be excluded as well. Subjects selected without evidence of clinical disease will differ greatly from a group of older persons that is chosen at random from a population, containing many individuals with serious medical illness. Some of these illnesses will include those with considerable impact on cognitive function, such as Alzheimer's disease (Odenheimer et al., 1994). Thus, optimally healthy individuals, although non-representative, can be of heuristic value, and may ultimately make it easier to identify interventions that can minimize age-related cognitive change.
Inter-individual differences and aging
In recent years, when researchers have focused their attention on animal models and human studies of aging, it has become clear that, even among optimally healthy subjects, there is considerable variability in both cognitive and physical abilities.
Normals (N = 42) and patients with mild memory difficulty (N = 123) were given a neuropsychological test battery, and then followed annually for 3 years to determine which individuals developed sufficient functional change that they met clinical criteria for AD. Twenty-three of the 123 participants with mild memory difficulty converted to a diagnosis of probable Alzheimer's disease (AD) within 3 years of follow-up. Four of the 20 neuropsychological measures obtained at baseline, were useful in discriminating the groups on the basis of their status 3 years after the tests were given. The 4 discriminating tests pertained to assessments of memory and executive function. When the controls were compared to the individuals with memory impairments who ultimately developed AD (the converters), the accuracy of discrimination was 89%, based on the neuropsychological measures at baseline. The discrimination of the controls from the individuals with mild memory problems who did not progress to the point where they met clinical criteria for probable AD over the 3 years of follow-up (the Questionables) was 74% and the discrimination of the questionables from the converters was 80%. The specific tests that contributed to these discriminations, in conjunction with recent neuropathological and neuroimaging data from preclinical cases, have implications for which brain regions may be affected during the prodromal phase of AD. (JINS, 2001, 7, 631–639.)
The ability to process emotional information was assessed in 42 individuals: 23 patients with Alzheimer's disease (AD) and 19 healthy elderly controls. Four tasks assessed the ability to recognize emotion in audiotaped voices, in drawings of emotional situations, and in videotaped vignettes displaying emotions in facial expression, gestures, and body movements. Hemispheric dominance for processing facial expressions of emotions was also examined. There were no consistent group differences in the ability to process emotion presented via the auditory domain (i.e., nonverbal sounds, such as crying or shrieking, and speech prosody). Controls were, however, significantly better than the AD patients in identifying emotions depicted in drawings of emotional situations and in videotaped scenes displaying faces, gestures, and body movements. These differences were maintained after statistically adjusting for the visuospatial abilities of the participants. After a statistical adjustment for abstraction ability, some of the tasks continued to differentiate the groups (e.g., the emotional drawings task, the videotaped displays of faces), but others did not. These results confirm and extend previous results indicating that AD patients do not have a primary deficit in the processing of emotion. They suggest that the difficulties of the AD patients in perceiving emotion are secondary to the cognitive impairments associated with AD. (JINS, 1999, 5, 32–40.)
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