Clinical and pathological data from the Rush Memory and Aging Project were used to test the hypothesis that distress proneness is associated with increased risk of Alzheimer's disease (AD). More than 600 older persons without dementia completed a 6-item measure of neuroticism, a stable indicator of proneness to psychological distress. At annual intervals thereafter, they underwent uniform evaluations that included clinical classification of AD and administration of 18 cognitive tests. Those who died underwent brain autopsy from which composite measures of AD pathology were derived. During a mean of about 3 years of follow-up, 55 people were clinically diagnosed with AD. In analyses that controlled for age, sex, and education, persons with a high level of distress proneness (score = 24, 90th percentile) were 2.7 times more likely to develop AD than those not prone to distress (score = 6, 10th percentile). Adjustment for depressive symptomatology or frequency of cognitive, social, and physical activity did not substantially change this effect. Distress proneness was also associated with more rapid cognitive decline. Among 45 participants who died and underwent brain autopsy, distress proneness was unrelated to diverse measures of AD pathology and was inversely related to cognition after controlling for AD pathology. The results support the hypothesis that distress proneness is associated with increased risk of dementia and suggest that neurobiologic mechanisms other than AD pathology may underlie the association.
"The link between distress and the diagnosis of dementia remained after controlling for depression, levels of social and physical activity, and recency of cognitive symptoms. Echoing their prior work, the authors concluded that psychological distress is associated with cognitive decline, but not specifically with AD . Peavy and colleagues performed a 3-year longitudinal study on 52 individuals, who were either cognitively intact or evidencing signs of mild cognitive impairment (MCI). "
[Show abstract][Hide abstract] ABSTRACT: The physiological consequences of acute and chronic stress on a range of organ systems have been well documented after the pioneering work of Hans Selye more than 70 years ago. More recently, an association between exposure to stressful life events and the development of later-life cognitive dysfunction has been proposed. Several plausible neurohormonal pathways and genetic mechanisms exist to support such an association. However, many logistical and methodological barriers must be overcome before a defined causal linkage can be firmly established. Here the authors review recent studies of the long-term cognitive consequences of exposures to cumulative ordinary life stressors as well as extraordinary traumatic events leading to posttraumatic stress disorder. Suggestive effects have been demonstrated for the role of life stress in general, and posttraumatic stress disorder in particular, on a range of negative cognitive outcomes, including worse than normal changes with aging, Alzheimer's disease, and vascular dementia. However, given the magnitude of the issue, well-controlled studies are relatively few in number, and the effects they have revealed are modest in size. Moreover, the effects have typically only been demonstrated on a selective subset of measures and outcomes. Potentially confounding factors abound and complicate causal relationships despite efforts to contain them. More well-controlled, carefully executed longitudinal studies are needed to confirm the apparent association between stress and dementia, clarify causal relationships, develop reliable antemortem markers, and delineate distinct patterns of risk in subsets of individuals.
Alzheimer's and Dementia 06/2014; 10(3):S155–S165. DOI:10.1016/j.jalz.2014.04.008 · 12.41 Impact Factor
"The rate of cognitive decline (disease progression) in 329 AD patients (214 from ANM, 87 from ARUK, and 28 from DCR) was calculated based on longitudinal MMSE assessments . For the ANM cohort, MMSE scores were gathered at five visits, in which visits were 3 months apart (1-year follow-up). "
[Show abstract][Hide abstract] ABSTRACT: Blood proteins and their complexes have become the focus of a great deal of interest in the context of their potential as biomarkers of Alzheimer's disease (AD). We used a SOMAscan assay for quantifying 1001 proteins in blood samples from 331 AD, 211 controls, and 149 mild cognitive impaired (MCI) subjects. The strongest associations of protein levels with AD outcomes were prostate-specific antigen complexed to α1-antichymotrypsin (AD diagnosis), pancreatic prohormone (AD diagnosis, left entorhinal cortex atrophy, and left hippocampus atrophy), clusterin (rate of cognitive decline), and fetuin B (left entorhinal atrophy). Multivariate analysis found that a subset of 13 proteins predicted AD with an accuracy of area under the curve of 0.70. Our replication of previous findings provides further evidence that levels of these proteins in plasma are truly associated with AD. The newly identified proteins could be potential biomarkers and are worthy of further investigation.
Alzheimer's & dementia: the journal of the Alzheimer's Association 04/2014; 10(6). DOI:10.1016/j.jalz.2013.09.016 · 12.41 Impact Factor
"The chronic stress that often characterizes the lives of those with cognitive impairment, as well as their caregivers, has been linked to adverse changes in sleep (30), mood (33, 34), and immunological function (33, 35), and elevated risk for metabolic syndrome, cardiovascular disease (CVD), and mortality (36, 37). Chronic psychological stress can have profound effects on memory and behavior in persons both with and without cognitive impairment, and has been prospectively linked to increased risk for incident MCI and dementia in older adults, and to accelerated cognitive decline (38–40). Chronic stress leads to deleterious neuroendocrine and associated inflammatory changes, to suppression of IGF-1 and other neuroprotective factors, and to impaired synaptic plasticity, suppressed neurogenesis, reduced neuronal survival, and other adverse morphological and functional changes in the hippocampus, prefrontal cortex, and other brain structures; all these changes can profoundly affect mood, sleep, memory, and learning (41–45). "
[Show abstract][Hide abstract] ABSTRACT: Alzheimer's disease (AD) is a chronic, progressive, brain disorder that affects at least 5.3 million Americans at an estimated cost of $148 billion, figures that are expected to rise steeply in coming years. Despite decades of research, there is still no cure for AD, and effective therapies for preventing or slowing progression of cognitive decline in at-risk populations remain elusive. Although the etiology of AD remains uncertain, chronic stress, sleep deficits, and mood disturbance, conditions common in those with cognitive impairment, have been prospectively linked to the development and progression of both chronic illness and memory loss and are significant predictors of AD. Therapies such as meditation that specifically target these risk factors may thus hold promise for slowing and possibly preventing cognitive decline in those at risk. In this study, we briefly review the existing evidence regarding the potential utility of meditation as a therapeutic intervention for those with and at risk for AD, discuss possible mechanisms underlying the observed benefits of meditation, and outline directions for future research.
Frontiers in Psychiatry 04/2014; 5:40. DOI:10.3389/fpsyt.2014.00040
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