Depressive Symptoms, Glial Fibrillary Acid Protein Concentrations, and Cognitive Decline in a Cohort Study.

BACKGROUND: Little is known about how depressive symptoms and glial fibrillary acid protein (GFAP) concentrations taken together may influence cognitive functioning. Understanding this relationship may inform strategies for screening and early intervention to decrease the rate of cognitive decline. METHODS: This study sample includes 1 169 participants from the Chicago Health and Aging Project (CHAP), consisting of 60% Black participants and 40% White participants, and 63% female participants and 37% male participants. CHAP is a population-based cohort study of older adults with a mean age of 77 years. Linear mixed-effects regression models tested the main effects of depressive symptoms and GFAP concentrations and their interactions on baseline cognitive function and cognitive decline over time. Models included adjustments for age, race, sex, education, chronic medical conditions, body mass index, smoking status, alcohol use, and their interactions with time. RESULTS: The interaction of depressive symptomology and GFAP (ß = -0.105 [standard error = 0.038], p = .006) on global cognitive function was statistically significant. Participants with depressive symptoms including and above the cutoff and high log of GFAP concentrations had more cognitive decline over time, followed by participants with depressive symptoms below the cutoff and high log of GFAP concentrations, depressive symptom scores including and above the cutoff and low log of GFAP concentrations, and depressive symptom scores below the cutoff and low log of GFAP concentrations. CONCLUSIONS: Depressive symptoms have an additive effect on the association between the log of GFAP and baseline global cognitive function.

Dementia and autopsy-verified causes of death in racially-diverse older Brazilians.

BACKGROUND: While dementia has been associated with specific causes of death, previous studies were relatively small autopsy series or population-based studies lacking autopsy confirmation and were restricted to Non-Latinx Whites. Here, we examine the association of dementia with autopsy-verified causes of death in racially-diverse older Brazilians. METHODS: As part of the Pathology, Alzheimer´s and Related Dementias Study (PARDoS), a community-based study in Brazil, we included 1941 racially-diverse deceased, 65 years or older at death. We conducted a structured interview with legal informants including the Clinical Dementia Rating (CDR) Scale for dementia proximate to death. Causes of death were assessed after full-body autopsy and macroscopic examination of the brain, thoracic and abdominal/pelvic organs. Up to four causes of death were reported for each decedent. Causes of death were classified as circulatory, infectious, cancer and other. Logistic regression was used to determine associations of dementia with cause of death, controlling for age, sex, race, and education. RESULTS: Dementia was associated with a higher odds of an infectious cause of death (OR = 1.81, 95%CI:1.45-2.25), and with a lower odds of a circulatory disease as cause of death (OR = 0.69, 95%CI:0.54-0.86) and cancer as cause of death (OR = 0.41, 95%CI:0.24-0.71). Dementia was associated with a higher odds of pneumonia (OR = 1.92, 95%CI:1.53-2.40) and pulmonary embolism (OR = 2.31, 95%CI:1.75-3.05) as causes of death and with a lower odds of acute myocardial infarction (OR = 0.42, 95%CI:0.31-0.56) and arterial disease (OR = 0.76, 95%CI:0.61-0.94) as causes of death. CONCLUSION: Racially-diverse older Brazilians with dementia had a higher odds of an infectious cause of death and a lower odds of cancer and circulatory disease as causes of death than those without dementia.

Cortical proteins may provide motor resilience in older adults.

Motor resilience proteins may be a high value therapeutic target that offset the negative effects of pathologies on motor function. This study sought to identify cortical proteins associated with motor decline unexplained by brain pathologies that provide motor resilience. We studied 1226 older decedents with annual motor testing, postmortem brain pathologies and quantified 226 proteotypic peptides in prefrontal cortex. Twenty peptides remained associated with motor decline in models controlling for ten brain pathologies (FDR < 0.05). Higher levels of nine peptides and lower levels of eleven peptides were related to slower decline. A higher motor resilience protein score based on averaging the levels of all 20 peptides was related to slower motor decline, less severe parkinsonism and lower odds of mobility disability before death. Cortical proteins may provide motor resilience. Targeting these proteins in further drug discovery may yield novel interventions to maintain motor function in old age.

Cognitive decline after elective and nonelective hospitalizations in older adults.

OBJECTIVE: To determine whether emergent and urgent (nonelective) hospitalizations are associated with faster acceleration of cognitive decline compared to elective hospitalizations, accounting for prehospital decline. METHODS: Data came from the Rush Memory and Aging Project, a prospective cohort study of community-dwelling older persons without baseline dementia. Annual measures of cognition via a battery of 19 tests were linked to 1999 to 2010 Medicare claims records. RESULTS: Of 777 participants, 460 (59.2%) were hospitalized over a mean of 5.0 (SD = 2.6) years; 222 (28.6%) had at least one elective and 418 (53.8%) at least one nonelective hospitalization. Mixed-effects regression models estimated change in global cognition before and after each type of hospitalization compared to no hospitalization, adjusted for age, sex, education, medical conditions, length of stay, surgery, intensive care unit, and comorbidities. Persons who were not hospitalized had a mean loss of 0.051 unit global cognition per year. In comparison, there was no significant difference in rate of decline before (0.044 unit per year) or after (0.048 unit per year) elective hospitalizations. In contrast, decline before nonelective hospitalization was faster (0.076 unit per year; estimate = -0.024, SE = 0.011, p = 0.032), and accelerated by 0.036 unit (SE = 0.005, p < 0.001) to mean loss of 0.112 unit per year after nonelective hospitalizations, more than doubling the rate in those not hospitalized. CONCLUSIONS: Nonelective hospitalizations are related to more dramatic acceleration in cognitive decline compared to elective hospitalizations, even after accounting for prehospital decline. These findings may inform which hospital admissions pose the greatest risk to the cognitive health of older adults.

Association of Financial Literacy With Hospitalization in Community-dwelling Older Adults.

BACKGROUND: Lowering the likelihood of hospitalization in older adults is a major public health goal for modern health care systems. Emerging data suggest that financial literacy is an important determinant of health outcomes in old age, but the relationship with hospitalization has not been explored. OBJECTIVE: To test the hypothesis that better financial literacy is related to lower risk of hospitalization in older persons. DESIGN: Prospective cohort study. PARTICIPANTS: Data came from community-dwelling older adults (n=388) without dementia enrolled in the Rush Memory and Aging Project. MAIN MEASURES: Participants underwent detailed assessment of financial literacy and cognition. Data on hospitalizations were obtained from linked Medicare claims records (MedPAR file). RESULTS: Over an average of 1.8 years, 117 participants (30%) were hospitalized, and a third of those hospitalized experienced multiple hospitalizations. In a modified Poisson regression model adjusted for age, sex, education, and cognition, better financial literacy was associated with lower risk of hospitalization. In a model further adjusted for income, physical activity, body mass index, smoking, social network size, chronic conditions, basic and instrumental activities of daily living disability, and depressive symptoms, the association was unchanged. Secondary analyses showed the association was primarily driven by conceptual knowledge rather than numeracy. CONCLUSIONS: Higher financial literacy is related to a lower risk of hospitalization in older persons without dementia, after adjusting for cognitive, health, functional, and socioeconomic factors. The ability to understand and utilize financial concepts may represent a potentially modifiable risk factor for hospitalization in later life.

Circulating Dkk1 and TRAIL Are Associated With Cognitive Decline in Community-Dwelling, Older Adults With Cognitive Concerns.

Background: Osteoporosis and Alzheimer's disease are common diseases of aging that would seem to be unrelated, but may be linked through the influence of bone-derived signals on brain function. The aim of the current study is to investigate the relationship between circulating levels of bone-related biomarkers and cognition. Methods: The population included 103 community-dwelling older individuals with memory concerns but without cognitive impairment. A global cognition summary measure was collected at baseline and 6, 12, and 18 months post-enrollment by converting raw scores from 19 cognitive function tests to z-scores and averaging. Baseline plasma concentrations of bone-related biomarkers, including undercarboxylated, carboxylated, and total osteocalcin, parathyroid hormone, C-terminal telopeptide of collagen 1 (CTX-1), procollagen type 1 amino-terminal propeptide, osteoprotegrin, osteopontin, Dickkopf WNT signaling pathway inhibitor 1 (Dkk1), sclerostin, and amyloid ß peptides (Aß40 and Aß42), were measured. Results: Using sex, age, and education-adjusted mixed-effects models, we found that baseline levels of TNF-related apoptosis-inducing ligand (TRAIL; p < .001), Dkk1 (p = .014), and CTX-1 (p = .046) were related to the annual rate of change of global cognition over the 18 month follow-up. In cognitive domain-specific analysis, baseline TRAIL was found to be positively related to the annual rate of change in episodic (p < .001) and working memory (p = .016), and baseline Dkk1 was positively related to semantic memory (p = .027) and negatively related to working memory (p = .016). Conclusions: These results further confirm the link between bone and brain health and suggest that circulating levels of bone-related biomarkers may have diagnostic potential to predict worsening cognition.

Loneliness 5 years ante-mortem is associated with disease-related differential gene expression in postmortem dorsolateral prefrontal cortex.

Subjective social isolation, loneliness, is associated with poor mental and physical health, but the underlying molecular mechanisms are poorly understood. Here we analyzed loneliness data collected on average 5 years ante-mortem and RNA gene expression at death in postmortem dorsolateral prefrontal cortex (DLPFC) from 181 participants in the Rush Memory and Aging Project (MAP), a longitudinal, prospective cohort study of common chronic conditions of aging. Our analytic protocol controlled for biographical variables (age, sex, education), psychological and health variables (depressive symptoms, interval between assessment and autopsy, slope of cognitive decline, AD pathology, presence of infarcts) and RNA integrity. Our results are based on a pre-ranked Gene Set Enrichment Analysis (GSEA) at FDR-corrected q-values <0.05, using these collections from the Molecular Signatures Database (v6.0 MSigDB): (1) Hallmarks, (2) Canonical, (3) Gene Ontology (GO), (4) Chemical and Genetic Perturbations, (5) Immunologic Signatures, (6) Oncogenic Signatures, and (7) Cancer Modules. We now report on 337 up-regulated and 43 down-regulated gene sets, among which the most significant ones were associated with Alzheimer's disease, psychiatric illness, immune dysfunction, and cancer. These gene sets constitute attractive targets for future studies into the molecular mechanisms by which loneliness exacerbates a wide range of neurodegenerative, psychiatric, and somatic illnesses.

TDP-43 pathology and memory impairment in elders without pathologic diagnoses of AD or FTLD.

OBJECTIVE: To investigate the association of TAR DNA-binding protein 43 (TDP-43) pathology with memory, other cognitive domains, and dementia in community-dwelling elders without pathologic diagnoses of Alzheimer disease (AD) or frontotemporal lobar degeneration (FTLD). METHODS: Of 1,058 autopsied participants, 343 (32.4%) did not have pathologic diagnoses of AD or FTLD. Diagnosis of dementia was based on clinical evaluation and cognitive performance tests, which were used to create summary measures of global cognition and of 5 cognitive domains. TDP-43 pathology evaluated in 6 brain regions by immunohistochemistry was converted into a summary measure of TDP-43 severity. RESULTS: Of 343 participants, 135 (39.4%) had TDP-43 pathology with a mean TDP-43 severity score of 0.394 (SD 0.490). TDP-43 inclusions were confined to the amygdala (stage 1) in 43.7% of participants, 40% showed additional involvement of the hippocampus or entorhinal cortex (stages 2), while fewer (16.3%) showed additional TDP-43 pathology in the temporal and frontal cortices (stage 3). Severity of TDP-43 pathology was independently related to lower function in global cognition and episodic and semantic memory while increased odds of dementia was only a trend. When participants with hippocampal sclerosis (HS) were excluded from the models, TDP-43 pathology remained associated with lower episodic memory but relationships with global cognition, semantic memory, and dementia were attenuated. CONCLUSIONS: TDP-43 pathology in elders, without pathologic diagnoses of AD or FTLD, is common and independently associated with lower function in episodic memory, while its associations with global cognitive impairment and dementia are difficult to separate from HS.

Association of Cancer History with Alzheimer's Disease Dementia and Neuropathology.

BACKGROUND: Cancer and Alzheimer's disease (AD) are common diseases of aging and share many risk factors. Surprisingly, however, epidemiologic data from several recent independent cohort studies suggest that there may be an inverse association between these diseases. OBJECTIVE: To determine the relationship between history of cancer and odds of dementia proximate to death and neuropathological indices of AD. METHODS: Using data from two separate clinical-pathologic cohort studies of aging and AD, the Religious Orders Study (ROS) and the Rush Memory and Aging Project (MAP), we compared odds of AD dementia proximate to death among participants with and without a history of cancer. We then examined the relation of history of cancer with measures of AD pathology at autopsy, i.e., paired helical filament tau (PHFtau) neurofibrillary tangles and amyloid-ß load. RESULTS: Participants reporting a history of cancer had significantly lower odds of AD (OR 0.70 [0.55-0.89], p = 0.0040) proximate to death as compared to participants reporting no prior history of cancer. The results remained significant after adjusting for multiple risk factors including age, sex, race, education, and presence of an APOEɛ4 allele. At autopsy, participants with a history of cancer had significantly fewer PHFtau tangles (p < 0.001) than participants without a history of cancer, but similar levels of amyloid-ß. CONCLUSIONS: Cancer survivors have reduced odds of developing AD and a lower burden of neurofibrillary tangle deposition.

Change in Cognitive Abilities in Older Latinos.

The aim of this study was to compare patterns of cognitive decline in older Latinos and non-Latinos. At annual intervals for a mean of 5.7 years, older Latino (n=104) and non-Latino (n=104) persons of equivalent age, education, and race completed a battery of 17 cognitive tests from which previously established composite measures of episodic memory, semantic memory, working memory, perceptual speed, and visuospatial ability were derived. In analyses adjusted for age, sex, and education, performance declined over time in each cognitive domain, but there were no ethnic group differences in initial level of function or annual rate of decline. There was evidence of retest learning following the baseline evaluation, but neither the magnitude nor duration of the effect was related to Latino ethnicity, and eliminating the first two evaluations, during which much of retest learning occurred, did not affect ethnic group comparisons. Compared to the non-Latino group, the Latino group had more diabetes (38.5% vs. 25.0; χ2[1]=4.4; p=.037), fewer histories of smoking (24.0% vs. 39.4%, χ2[1]=5.7; p=.017), and lower childhood household socioeconomic level (-0.410 vs. -0.045, t[185.0]=3.1; p=.002), but controlling for these factors did not affect results. Trajectories of cognitive aging in different abilities are similar in Latino and non-Latino individuals of equivalent age, education, and race. (JINS, 2016, 22, 58-65).

Purpose in life and cerebral infarcts in community-dwelling older people.

BACKGROUND AND PURPOSE: Purpose in life, the sense that life has meaning and direction, is associated with reduced risks of adverse health outcomes. However, it remains unknown whether purpose in life protects against the risk of cerebral infarcts among community-dwelling older people. We tested the hypothesis that greater purpose in life is associated with lower risk of cerebral infarcts. METHODS: Participants came from the Rush Memory and Aging Project. Each participant completed a standard measure of purpose in life. Uniform neuropathologic examination identified macroscopic infarcts and microinfarcts, blinded to clinical information. Association of purpose in life with cerebral infarcts was examined in ordinal logistic regression models using a semiquantitative outcome. RESULTS: Four hundred fifty-three participants were included in the analyses. The mean score on the measure of purpose was 3.5 (SD, 0.5; range, 2.1-5.0). Macroscopic infarcts were found in 154 (34.0%) people, and microinfarcts were found in 128 (28.3%) people. Greater purpose in life was associated with a lower odds of having more macroscopic infarcts (odds ratio, 0.535; 95% confidence interval, 0.346-0.826; P=0.005), but we did not find association with microinfarcts (odds ratio, 0.780; 95% confidence interval, 0.495-1.229; P=0.283). These results persisted after adjusting for vascular risk factors of body mass index, history of smoking, diabetes mellitus, and blood pressure, as well as measures of negative affect, physical activity, and clinical stroke. The association with macroscopic infarcts was driven by lacunar infarcts, and was independent of cerebral atherosclerosis and arteriolosclerosis. CONCLUSIONS: Purpose in life may affect risk for cerebral infarcts, specifically macroscopic lacunar infarcts.

Perceived stress and change in cognitive function among adults 65 years and older.

OBJECTIVE: Exposure to acute and chronic stress can affect learning and memory, but most evidence comes from animal studies or clinical observations. Almost no population-based studies have investigated the relation of stress to cognition or changes in cognition over time. We examined whether higher levels of perceived stress were associated with accelerated decline in cognitive function in older blacks and whites from a community-based population sample. METHODS: Participants included 6207 black and white adults (65.7% black, 63.3% women) from the Chicago Health and Aging Project. Two to five in-home assessments were completed over an average of 6.8 years of follow-up and included sociodemographics, health behaviors, psychosocial measures, cognitive function tests, and health history. Perceived stress was measured by a six-item scale, and a composite measure of four tests of cognition was used to determine cognitive function at each assessment. RESULTS: Mixed-effects regression models showed that increasing levels of perceived stress were related to lower initial cognitive scores (B = -0.0379, standard error = 0.0025, p < .001) and a faster rate of cognitive decline (stress × time interaction: B = -0.0015, standard error = 0.0004, p < .001). Results were similar after adjusting for demographic variables, smoking, systolic blood pressure, body mass index, chronic medical conditions, and psychosocial factors and did not vary by race, sex, age, or education. CONCLUSIONS: Increasing levels of stress are independently associated with accelerated declines in cognitive function in black and white adults 65 years and older.

Accounting for bias due to selective attrition: the example of smoking and cognitive decline.

BACKGROUND: Selective attrition may introduce bias into analyses of the determinants of cognitive decline. This is a concern especially for risk factors, such as smoking, that strongly influence mortality and dropout. Using inverse-probability-of-attrition weights, we examined the influence of selective attrition on the estimated association of current smoking (vs. never smoking) with cognitive decline. METHODS: Chicago Health and Aging Project participants (n = 3713), aged 65-109 years, who were current smokers or never- smokers, underwent cognitive assessments up to 5 times at 3-year interval. We used pooled logistic regression to fit predictive models of attrition due to death or study dropout across the follow-up waves. With these models, we computed inverse-probability-of-attrition weights for each observation. We fit unweighted and weighted, multivariable-adjusted generalized-estimating-equation models, contrasting rates of change in cognitive scores in current versus never-smokers. Estimates are expressed as rates of change in z score per decade. RESULTS: During the 12 years of follow-up, smokers had higher mortality than never-smokers (hazard ratio = 1.93 [95% confidence interval = 1.67 to 2.23]). Higher previous cognitive score was associated with increased likelihood of survival and continued participation. In unweighted analyses, current smokers' cognitive scores declined 0.11 standard units per decade more rapidly than never-smokers' (95% CI = -0.20 to -0.02). Weighting to account for attrition yielded estimates that were 56% to 86% larger, with smokers' estimated 10-year rate of decline up to 0.20 units faster than never-smokers' (95% CI = -0.36 to -0.04). CONCLUSIONS: Estimates of smoking's effects on cognitive decline may be underestimated due to differential attrition. Analyses that weight for the inverse probability of attrition help compensate for this attrition.

Olfactory identification and incidence of mild cognitive impairment in older age.

CONTEXT: Mild cognitive impairment (MCI) is often a precursor to Alzheimer disease, but knowledge about factors that predict its development is limited. OBJECTIVE: To test the hypothesis that impaired odor identification is related to increased risk of incident MCI. DESIGN: Longitudinal cohort study. SETTING: Academic research. PARTICIPANTS: Subjects were 589 community-dwelling older persons without cognitive impairment at study baseline, at which time odor identification was assessed using the 12-item Brief Smell Identification Test (mean +/- SD score, 9.3 +/- 1.9). MAIN OUTCOME MEASURES: Incidence of MCI and rate of decline in cognitive function. RESULTS: During annual observation of up to 5 years, 177 subjects developed MCI. In a proportional hazards model adjusted for age, sex, and education, odor identification score predicted development of MCI (relative risk, 1.15; 95% confidence interval, 1.07-1.23), with risk increased by 50% in persons with below-average (score of 8 [25th percentile]) compared with above-average (score of 11 [75th percentile]) odor identification scores. Results were not substantially changed in subsequent analyses that controlled for level of cognitive function or disability, presence of stroke, or smoking status at baseline or that required MCI to persist for at least 1 year. Impaired odor identification was also associated with a lower level of global cognition at baseline and with more rapid decline in episodic memory, semantic memory, and perceptual speed. CONCLUSION: Among older persons without manifest cognitive impairment, difficulty in identifying odors predicts subsequent development of MCI.

Diabetes and parkinsonian signs in older persons.

We examined the relation of type 2 diabetes mellitus to parkinsonian signs in older persons. Participants were 1030 women and men (mean age 80.3 y, education 14.5 y, Mini-Mental State Examination 27.9) without dementia or Parkinson disease, enrolled in the Rush Memory and Aging Project, an epidemiologic study of aging. We used separate linear and logistic regression models, adjusted for age, sex, and education, to examine the relation of diabetes, identified by history and medication inspection, to each of the scores of global parkinsonian signs and 4 separate parkinsonian signs. Diabetes was present in 140 (14%) participants. Most participants had mild parkinsonian signs. Diabetes was associated with a more severe global parkinsonian signs score (beta=0.20, SE=0.10, P=0.05) and postural reflex impairment-gait disturbance (beta=0.40, SE=0.17, P=0.02), but not with bradykinesia, rigidity, or tremor. Associations were no longer significant after controlling for vascular risk factors or conditions, particularly body mass index and congestive heart failure. Overall, there was no evidence that vascular variables modified the relation of diabetes to parkinsonian signs. In summary, we found that diabetes was associated with parkinsonian signs, especially postural reflex impairment-gait disturbance, and that vascular factors may play a role in this association.

The relation of cigarette smoking to incident Alzheimer's disease in a biracial urban community population.

The relationship between smoking status and incident Alzheimer's disease (AD) was investigated in a random stratified sample of a biracial community in Chicago. Analyses are based on 1,064 persons (of 1,134 evaluated) who had data on smoking status, disease incidence, and key covariates such as apolipoprotein allele status. During a mean of about 4 years of follow-up, 170 persons met criteria for incident AD. Current smoking was associated with increased risk of incident AD (OR = 3.4, 95% CI = 1.4-8.0) compared to persons who never smoked. There was no apparent increase in risk of AD for former smokers compared to persons who never smoked (OR = 0.9, 95% CI = 0.5-1.7). Apolipoprotein E allele status modified this association in that former smokers with a upsilon4 allele were less likely to develop AD (p = 0.04) than those who never smoked. Former smokers also appeared to have a reduced risk of developing AD as their pack-years of smoking increased (p = 0.02)such that the odds of developing AD increased by 50% for every 10 years of smoking cessation (OR = 1.3, CI = 0.9-1.7). The results suggest that older people who currently smoke are more likely to develop AD compared to those who never smoked; the relation between those who used to smoke but quit and the risk of AD is complex and requires further research.

Odor identification and decline in different cognitive domains in old age.

The authors examined the association of odor identification with rate of decline in different cognitive systems. Participants are 481 older persons from the Rush Memory and Aging Project. At baseline, the Brief Smell Identification Test was administered. At annual intervals for up to 3 years, a battery of 19 cognitive tests was administered from which previously established composite measures of 5 cognitive domains were derived. In mixed-effects models adjusted for age, sex, and education, lower odor identification score was associated with lower function at baseline in each cognitive domain. Lower score was also associated with more rapid decline in perceptual speed (estimate=0.015, SE=0.006, p=0.013) and episodic memory (estimate=0.012, SE=0.006, p=0.030) but not with rate of decline in semantic memory, working memory, or visuospatial ability. Thus, on average, a person with a low odor identification score (6, 10th percentile) declined more than twice as rapidly in perceptual speed and episodic memory as a person with a high score (11, 90th percentile). Results were unchanged in subsequent analyses that controlled for cigarette smoking or clinically diagnosed stroke. The results indicate that impaired odor identification in old age is associated with impaired global cognition and more rapid decline in perceptual processing speed and episodic memory.

Effect of hydration variability on hybrid layer properties of a self-etching versus an acid-etching system.

The hypothesis tested in this study was that the self-etching system (Clearfil SE Bond, CSE) is less sensitive to surface moisture variability than the system that uses a separate acid-etching step (Single Bond, SB). Eighteen dentin specimens were bonded to composite using CSE or SB. Three different surface moisture conditions per bonding type (overwet, w; dry, d; and visibly moist, n [normal]) were applied prior to bonding dentin to composite. One cross section of each sample was analyzed with lines of nanoindentations crossing perpendicular to the bonding interface. An additional set of bonded samples was fixed and cross sectioned before the hybrid layer thickness was measured in scanning electron microscopy. The nanoindentations revealed significant differences in indentation modulus (E(i)) and hardness (H) for the hybrid layer comparing SBn, E(i) = 2.7(+/-1.6); H = 0.24(+/-0.1) GPa with SBd, E(i) = 0.9(+/-0.7); H = 0.9(+/-0.05) GPa, respectively, while CSE showed no differences among the groups. A significantly greater demineralized zone below the hybrid layer was found for SBd. The hybrid layer was wider for both CSEd and SBd. In conclusion the hypothesis was verified; CSE exhibited no significant changes of hybrid layer properties (E(i), H) at different hydration conditions, while SB had significant differences, especially after air-drying.

Negative affect and mortality in older persons.

The authors examined the relation of negative affect to mortality in the Religious Orders Study, a longitudinal cohort study of older persons, between 1994 and 2002. Participants were 851 Catholic clergy members without dementia at baseline (mean age, 75.4 (standard deviation, 6.9) years; 68% women). They completed standard measures of depressive symptoms, proneness to anxiety and anger, and patterns of anger expression at baseline and then underwent annual clinical evaluations for a mean of 4.7 (standard deviation, 2.7) years. The association of each scale with mortality was examined in proportional hazards models adjusted for age, sex, education, measures of cognitive function, lower limb function, chronic illness, smoking, alcohol, and obesity. During follow-up, 164 persons died. Measures of internally experienced negative affect, such as depressive symptoms and suppressed anger, were related to mortality, but measures of externally directed negative affect, such as the tendencies to be angry with others and to express anger overtly, were not. Persons with a high score (90th percentile) on a summary measure of internally experienced negative affect were nearly twice as likely to die as persons with a low score (10th percentile). The results suggest that negative affect in older persons, especially internally experienced distress, is associated with an increased mortality risk.

Vitamin E and cognitive decline in older persons.

BACKGROUND: Previous studies raise the possibility that antioxidants protect against neurodegenerative diseases. OBJECTIVE: To examine whether intake of antioxidant nutrients, including vitamin E, vitamin C, and carotene, is associated with reduced cognitive decline with age. DESIGN: Longitudinal population-based study conducted from September 17, 1993, to November 20, 2000, with an average follow-up of 3.2 years. PATIENTS: The patients were 2889 community residents, aged 65 to 102 years, who completed a food frequency questionnaire, on average 18 months after baseline. MAIN OUTCOME MEASURE: Cognitive change as measured by 4 tests (the East Boston Memory Test, which tests immediate and delayed recall; the Mini-Mental State Examination; and the Symbol Digit Modalities Test) at baseline and 3 years for all participants, and at 6 months for 288 randomly selected participants. RESULTS: We used random-effects models to estimate nutrient effects on individual change in the average score of the 4 cognitive tests. The cognitive score declined on average by 5.0 x 10(-2) standardized units per year. There was a 36% reduction in the rate of decline among persons in the highest quintile of total vitamin E intake (-4.3 x 10(-2) standardized units per year) compared with those in the lowest quintile (-6.7 x 10(-2) standardized units per year) (P =.05), in a model adjusted for age, race, sex, educational level, current smoking, alcohol consumption, total calorie (energy) intake, and total intakes of vitamin C, carotene, and vitamin A. We also observed a reduced decline with higher vitamin E intake from foods (P =.03 for trend). There was little evidence of association with vitamin C or carotene intake. CONCLUSION: Vitamin E intake, from foods or supplements, is associated with less cognitive decline with age.