PubMed Health⌕ Search

Biomedical subjects

R S Wilson

Publications and source records attributed to R S Wilson.

At least 19 recordsLinked to original sources
PubMed2007

Physical activity and motor decline in older persons.

We tested the hypothesis that physical activity modifies the course of age-related motor decline. More than 850 older participants of the Rush Memory and Aging Project underwent baseline assessment of physical activity and annual motor testing for up to 8 years. Nine strength measures and nine motor performance measures were summarized into composite measures of motor function. In generalized estimating equation models, global motor function declined during follow-up (estimate, -0.072; SE, 0.008; P < 0.001). Each additional hour of physical activity at baseline was associated with about a 5% decrease in the rate of global motor function decline (estimate, 0.004; SE, 0.001; P = 0.007). Secondary analyses suggested that the association of physical activity with motor decline was mostly due to the effect of physical activity on the rate of motor performance decline. Thus, higher levels of physical activity are associated with a slower rate of motor decline in older persons.

Activities of Daily Living↗
PubMed2006

Body mass index in older persons is associated with Alzheimer disease pathology.

OBJECTIVE: We examined the extent to which body mass index (BMI) in older persons is associated with common age-related neuropathologies known to contribute to dementia including Alzheimer disease (AD) pathology, cerebral infarction, and Lewy body disease. METHODS: We studied brain autopsies from 298 deceased Catholic clergy participating in the Religious Orders Study, a longitudinal clinical-pathologic investigation. BMI was assessed at annual clinical evaluations during an average follow-up of 4.9 years (SD = 2.7 years). Each person's average BMI, derived from all evaluations, was used in analyses. Multiple regression analyses were used to examine the relation of common postmortem neuropathologic findings to average BMI prior to death. RESULTS: Mean age at death was 85.7 years (SD = 6.8 years), and average BMI during the course of the study was 26.0 (SD = 5.1). A series of linear regression models was performed with average BMI as the outcome and controlling for age, sex, and education. Level of AD pathology was associated with BMI proximate to death (estimate = -1.15; SE = 0.42; p = 0.007). However, Lewy body pathology (estimate = -0.45; SE = 0.73; p = 0.53) and cerebral infarctions (estimate = -0.10; SE = 0.61; p = 0.88) were not associated with average BMI. The association of AD pathology with BMI was unchanged after controlling for dementia, chronic diseases, and physical activity. CONCLUSION: Body mass in old age is associated with Alzheimer disease pathology in persons with and without dementia.

Aged↗
PubMed2006

Diabetes is related to cerebral infarction but not to AD pathology in older persons.

OBJECTIVE: To examine the potential relation of diabetes to common neuropathologic causes of dementia, cerebral infarction and Alzheimer disease (AD) neuropathology. METHODS: Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). Diabetes was identified by annual direct medication inspection and history. Cognitive function proximate to death was summarized into five cognitive domains, based on 19 neuropsychological tests. Macroscopic cerebral infarctions were recorded from 1 cm coronal slabs. Neuritic plaques, diffuse plaques, and neurofibrillary tangles were counted in Bielschowsky silver-stained sections and summarized to yield composite measures of neuritic plaques, diffuse plaques, tangles, and overall AD pathology. We also used immunohistochemistry with antibodies to amyloid-beta and PHF-tau to obtain quantitative measures of amyloid burden and neurofibrillary tangle density. Multiple logistic and linear regression analyses were used to examine the relation of diabetes to cerebral infarctions and AD pathology, controlling for age, sex, and education. RESULTS: AD pathology was related to all five cognitive domains (p < 0.01) and infarctions were related to perceptual speed (p < 0.001). Diabetes (present in 15% subjects) was associated with an increased odds of infarction (OR = 2.47, 95% CI: 1.16, 5.24). Diabetes was not related to global AD pathology score, or to specific measures of neuritic plaques, diffuse plaques or tangles, or to amyloid burden or tangle density. CONCLUSION: We found a relation between diabetes and cerebral infarction but not between diabetes and Alzheimer disease pathology in older persons.

Aged↗
PubMed2006

Associations of vegetable and fruit consumption with age-related cognitive change.

OBJECTIVE: To examine the association between rates of cognitive change and dietary consumption of fruits and vegetables among older persons. METHODS: The authors conducted a prospective cohort study of 3,718 participants, aged 65 years and older of the Chicago Health and Aging Project. Participants completed a food frequency questionnaire and were administered at least two of three cognitive assessments at baseline, 3-year, and 6-year follow-ups. Cognitive function was measured using the average z-score of four tests: the East Boston Tests of immediate memory and delayed recall, the Mini-Mental State Examination, and the Symbol Digit Modalities Test. RESULTS: The mean cognitive score at baseline for the analyzed cohort was 0.18 (range: -3.5 to 1.6), and the overall mean change in score per year was a decline of 0.04 standardized units. In mixed effects models adjusted for age, sex, race, and education, compared with the rate of cognitive decline among persons in the lowest quintile of vegetable intake (median of 0.9 servings/day), the rate for persons in the fourth quintile (median, 2.8 servings/day) was slower by 0.019 standardized units per year (p = 0.01), a 40% decrease, and by 0.018 standardized units per year (p = 0.02) for the fifth quintile (median, 4.1 servings/day), or a 38% decrease in rates. The association remained significant (p for linear trend = 0.02) with further control of cardiovascular-related conditions and risk factors. Fruit consumption was not associated with cognitive change. CONCLUSION: High vegetable but not fruit consumption may be associated with slower rate of cognitive decline with older age.

Aged↗
PubMed2006

The relationship between cerebral Alzheimer's disease pathology and odour identification in old age.

BACKGROUND: Olfactory dysfunction is common in old age, but its basis is uncertain. OBJECTIVE: To test the hypothesis that difficulty in identifying odours in old age is related to the accumulation of Alzheimer's disease pathology. METHODS: As part of the Rush Memory and Aging Project, participants completed the 12-item Brief Smell Identification Test, a standard measure of odour identification. During a mean (standard deviation (SD)) of 2.2 (1.2) years of follow-up (range 0.2-4.9), 166 people died, with brain autopsies performed on 129 (77.7%) people and neuropathological examinations completed on 77 (mean (SD) age at death 87.5 (5.9) years; median postmortem interval 6.1 h). From a uniform postmortem examination of multiple brain regions, summary measures of plaque and tangle pathology were derived on the basis of silver staining, and those of amyloid beta burden, tangle density and Lewy bodies on the basis of immunohistochemistry. RESULTS: Odour identification performance ranged from 0 to 12 correct (mean (SD) 8.0 (2.6)). In analyses adjusted for age, sex and education, a composite measure of plaques and tangles accounted for >12% of the variation in odour identification. The association remained after controlling for dementia or semantic memory. Density of tau tangles was inversely related to odour identification. A similar effect for amyloid burden was attenuated after controlling for tangles. The association with odour identification was robust for tangles in the entorhinal cortex and CA1/subiculum area of the hippocampus, but not for tangles in other cortical sites. Lewy bodies, identified in 12.5%, were not related to odour identification, probably partly due to to their relative infrequency. CONCLUSION: The results suggest that difficulty in identifying familiar odours in old age is partly due to the accumulation of neurofibrillar pathology in central olfactory regions.

Aged↗
PubMed2006

Mild cognitive impairment: risk of Alzheimer disease and rate of cognitive decline.

OBJECTIVE: To examine the extent to which persons with mild cognitive impairment (MCI) have an increased risk of Alzheimer disease (AD) and a more rapid rate of decline in cognitive function compared to similar persons without cognitive impairment. METHOD: Participants were 786 community-based persons (221 with MCI and 565 without cognitive impairment) from the Rush Memory and Aging Project, an ongoing longitudinal clinical-pathologic study of common chronic conditions of old age. All participants underwent detailed annual clinical and neuropsychological evaluations. The authors examined the risk of incident AD and rate of change in global cognitive function among persons with MCI and those without cognitive impairment; all statistical models controlled for age, sex, and education. RESULTS: Over an average of 2.5 years of follow-up, 57 persons with MCI (25.8%) developed AD, a rate 6.7 times higher than those without cognitive impairment. In addition, persons with MCI declined considerably more rapidly each year on a measure of global cognitive function than those without cognitive impairment. CONCLUSIONS: Mild cognitive impairment is associated with a greatly increased risk of incident Alzheimer disease and a more rapid rate of decline in cognitive function.

Age Factors↗
PubMed2006

Neuropathology of older persons without cognitive impairment from two community-based studies.

OBJECTIVE: To examine the relation of National Institute on Aging-Reagan (NIA-Reagan) neuropathologic criteria of Alzheimer disease (AD) to level of cognitive function in persons without dementia or mild cognitive impairment (MCI). METHODS: More than 2,000 persons without dementia participating in the Religious Orders Study or the Memory and Aging Project agreed to annual detailed clinical evaluation and brain donation. The studies had 19 neuropsychological performance tests in common that assessed five cognitive domains, including episodic memory, semantic memory, working memory, perceptual speed, and visuospatial ability. A total of 134 persons without cognitive impairment died and underwent brain autopsy and postmortem assessment for AD pathology using NIA-Reagan neuropathologic criteria for AD, cerebral infarctions, and Lewy bodies. Linear regression was used to examine the relation of AD pathology to level of cognitive function proximate to death. RESULTS: Two (1.5%) persons met NIA-Reagan criteria for high likelihood AD, and 48 (35.8%) met criteria for intermediate likelihood; 29 (21.6%) had cerebral infarctions, and 18 (13.4%) had Lewy bodies. The mean Mini-Mental State Examination score proximate to death was 28.2 for those meeting high or intermediate likelihood AD by NIA-Reagan criteria and 28.4 for those not meeting criteria. In linear regression models adjusted for age, sex, and education, persons meeting criteria for intermediate or high likelihood AD scored about a quarter standard unit lower on tests of episodic memory (p = 0.01). There were no significant differences in any other cognitive domain. CONCLUSIONS: Alzheimer disease pathology can be found in the brains of older persons without dementia or mild cognitive impairment and is related to subtle changes in episodic memory.

Age Factors↗
PubMed2006

Substantial changes in the genetic basis of tadpole morphology of Rana lessonae in the presence of predators.

Predator-induced morphological plasticity is a model system for investigating phenotypic plasticity in an ecological context. We investigated the genetic basis of the predator-induced plasticity in Rana lessonae by determining the pattern of genetic covariation of three morphological traits that were found to be induced in a predatory environment. Body size decreased and tail dimensions increased when reared in the presence of preying dragonfly larvae. Genetic variance in body size increased by almost an order of magnitude in the predator environment, and the first genetic principal component was found to be highly significantly different between the two environments. The across environment genetic correlation for body size was significantly below 1 indicating that different genes contributed to this trait in the two environments. Body size may therefore be able to respond to selection independently in the two environments to some extent.

Animals↗
PubMed2005

Parkinsonian signs in subjects with mild cognitive impairment.

BACKGROUND: Parkinsonian signs such as gait disturbance, rigidity, bradykinesia, and tremor are common among individuals with dementia and are associated with negative outcomes, but little is known about parkinsonian signs among individuals with mild cognitive impairment (MCI). OBJECTIVE: To examine the extent to which MCI is associated with parkinsonian signs and the relation between cognitive abilities and parkinsonism among individuals with MCI. METHODS: Participants included 835 individuals from the Rush Memory and Aging Project, a clinical-pathologic study of common chronic conditions of old age. All participants underwent detailed clinical evaluations which included assessments of parkinsonian signs and cognitive function, and linear regression models were used to examine the associations of MCI and parkinsonism. RESULTS: In a series of analyses controlled for age, sex, and education, individuals with MCI exhibited significantly more parkinsonism than individuals without cognitive impairment, particularly gait disturbance, bradykinesia, and rigidity. Among individuals with MCI, lower levels of cognitive function, particularly in perceptual speed, were associated with higher levels of parkinsonism; when classified according to MCI subtype, individuals with amnestic vs non-amnestic MCI differed from each other on only one parkinsonian sign, with non-amnestic MCI showing more gait disturbance. Because vascular factors can contribute to cognitive impairment and parkinsonian signs, the authors repeated the core analyses including terms for vascular risk factors and vascular disease and the associations between MCI and parkinsonism persisted. CONCLUSIONS: Mild cognitive impairment (MCI) is accompanied by parkinsonian signs, which are related to the severity and type of cognitive impairment. The association between MCI and parkinsonism is not explained by vascular risk factors or vascular disease.

Aged↗
PubMed2005

Hallucinations, cognitive decline, and death in Alzheimer's disease.

The relation of psychotic symptoms to cognitive decline and mortality in Alzheimer's disease (AD) was examined during a mean of 2.2 years in 478 persons selected from clinical settings. Psychotic symptoms were ascertained at baseline and cognition was assessed semiannually with nine tests from which a global measure was formed. In analyses that controlled for age, sex, race, and education, hallucinations (29.6%), especially visual ones, were associated with more rapid global cognitive decline and increased mortality, even after controlling for baseline level of cognition and use of antipsychotic medication, and the association with mortality increased with higher level of education. Delusions and misperceptions were not strongly related to cognitive decline or mortality. The results suggest that hallucinations in Alzheimer's disease, particularly visual ones, are associated with more rapid progression.

Aged↗
PubMed2005

Change in body mass index and risk of incident Alzheimer disease.

OBJECTIVE: To examine the association of change in body mass index (BMI) with risk of Alzheimer disease (AD). METHODS: Nine hundred eighteen older Catholic clergy participating in the Religious Orders Study without dementia at baseline were studied. Outcome measures were the clinical diagnosis of AD and change in cognitive function. RESULTS: During a mean follow-up of 5.5 years, 151 persons developed AD. BMI averaged 27.4 at baseline and declined in about half the participants. In a proportional hazards model adjusted for age, sex, and education, each 1-unit less of BMI at baseline was associated with about a 5% increase in the risk of AD (hazard ratio = 0.944; 95% CI = 0.908 to 0.981), and each 1-unit annual decline in BMI (about the 10th percentile) was associated with about a 35% increase in the risk of AD compared with a person experiencing no change in BMI (about the 50th percentile) (hazard ratio = 0.730; 95% CI = 0.625 to 0.852). The results were similar after controlling for chronic diseases and excluding persons who developed AD during the first 4 years of observation. Random effects models showed that the rate of cognitive decline increased by about 8% for each 1-unit less of BMI at baseline and declined an additional 40%/year in persons losing 1 unit of BMI/year compared with those with no change in BMI. CONCLUSION: Declining body mass index (BMI) is associated with increased risk of incident Alzheimer disease (AD). Loss of BMI may reflect pathologic processes that contribute to the subsequent development of AD.

Age Factors↗
PubMed2005

Education modifies the association of amyloid but not tangles with cognitive function.

The authors quantified amyloid and tau tangles in Religious Orders Study participants. In separate analyses, amyloid and tangles were related to level of cognition. When terms for education's interaction with amyloid and tangles were added, education dampened the association of amyloid with level of cognition (p = 0.02) but not the association of neurofibrillary tangles with level of cognition, suggesting that education is related to factors that reduce the effect of amyloid on cognition.

Activities of Daily Living↗
PubMed2005

The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons.

BACKGROUND AND PURPOSE: Studies investigating the relation of the apolipoprotein E (apoE) epsilon4 allele to clinical stroke and to vascular changes on magnetic resonance imaging have been conflicting. Little data are available regarding the relation of apoE epsilon4 to cerebral infarctions documented on postmortem examination. METHODS: We studied the apoE epsilon4 allele in 214 deceased members of the Religious Orders Study, a longitudinal clinical-pathologic study of aging and Alzheimer disease. The apoE genotype was determined using DNA from lymphocytes. Brains were removed a median of 5 hours (interquartile range, 5.5) after death. At postmortem examination, age, location, and size of macroscopic chronic cerebral infarctions were recorded from 1-cm coronal slabs after paraformaldehyde fixation. We also examined 20-microm paraffin-embedded sections of midfrontal and calcarine cortex for amyloid angiopathy on a scale of 1 to 4. RESULTS: Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). Sixty-five subjects (30.4%) had at least 1 apoE epsilon4 allele and 76 (35.5%) exhibited cerebral infarctions. More than 74% of the subjects exhibited amyloid angiopathy with a mean score of 1.4+/-1.2. After controlling for age and sex, apoE epsilon4 increased the odds of cerebral infarction by 2.3-fold (95% CI, 1.2 to 4.2). apoE epsilon4 increased the odds of cortical 3.2-fold (95% CI, 1.3 to 7.7) and subcortical infarctions 2.3-fold (95% CI, 1.2 to 4.5). The effect was unchanged after accounting for amyloid angiopathy. CONCLUSIONS: apoE epsilon4 increases the odds of chronic cerebral infarction detected at autopsy in older persons.

Aged↗
PubMed2005

Mild cognitive impairment is related to Alzheimer disease pathology and cerebral infarctions.

OBJECTIVES: To examine the extent to which persons with mild cognitive impairment have intermediate levels of Alzheimer disease (AD) pathology, cerebral infarcts, and Lewy body disease. METHODS: A total of 180 Catholic clergy participating in the Religious Orders Study underwent annual detailed evaluation and brain autopsy. Blocks of midfrontal, superior temporal, medial temporal lobe, inferior parietal, entorhinal cortex, hippocampus, and substantia nigra were paraffin embedded, and sectioned at 6 mum. Cortical neuritic plaques, diffuse plaques, and neurofibrillary tangles were visualized with Bielschowsky silver stain, and counted and summarized to yield a Braak stage, Consortium to Establish a Registry for Alzheimer's Disease (CERAD) diagnosis, National Institute on Aging (NIA)-Reagan diagnosis, and composite measure of AD pathology. The authors recorded the number and location of all gross chronic cerebral infarctions. Lewy bodies were identified with antibodies to alpha-synuclein. Multiple regression analyses were used to examine the relation of AD pathology and cerebral infarctions to clinical diagnosis proximate to death, controlling for age, sex, and education. RESULTS: A total of 37 had mild cognitive impairment, 60 did not have cognitive impairment, and 83 had dementia proximate to death. Nearly all persons had at least some AD pathology. Cerebral infarctions were present in 35.2%, and 15.6% had Lewy body disease. Persons with mild cognitive impairment were intermediate in terms of Braak stage and CERAD and NIA-Reagan neuropathologic criteria for AD compared to the other two groups. In multiple regression analyses, persons with mild cognitive impairment had intermediate levels of AD pathology from those without cognitive impairment and those with dementia (test for trend, F = 45.2, p < 0.001). Further, the relation between cognition and AD pathology in persons with mild cognitive impairment did not differ significantly from the relation between cognition and AD pathology in persons with dementia or those without cognitive impairment. Persons with mild cognitive impairment also had intermediate levels of cerebral infarctions (test for trend, p = 0.04). Only 3 (8.1%) persons with mild cognitive impairment had Lewy body disease. CONCLUSION: These data suggest that mild cognitive impairment may be the earliest clinical manifestation of common age-related neurologic diseases.

Age Factors↗
PubMed2005

Proneness to psychological distress and risk of Alzheimer disease in a biracial community.

Persons without dementia residing in a biracial community completed a brief scale of proneness to psychological distress, and 1,064 were subsequently examined for incident Alzheimer disease (AD) 3 to 6 years later. In analyses controlling for selected demographic and clinical variables, persons prone to distress were 2.4 times more likely to develop AD than persons not distress prone. This effect was substantially stronger in white persons compared to African Americans.

Black or African American↗
PubMed2005

Mild cognitive impairment in different functional domains and incident Alzheimer's disease.

BACKGROUND: Little is known about factors that predict transition from mild cognitive impairment to Alzheimer's disease (AD). OBJECTIVE: To examine the relation of impairment in different cognitive systems to risk of developing AD in persons with mild cognitive impairment. METHODS: Participants are 218 older Catholic clergy members from the Religious Orders Study. At baseline, they met criteria for mild cognitive impairment based on a uniform clinical evaluation that included detailed cognitive testing. Evaluations were repeated annually for up to 10 years. Analyses were controlled for age, sex, and education. RESULTS: Eighty two persons (37.6%) developed AD. In separate analyses, episodic memory, semantic memory, working memory, and perceptual speed, but not visuospatial ability, were associated with risk of AD, but when analysed together only episodic memory and perceptual speed were associated with AD incidence, with the effect for episodic memory especially strong. Overall, those with impaired episodic memory were more than twice as likely to develop AD as those with impairment in other cognitive domains (relative risk (RR) = 2.45; 95% confidence interval (CI): 1.53 to 3.92), and they experienced more rapid cognitive decline. Lower episodic memory performance was associated with increased risk of AD throughout the observation period, whereas impairment in other cognitive domains was primarily associated with risk during the following year but not thereafter. CONCLUSION: Among persons with mild cognitive impairment, episodic memory impairment is associated with a substantial and persistent elevation in risk of developing AD compared to impairment in other cognitive systems.

Aged↗
PubMed2005

Amyloid mediates the association of apolipoprotein E e4 allele to cognitive function in older people.

BACKGROUND: The neurobiological changes underlying the association of the apolipoprotein E (APOE) e4 allele with level of cognition are poorly understood. OBJECTIVE: To test the hypothesis that amyloid load can account for (mediate) the association of the APOE e4 allele with level of cognition assessed proximate to death. METHODS: There were 44 subjects with clinically diagnosed Alzheimer's disease and 50 without dementia, who had participated in the Religious Orders Study. They underwent determination of APOE allele status, had comprehensive cognitive testing in the last year of life, and brain autopsy at death. The percentage area of cortex occupied by amyloid beta and the density of tau positive neurofibrillary tangles were quantified from six brain regions and averaged to yield summary measures of amyloid load and neurofibrillary tangles. Multiple regression analyses were used to examine whether amyloid load could account for the effect of allele status on level of cognition, controlling for age, sex, and education. RESULTS: Possession of at least one APOE e4 allele was associated with lower level of cognitive function proximate to death (p = 0.04). The effect of the e4 allele was reduced by nearly 60% and was no longer significant after controlling for the effect of amyloid load, whereas there was a robust inverse association between amyloid and cognition (p = 0.001). Because prior work had suggested that neurofibrillary tangles could account for the association of amyloid on cognition, we next examined whether amyloid could account for the effect of allele status on tangles. In a series of regression analyses, e4 was associated with density of tangles (p = 0.002), but the effect of the e4 allele was reduced by more than 50% and was no longer significant after controlling for the effect of amyloid load. CONCLUSION: These findings are consistent with a sequence of events whereby the e4 allele works through amyloid deposition and subsequent tangle formation to cause cognitive impairment.

Aged↗