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Articles by Claudia H. Kawas
Total Records ( 7 ) for Claudia H. Kawas
  B. Adar Kravitz , Maria M. Corrada and Claudia H. Kawas
  Background C-reactive protein (CRP) is a nonspecific marker of inflammation that is increased in the brain and serum of patients with Alzheimer's disease (AD), and has been associated with increased risk of developing dementia. Inflammation increases with age, and the number of people reaching age 90 years and older is growing, making the association between inflammation and dementia increasingly relevant. Using a cross-sectional design, we examined whether high levels of serum CRP are associated with increased odds of prevalent dementia in the oldest-old. Methods Serum CRP levels of 305 participants (mean age ± standard deviation, 94.3 ± 2.9 years) from the 90+ Study, a longitudinal cohort study of people aged 90 years and older, were evaluated with respect to all-cause dementia. Levels of CRP were divided into three categories: undetectable (<0.5 mg/dL), detectable (0.5–0.7 mg/dL), and elevated (≥0.8 mg/dL). Odds ratios (ORs) were calculated using logistic regression, and were adjusted for covariates. Results Relative to participants with undetectable CRP levels, participants with detectable or elevated CRP levels had increased odds of all-cause dementia (detectable: OR, 3.0; 95% confidence interval, 1.2–7.3; elevated: OR, 5.0; 95% confidence interval, 1.9–12.9). When participants were subdivided by gender, significantly increased ORs were seen only in women. Conclusions In the oldest-old, high CRP levels are associated with increased odds of all-cause dementia, particularly in women. Prospective studies are necessary to confirm whether increased CRP levels are associated with an increased risk of developing dementia in this age group.
  Sudha Seshadri , Alexa Beiser , Rhoda Au , Philip A. Wolf , Denis A. Evans , Robert S. Wilson , Ronald C. Petersen , Ronald C. Petersen , Walter A. Rocca , Claudia H. Kawas , Maria M. Corrada , Brenda L. Plassman , Kenneth M. Langa and Helena C. Chui
  This article focuses on the effects of operational differences in case ascertainment on estimates of prevalence and incidence of cognitive impairment and/or dementia of the Alzheimer type. Experience and insights are discussed by investigators from the Framingham Heart Study, the East Boston Senior Health Project, the Chicago Health and Aging Project, the Mayo Clinic Study of Aging, the Baltimore Longitudinal Study of Aging, and the Aging, Demographics, and Memory Study. There is a general consensus that the single most important factor determining prevalence estimates of Alzheimer‘s disease (AD) is the severity of cognitive impairment used as a threshold to define cases. Studies that require a level of cognitive impairment in which persons are unable to provide self-care will have much lower estimates than the studies aimed at identifying persons in the earliest stages of AD. There are limited autopsy data from the aforementioned epidemiological studies to address accuracy in the diagnosis of etiological subtype, namely the specification of AD alone or in combination with other types of pathology. However, other community-based cohort studies show that many persons with mild cognitive impairment and also some persons without dementia or mild cognitive impairment meet pathological criteria for AD, thereby suggesting that the number of persons who would benefit from an effective secondary prevention intervention is probably higher than the published prevalence estimates. Improved accuracy in the clinical diagnosis of AD is anticipated with the addition of molecular and structural biomarkers in the next generation of epidemiological studies.
  Guy M. McKhann , David S. Knopman , Howard Chertkow , Howard Chertkow , Clifford R. Jack , Claudia H. Kawas , William E. Klunk , Walter J. Koroshetz , Jennifer J. Manly , Richard Mayeux , Richard C. Mohs , John C. Morris , Martin N. Rossor , Philip Scheltens , Maria C. Carrillo , Bill Thies , Sandra Weintraub and Creighton H. Phelps
  The National Institute on Aging and the Alzheimer‘s Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer‘s disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia.
  Carrie B. Peltz , Maria M. Corrada , Daniel J. Berlau and Claudia H. Kawas
  Objective To determine the prevalence and types of cognitive impairment in a sample of nondemented participants aged ≥90 (the oldest-old) and to examine the relationships between cognitive impairment and cardiovascular risk factors. Participants The participants were 420 nondemented individuals from The 90+ Study, a study of aging and dementia in the oldest-old. These participants were categorized into four nonoverlapping groups: normal cognition, amnestic mild cognitive impairment (aMCI), nonamnestic MCI (naMCI), and other cognitive impairment (OCI). History of cardiovascular risk factors was assessed through self-report. Results The overall prevalence of cognitive impairment in nondemented participants was 34.0% (95% CI: 29.5–38.5). The prevalence of OCI was highest (17.4%; 95% CI: 13.9–21.4), followed by aMCI (8.3%; 95% CI: 5.9–11.4) and naMCI (8.3%; 95% CI: 5.9–11.4). Normal cognition was present in 66.0% (95% CI: 61.2–70.5) of participants. History of hypertension and stroke were the only risk factors that varied between the groups, occurring more frequently in participants with naMCI (χ2 = 3.82; P < .05) and OCI (χ2 = 5.51; P < .05). Conclusions This study found a high prevalence of cognitive impairment in a sample of nondemented oldest-old. We did not find a strong relationship between cardiovascular risk factors and the cognitive impairment groups, other than between hypertension and naMCI and stroke and OCI. Future studies comparing the incidence of dementia in these groups will ultimately determine their predictive utility in the oldest-old.
  Sevil Yasar , Fu-Mei Lin , Linda P. Fried , Claudia H. Kawas , Kaycee M. Sink , Steven T. DeKosky and Michelle C. Carlson
  Background To investigate the association between diuretics, angiotensin-converting enzyme inhibitors (ACE-I), angiotensin II receptor blockers (AT2RB), and cognitive function. Methods This post hoc analysis of the randomized controlled Ginkgo Evaluation of Memory Study trial focuses on 3069 nondemented community-dwelling participants aged >75 years. At baseline visit, detailed information about medication use was collected and five cognitive domains were assessed. Multivariate linear regression analyses were used to assess cross-sectional associations between medication use and cognitive function. Results In all, 36% of participants reported history of hypertension and 53% reported antihypertensive medication use, with 17% reporting diuretic, 11% ACE-I, and 2% AT2RB use. Potassium-sparing diuretic use (N = 192) was associated with better verbal learning and memory measured by California Verbal Learning Test as compared with no antihypertensive medication users (β = 0.068, P = .01; β = 0.094, P < .001) and other antihypertensive medication users (β = 0.080, P = .03; β = 0.153, P < .001). Use of ACE-I or AT2RB was not associated with better cognitive function. Conclusion Results warrant further investigation into possible protective effects of potassium-sparing diuretics and the role of potassium in mitigating cognitive decline.
  Maria M. Corrada , Annlia Paganini- Hill , Daniel J. Berlau and Claudia H. Kawas
  Background Although the apolipoprotein E (APOE) ɛ4 allele is a major genetic risk factor for Alzheimer‘s disease (AD), it is not clear whether this relationship persists among the oldest old. Several European studies suggest that the effect of the APOE ɛ4 allele on dementia and mortality disappears in very old age. We describe the APOE allele and genotype frequencies and examine whether the presence of the APOE ɛ4 or APOE ɛ2 alleles is related to prevalent dementia, incident dementia, and mortality in a population-based cohort of oldest-old participants in the United States. Methods We studied 904 participants aged 90 years and older from The 90+ Study. Eight hundred two (89%) participants were genotyped and included in the prevalent dementia and mortality analyses. The 520 initially nondemented participants were included in the incident dementia analyses and were evaluated for dementia every 6 months. Results The APOE ɛ4 allele was significantly associated with prevalent dementia (odds ratio = 2.06) and AD (odds ratio = 2.37) in women but not in men. The APOE ɛ2 allele was not related to prevalent dementia in either sex. After an average follow-up of 2.4 years, 188 incident dementia cases were identified. Neither the APOE ɛ4 nor the APOE ɛ2 allele was related to incident dementia or AD. Five hundred ten (64%) participants died after an average follow-up of 2.3 years, and their mortality was not related to the presence of either the APOE ɛ2 or APOE ɛ4 allele. Conclusions Our findings suggest that the associations between APOE ɛ4, dementia, and mortality are age dependent, and that APOE ɛ4 no longer plays a role in dementia and mortality at very old ages.
  Claudia H. Kawas , Dana E. Greenia , Szofia S. Bullain , Christopher M. Clark , Michael J. Pontecorvo , Abhinay D. Joshi and Maria M. Corrada
  Background The goal of this study was to examine cross-sectional and longitudinal associations between cognitive performance and beta amyloid (Aβ) load determined by florbetapir F18 positron emission tomography (PET) in nondemented oldest-old. Methods Thirteen nondemented (normal or cognitively impaired nondemented) participants (median age, 94.2 years) from The 90+ Study underwent florbetapir-PET scanning within 3 months of baseline neuropsychological testing. Amyloid load was measured with a semi-automated quantitative analysis of average cortical-to-cerebellar standardized uptake value ratio (SUVr) and a visual interpretation (Aβ– or Aβ+). Neuropsychological testing was repeated every 6 months. Results At baseline, SUVr correlated significantly with tests of global cognition and memory. During follow-up (median, 1.5 years), the Aβ+ group had steeper declines on most cognitive tests, particularly global cognitive measures. Conclusion This preliminary study suggests that greater amyloid load is associated with poorer cognition and faster cognitive decline in nondemented oldest-old. Amyloid load may identify individuals at increased risk of developing Alzheimer‘s disease.
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