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Articles by David S. Knopman
Total Records ( 8 ) for David S. Knopman
  David S. Knopman , Thomas H. Mosley , Diane J. Catellier , Laura H. Coker and Atherosclerosis Risk in Communities Study Brain MRI Study
  Background Strokes, vascular risk factors, and apolipoprotein E (APOE) genotype are associated with cognitive decline in the elderly, but definitive evidence that these affect cognition as early as middle age is limited. Objective We describe the relationships of APOE genotype, stroke, and vascular risk factors with cognitive change over a 14-year follow-up in the Atherosclerosis Risk in Communities (ARIC) Study cohort recruited while in middle age. Methods Participants included a subset of the ARIC Study who underwent assessments of cognitive function and vascular risk factors. Four cognitive assessments were performed between 1990–1992 and 2004–2006. Cognitive assessments included the Delayed Word Recall (DWR) Test, the Digit Symbol Substitution (DSS) Test, and the Word Fluency (WF) Test. Vascular risk factors were assessed during the baseline visit in 1990–1992. Incident stroke was recorded over the 14 years of follow-up. Results There were 1130 participants (mean age, 59 ± 4.3 [SD] years; 62% women; 52% African-American) with longitudinal data. In multivariate, random-effects linear models adjusted for age, education, gender, and race, the risk factors diabetes and APOE ɛ4 genotype were independently associated with a decline in performance on the DSS test (both P < .005), whereas hypertension and stroke were not. For DWR, stroke and APOE ɛ4 genotype were independent predictors of decline (both P < .001). For the WF test, metabolic syndrome, hypertension, and stroke were independently associated with decline (all P < .005). No evidence of differential effects of risk factors on cognitive decline by race, gender, or interactions between risk factors was found. Conclusions The vascular risk factors diabetes and hypertension, a history of stroke itself, and APOE ɛ4 genotype independently contribute to cognitive decline in late middle age and early elderly years.
  Rosebud O. Roberts , Yonas E. Geda , David S. Knopman , Bradley F. Boeve , Teresa J.H. Christianson , V. Shane Pankratz , Iftikhar J. Kullo , Eric G. Tangalos , Robert J. Ivnik and Ronald C. Petersen
  Background Inflammation is proposed to play a role in the development of Alzheimer's disease, and may also be involved in the pathogenesis of mild cognitive impairment (MCI). This study examined the association of inflammatory markers in serum or plasma with prevalent MCI and MCI subtypes in a population-based sample. Methods Olmsted County, MN, residents aged 70–89 years on October 1, 2004, were evaluated using the Clinical Dementia Rating Scale, a neurological evaluation, and neuropsychological testing. Information ascertained for each participant was reviewed by an expert panel of neuropsychologists, physicians, and nurses, and a diagnosis of normal cognition, MCI, or dementia was made by consensus. C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis alpha (TNFα), and adiponectin were measured at baseline. Results Among 313 subjects with MCI and 1570 cognitively normal subjects, a CRP level in the upper quartile (>3.3 mg/L) was significantly associated with MCI (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.00–2.01) and with nonamnestic MCI (OR, 2.05; 95% CI, 1.12–3.78) after adjusting for age, sex, and years of education. However, there was no association with amnestic MCI (OR, 1.21; 95% CI, 0.81–1.82). No association was observed with the other inflammatory markers. Conclusions Plasma CRP is associated with prevalent MCI and with nonamnestic MCI in elderly, nondemented persons in a population-based setting. These findings suggest the involvement of inflammation in the pathogenesis of MCI.
  David S. Knopman , Ronald C. Petersen , Walter A. Rocca , Eric B. Larson and Mary Ganguli
  Passive surveillance for disease is a public health approach that relies on documentation available within existing health records for the region or community being studied. Its two primary advantages over active case-finding are the lower cost of research and the lower burden on the population under study. The effectiveness of passive case-finding depends on the comprehensiveness of the healthcare coverage in a given community and the adequacy of the available medical records. The Rochester Epidemiology Project has permitted dementia case detection for Olmsted County, Minnesota, using a medical records-linkage system. These data were compared with case ascertainment using direct assessment of individuals in an epidemiological study of the same community. At the Group Health Research Institute, investigators compared dementia and Alzheimer‘s disease cases detected using an electronic medical record database search with those identified by a parallel active case-finding study. In this article, the advantages and disadvantages of passive case-finding were discussed, and the following conclusion was drawn: the purpose of the study being conducted should determine the case-finding approach that is to be used.
  Walter A. Rocca , Ronald C. Petersen , David S. Knopman , Liesi E. Hebert , Denis A. Evans , Kathleen S. Hall , Sujuan Gao , Frederick W. Unverzagt , Kenneth M. Langa , Eric B. Larson and Lon R. White
  Declines in heart disease and stroke mortality rates are conventionally attributed to reductions in cigarette smoking, recognition and treatment of hypertension and diabetes, effective medications to improve serum lipid levels and to reduce clot formation, and general lifestyle improvements. Recent evidence implicates these and other cerebrovascular factors in the development of a substantial proportion of dementia cases. Analyses were undertaken to determine whether corresponding declines in age-specific prevalence and incidence rates for dementia and cognitive impairment have occurred in recent years. Data spanning 1 or 2 decades were examined from community-based epidemiological studies in Minnesota, Illinois, and Indiana, and from the Health and Retirement Study, which is a national survey. Although some decline was observed in the Minnesota cohort, no statistically significant trends were apparent in the community studies. A significant reduction in cognitive impairment measured by neuropsychological testing was identified in the national survey. Cautious optimism appears justified.
  Stephen D. Weigand , Prashanthi Vemuri , Heather J. Wiste , Matthew L. Senjem , Vernon S. Pankratz , Paul S. Aisen , Michael W. Weiner , Ronald C. Petersen , Leslie M. Shaw , John Q. Trojanowski , David S. Knopman and Clifford R. Jack
  Background Positron-emission tomography (PET) imaging of amyloid with Pittsburgh Compound B (PIB) and Aβ42 levels in the cerebrospinal fluid (CSF Aβ42) demonstrate a highly significant inverse correlation. Both these techniques are presumed to measure brain Aβ amyloid load. The objectives of this study were to develop a method to transform CSF Aβ42 measures into calculated PIB measures (PIBcalc) of Aβ amyloid load, and to partially validate the method in an independent sample of subjects. Methods In all, 41 subjects from the Alzheimer‘s Disease Neuroimaging Initiative (ADNI) underwent PIB PET imaging and lumbar puncture (LP) at the same time. This sample, referred to as the ”training“ sample (nine cognitively normal subjects, 22 subjects with mild cognitive impairment, and 10 subjects with Alzheimer‘s disease), was used to develop a regression model by which CSF Aβ42 (with apolipoprotein E ɛ4 carrier status as a covariate) was transformed into units of PIB PET (PIBcalc). An independent ”supporting“ sample of 362 ADNI subjects (105 cognitively normal subjects, 164 subjects with mild cognitive impairment, and 93 subjects with Alzheime‘s disease) who underwent LP but not PIB PET imaging had their CSF Aβ42 values converted to PIBcalc. These values were compared with the overall PIB PET distribution found in the ADNI subjects (n = 102). Results A linear regression model demonstrates good prediction of actual PIB PET from CSF Aβ42 measures obtained in the training sample (R2 = 0.77, P < .001). PIBcalc data (derived from CSF Aβ42) in the supporting sample of 362 ADNI subjects who underwent LP but not PIB PET imaging demonstrate group-wise distributions that are highly consistent with the larger ADNI PIB PET distribution and with published PIB PET imaging studies. Conclusion Although the precise parameters of this model are specific for the ADNI sample, we conclude that CSF Aβ42 can be transformed into PIBcalc measures of Aβ amyloid load. Brain Aβ amyloid load can be ascertained at baseline in therapeutic or observational studies by either CSF or amyloid PET imaging and the data can be pooled using well-established multiple imputation techniques that account for the uncertainty in a CSF-based PIBcalc value.
  Clifford R. Jack , Marilyn S. Albert , David S. Knopman , Guy M. McKhann , Reisa A. Sperling , Maria C. Carrillo , Bill Thies and Creighton H. Phelps
  Background Criteria for the clinical diagnosis of Alzheimer's disease (AD) were established in 1984. A broad consensus now exists that these criteria should be revised to incorporate state-of-the-art scientific knowledge. Methods The National Institute on Aging (NIA) and the Alzheimer's Association sponsored a series of advisory round table meetings in 2009 whose purpose was to establish a process for revising diagnostic and research criteria for AD. The recommendation from these advisory meetings was that three separate work groups should be formed with each assigned the task of formulating diagnostic criteria for one phase of the disease: the dementia phase; the symptomatic, pre-dementia phase; and the asymptomatic, preclinical phase of AD. Results Two notable differences from the AD criteria published in 1984 are incorporation of biomarkers of the underlying disease state and formalization of different stages of disease in the diagnostic criteria. There was a broad consensus within all three workgroups that much additional work is needed to validate the application of biomarkers for diagnostic purposes. In the revised NIA-Alzheimer's Association criteria, a semantic and conceptual distinction is made between AD pathophysiological processes and clinically observable syndromes that result, whereas this distinction was blurred in the 1984 criteria. Conclusions The new criteria for AD are presented in three documents. The core clinical criteria of the recommendations regarding AD dementia and MCI due to AD are intended to guide diagnosis in the clinical setting. However, the recommendations of the preclinical AD workgroup are intended purely for research purposes.
  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.
  David S. Knopman , Sandra Weintraub and Vernon S. Pankratz
  Background The six domain standard Clinical Dementia Rating Scale (CDRstd) has been successful for staging patients with the clinical syndrome of probable Alzheimer‘s disease (AD). The CDRstd does not specifically address language dysfunction or alteration in personality and social behaviors which are prominent in behavioral variant frontotemporal dementia (bvFTD) and primary progressive aphasia (PPA). Objective To determine the value of adding domains of Language (LANG), and Behavior, Comportment, and Personality (BEHAV) to the CDRstd for the evaluation of patients with bvFTD and PPA. Methods Two new domains, LANG and BEHAV, were constructed to parallel the six domains sampled in the CDRstd. Clinical and neuropsychological test data were obtained from the National Alzheimer‘s Coordinating Center. The dataset contained information on 2550 probable AD, 88 vascular dementia, 281 dementia with Lewy body, 234 bvFTD, and 137 PPA patients. Results There were 76.5% of bvFTD and 99.3% of PPA patients with abnormal ratings (>0) on the LANG domain; 90.2% of bvFTD and 63.5% of PPA had abnormal ratings on the BEHAV domain. In patients with a CDRstd sum of boxes score of <4, 53.7% of bvFTD had BEHAV domain and 78.6% of PPA patients had LANG domain scores >1. Among probable AD patients, 3.7% had LANG ratings that were ≥1 and 3.8% had BEHAV ratings that were ≥1. Logistic regression analyses showed that adding either the LANG or BEHAV domains to the CDRstd sum of boxes score significantly improved the discrimination between probable AD, bvFTD, and PPA. Conclusions The new LANG and BEHAV domains add value to the CDRstd for the characterization of the nonamnestic symptoms that are prominent in patients with bvFTD and PPA but that also occur in those with probable AD.
 
 
 
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