Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by Kaj Blennow
Total Records ( 6 ) for Kaj Blennow
  John Q. Trojanowski , Hugo Vandeerstichele , Magdalena Korecka , Christopher M. Clark , Paul S. Aisen , Ronald C. Petersen , Kaj Blennow , Holly Soares , Adam Simon , Piotr Lewczuk , Robert Dean , Eric Siemers , William Z. Potter , Michael W. Weiner , Clifford R. Jack Jr. , William Jagust , Arthur W. Toga , Virginia M.-Y. Lee and Leslie M. Shaw
  Here, we review progress by the Penn Biomarker Core in the Alzheimer's Disease Neuroimaging Initiative (ADNI) toward developing a pathological cerebrospinal fluid (CSF) and plasma biomarker signature for mild Alzheimer's disease (AD) as well as a biomarker profile that predicts conversion of mild cognitive impairment (MCI) and/or normal control subjects to AD. The Penn Biomarker Core also collaborated with other ADNI Cores to integrate data across ADNI to temporally order changes in clinical measures, imaging data, and chemical biomarkers that serve as mileposts and predictors of the conversion of normal control to MCI as well as MCI to AD, and the progression of AD. Initial CSF studies by the ADNI Biomarker Core revealed a pathological CSF biomarker signature of AD defined by the combination of Aβ1-42 and total tau (T-tau) that effectively delineates mild AD in the large multisite prospective clinical investigation conducted in ADNI. This signature appears to predict conversion from MCI to AD. Data fusion efforts across ADNI Cores generated a model for the temporal ordering of AD biomarkers which suggests that Aβ amyloid biomarkers become abnormal first, followed by changes in neurodegenerative biomarkers (CSF tau, F-18 fluorodeoxyglucose-positron emission tomography, magnetic resonance imaging) with the onset of clinical symptoms. The timing of these changes varies in individual patients due to genetic and environmental factors that increase or decrease an individual's resilience in response to progressive accumulations of AD pathologies. Further studies in ADNI will refine this model and render the biomarkers studied in ADNI more applicable to routine diagnosis and to clinical trials of disease modifying therapies.
  Hans Brunnstrom , Nina Rawshani , Henrik Zetterberg , Kaj Blennow , Lennart Minthon , Ulla Passant and Elisabet Englund
  Background Clinical dementia diagnoses are not always consistent with neuropathological findings. As correct diagnosis is important for treatment and care, new diagnostic possibilities for dementia are in demand. Cerebrospinal fluid biomarkers should ideally be able to identify ongoing processes in the brain, but need to be further compared with neuropathological findings for evaluation of their diagnostic validity. Methods This study included 43 patients with a clinical dementia disorder. All patients were neuropathologically examined at the University Hospital in Lund, Sweden, during the years 2001-2008, and all had a lumbar puncture carried out as part of the clinical investigation during the time of cognitive impairment. Results Of eight patients, five with Alzheimer's disease had elevated total tau protein (T-tau) and decreased amyloid beta 1-42 protein (Aβ42), while both values for the other three patients were normal. Slightly elevated T-tau and/or decreased Aβ42 were also seen in several patients with other dementia diagnoses such as Lewy body disease, frontotemporal lobar degeneration and vascular dementia. Furthermore, T-tau levels did not differ markedly between patients with morphologically tau-positive and tau-negative frontotemporal lobar degeneration. Also, seven of nine patients with Creutzfeldt-Jacob disease exhibited pronounced elevation in T-tau concentration. Conclusion From this rather limited study, being the first of its kind in Sweden, we may conclude that there is no perfect concordance between cerebrospinal fluid biomarker levels and pathological findings, which should be taken into account in the clinical diagnostic setting.
  Hugo Vanderstichele , Mirko Bibl , Sebastiaan Engelborghs , Nathalie Le Bastard , Piotr Lewczuk , Jose Luis Molinuevo , Lucilla Parnetti , Armand Perret- Liaudet , Leslie M. Shaw , Charlotte Teunissen , Dirk Wouters and Kaj Blennow
  Background Numerous studies show that the cerebrospinal fluid biomarkers total tau (T-tau), tau phosphorylated at threonine 181 (P-tau181P), and amyloid-β (1–42) (Aβ1–42) have high diagnostic accuracy for Alzheimer‘s disease. Variability in concentrations for Aβ1–42, T-tau, and P-tau181P drives the need for standardization. Methods Key issues were identified and discussed before the first meeting of the members of the Alzheimer‘s Biomarkers Standardization Initiative (ABSI). Subsequent ABSI consensus meetings focused on preanalytical issues. Results Consensus was reached on preanalytical issues such as the effects of fasting, different tube types, centrifugation, time and temperature before storage, storage temperature, repeated freeze/thaw cycles, and length of storage on concentrations of Aβ1–42, T-tau, and P-tau181P in cerebrospinal fluid. Conclusions The consensus reached on preanalytical issues and the recommendations put forward during the ABSI consensus meetings are presented in this paper.
  Mary D. Naylor , Jason H. Karlawish , Steven E. Arnold , Ara S. Khachaturian , Zaven S. Khachaturian , Virginia M.-Y. Lee , Matthew Baumgart , Sube Banerjee , Cornelia Beck , Kaj Blennow , Ron Brookmeyer , Kurt R. Brunden , Kathleen C. Buckwalter , Meryl Comer , Kenneth Covinsky , Lynn Friss Feinberg , Giovanni Frisoni , Colin Green , Renato Maia Guimaraes , Lisa P. Gwyther , Franz F. Hefti , Michael Hutton , Claudia Kawas , David M. Kent , Lewis Kuller , Kenneth M. Langa , Robert W. Mahley , Katie Maslow , Colin L. Masters , Diane E. Meier , Peter J. Neumann , Steven M. Paul , Ronald C. Petersen , Mark A. Sager , Mary Sano , Dale Schenk , Holly Soares , Reisa A. Sperling , Sidney M. Stahl , Vivianna van Deerlin , Yaakov Stern , David Weir , David A. Wolk and John Q. Trojanowski
  To address the pending public health crisis due to Alzheimer‘s disease (AD) and related neurodegenerative disorders, the Marian S. Ware Alzheimer Program at the University of Pennsylvania held a meeting entitled "State of the Science Conference on the Advancement of Alzheimer's Diagnosis, Treatment and Care," on June 21-22, 2012. The meeting comprised four workgroups focusing on Biomarkers; Clinical Care and Health Services Research; Drug Development; and Health Economics, Policy, and Ethics. The workgroups shared, discussed, and compiled an integrated set of priorities, recommendations, and action plans, which are presented in this article.
  Maria C. Carrillo , Kaj Blennow , Holly Soares , Piotr Lewczuk , Niklas Mattsson , Pankaj Oberoi , Robert Umek , Manu Vandijck , Salvatore Salamone , Tobias Bittner , Leslie M. Shaw , Diane Stephenson , Lisa Bain and Henrik Zetterberg
  Recognizing that international collaboration is critical for the acceleration of biomarker standardization efforts and the efficient development of improved diagnosis and therapy, the Alzheimer's Association created the Global Biomarkers Standardization Consortium (GBSC) in 2010. The consortium brings together representatives of academic centers, industry, and the regulatory community with the common goal of developing internationally accepted common reference standards and reference methods for the assessment of cerebrospinal fluid (CSF) amyloid β42 (Aβ42) and tau biomarkers. Such standards are essential to ensure that analytical measurements are reproducible and consistent across multiple laboratories and across multiple kit manufacturers. Analytical harmonization for CSF Aβ42 and tau will help reduce confusion in the AD community regarding the absolute values associated with the clinical interpretation of CSF biomarker results and enable worldwide comparison of CSF biomarker results across AD clinical studies.
  Niklas Mattsson , Ulf Andreasson , Staffan Persson , Maria C. Carrillo , Steven Collins , Sonia Chalbot , Neal Cutler , Diane Dufour- Rainfray , Anne M. Fagan , Niels H.H. Heegaard , Ging-Yuek Robin Hsiung , Bradley Hyman , Khalid Iqbal , D. Richard Lachno , Alberto Lleo , Piotr Lewczuk , Jose L. Molinuevo , Piero Parchi , Axel Regeniter , Robert Rissman , Hanna Rosenmann , Giuseppe Sancesario , Johannes Schroder , Leslie M. Shaw , Charlotte E. Teunissen , John Q. Trojanowski , Hugo Vanderstichele , Manu Vandijck , Marcel M. Verbeek , Henrik Zetterberg , Kaj Blennow and Stephan A. Kaser
  Background The cerebrospinal fluid (CSF) biomarkers amyloid beta 1–42, total tau, and phosphorylated tau are used increasingly for Alzheimer's disease (AD) research and patient management. However, there are large variations in biomarker measurements among and within laboratories. Methods Data from the first nine rounds of the Alzheimer's Association quality control program was used to define the extent and sources of analytical variability. In each round, three CSF samples prepared at the Clinical Neurochemistry Laboratory (Molndal, Sweden) were analyzed by single-analyte enzyme-linked immunosorbent assay (ELISA), a multiplexing xMAP assay, or an immunoassay with electrochemoluminescence detection. Results A total of 84 laboratories participated. Coefficients of variation (CVs) between laboratories were around 20% to 30%; within-run CVs, less than 5% to 10%; and longitudinal within-laboratory CVs, 5% to 19%. Interestingly, longitudinal within-laboratory CV differed between biomarkers at individual laboratories, suggesting that a component of it was assay dependent. Variability between kit lots and between laboratories both had a major influence on amyloid beta 1–42 measurements, but for total tau and phosphorylated tau, between-kit lot effects were much less than between-laboratory effects. Despite the measurement variability, the between-laboratory consistency in classification of samples (using prehoc-derived cutoffs for AD) was high (>90% in 15 of 18 samples for ELISA and in 12 of 18 samples for xMAP). Conclusions The overall variability remains too high to allow assignment of universal biomarker cutoff values for a specific intended use. Each laboratory must ensure longitudinal stability in its measurements and use internally qualified cutoff levels. Further standardization of laboratory procedures and improvement of kit performance will likely increase the usefulness of CSF AD biomarkers for researchers and clinicians.
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility