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1. MicroRNAs as Biomarkers of Brain Tumor

Author

Jelski W and Mroczko B

Subjects
micrornas, brain tumor, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Wojciech Jelski,1 Barbara Mroczko1,2 1Department of Biochemical Diagnostics, Medical University, Bialystok, Poland; 2Department of Neurodegeneration Diagnostics, Medical University, Bialystok, PolandCorrespondence: Wojciech Jelski, Department of Biochemical Diagnostics, Medical University, Waszyngtona 15 A, Bialystok, 15-269, Poland, Tel +48 85 746 8587, Fax +48 85 746 8585, Email wjelski@umb.edu.plAbstract: Brain tumors have been deadly cancers for years, and in most cases they are difficult to diagnose in their early stages. For this reason, researchers need to develop low-cost, sensitive methods for examining cancer biomarkers. Such biomarkers include microRNA. MicroRNA expression in various body fluids shows a high correlation with cancer. A number of studies have demonstrated changes in microRNA expression in cerebrospinal fluid and blood samples from patients with brain tumors. New biomarkers such as microRNAs may help diagnose brain tumors at the very beginning of the disease, enabling early treatment and increasing the chances of survival. This review describes the diagnostic role of microRNAs and the prospects for their use as biomarkers in patients with brain tumors.Keywords: microRNAs, brain tumor

Published
2024

2. Potential Diagnostic Utility of microRNAs in Gastrointestinal Cancers

Author

Jelski W and Mroczko B

Subjects
mirna, gastric cancer, colorectal cancer, esophageal cancer, diagnosis, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Wojciech Jelski,1 Barbara Mroczko1,2 1Department of Biochemical Diagnostics, Medical University, Bialystok, Poland; 2Department of Neurodegeneration Diagnostics, Medical University, Bialystok, PolandCorrespondence: Wojciech Jelski, Department of Biochemical Diagnostics, Medical University, Waszyngtona 15 A, Bialystok, 15– 269, Poland, Tel +48 85 746 8587, Fax +48 85 746 8585, Email wjelski@umb.edu.plAbstract: Early detection of gastrointestinal cancers is beneficial for patient survival and prognosis. MiRNAs have been shown to be potential cancer biomarkers that can be used to diagnose cancers. MiRNAs are single-stranded, small non-coding RNAs that are involved in the post-transcriptional regulation of the expression of different oncogenes. Cancer tissues contain miRNAs that play a special role in the etiology of cancer development or limiting cancer suppression. Dysregulation of miRNAs occurs in a variety of malignancies, including gastrointestinal cancers. MiRNAs are stable and protected against degradation by RNase, which enables their detection in tissues and biological fluids. The results of many studies suggest that miRNAs have a relatively higher diagnostic efficiency in distinguishing cancer patients from healthy people. The researchers have identified many miRNA signature in the blood for the detection of gastrointestinal cancers. This review focuses on the role and potential utility of miRNAs in the early detection, prognosis and evaluation of the treatment effectiveness of gastrointestinal cancers.Keywords: miRNA, gastric cancer, colorectal cancer, esophageal cancer, diagnosis

Published
2023

3. Biochemical Markers of Colorectal Cancer – Present and Future

Author

Jelski W and Mroczko B

Subjects
tumor markers, colorectal cancer, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Wojciech Jelski,1 Barbara Mroczko1,2 1Department of Biochemical Diagnostics, Medical University of Bialystok, Bialystok, Poland; 2Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Bialystok, PolandCorrespondence: Wojciech JelskiDepartment of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15 A, Bialystok 15– 269, PolandTel +48 85 746 8587Fax +48 85 746 8585Email wjelski@umb.edu.plAbstract: According to a report by the National Cancer Institute, colorectal cancer (CRC) is one of the most common types of cancer worldwide. CRC is often recognized too late for successful therapy. Tumor markers have been sought for a number of years to detect the transformation of malignant cells at the earliest possible stage. They are usually proteins associated with a malignancy and might be clinically useful in patients with cancer. Several classical markers have been used to recognize colorectal cancer, including carcinoembryonic antigen (CEA), carbohydrate antigen (CA 19.9), tissue polypeptide specific antigen (TPS) and tumor-associated glycoprotein-72 (TAG-72). None of these tests, however, have excellent diagnostic accuracy. Recent studies have been conducted on the use of hematopoietic growth factors (HGFs) and various enzymes in the diagnosis and prognosis of colorectal cancer. These include macrophage-colony stimulating factor (M-CSF) and granulocyte-macrophage-colony stimulating factor (GM-CSF), interleukin-3, interleukin-6 and enzymes (alcohol dehydrogenase and lysosomal exoglycosidases). Significantly, most cancer deaths are not caused by the primary tumor itself but by its spread. Analysis of circulating cancer cells (CTCs), ie, factors responsible for metastasis, may be a source of information useful in the treatment of patients with colorectal cancer. Currently available markers have significant limitations.Keywords: tumor markers, colorectal cancer

Published
2020

9. Seroprevalence of Helicobacter pylori infection in Polish children and adults depending on socioeconomic status and living conditions

Author

Annabhani, A., Bała, G., Bąk-Romaniszyn, L., Budzyńska, A., Cader, J., Celiński, K., Cichy, W., Czerwionka-Szaflarska, M., Czkwianianc, E., Czosnek, R., Czykwin, M., Daniluk, J., Długosz, J., Dzieniszewski, J., Dzierżanowska, D., Dzierżanowska-Fangrat, K., Forencewicz, J., Gościniak, G., Ignyś, I., Jarosz, M., Jaroszewicz-Heidelmann, H., Jędrychowski, W., Kaczmarski, M., Kemona, A., Kiełtyka, A., Klincewicz, B., Kosidło, S., Maciorkowska, E., Marlicz, K., Matusiewicz, K., Mierzwa, G., Mroczko, B., Nowak, A., Paradowski, L., Płaneta-Małecka, I., Pytrus, T., Roszko, I., Romańczuk, W., Rożynek, E., Rymarczyk, G., Słomka, M., Smereka, A., Starzyńska, T., Swincow, G., Szaflarska, M., Szaflarska-Popławska, A., Szafraniec, K., Szmitkowski, M., Wasielica-Berger, J., Wereszczyńska-Siemiątkowska, U., Wogtt, E., Wojda, U., Wróblewski, E., Zielińska, I., Zimnicki, P., Łaszewicz, Wiktor, Iwańczak, Franciszek, and Iwańczak, Barbara

Published
2014
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13. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview

Author

Delaby, C., Teunissen, C.E., Blennow, K., Alcolea, D., Arisi, I., Amar, E.B., Beaume, A., Bedel, A., Bellomo, G., Bigot-Corbel, E., Bjerke, M., Blanc-Quintin, M.C., Boada, M., Bousiges, O., Chapman, M.D., DeMarco, M.L., D'Onofrio, M., Dumurgier, J., Dufour-Rainfray, D., Engelborghs, S., Esselmann, H., Fogli, A., Gabelle, A., Galloni, E., Gondolf, C., Grandhomme, F., Grau-Rivera, O., Hart, M., Ikeuchi, T., Jeromin, A., Kasuga, K., Keshavan, A., Khalil, M., Körtvelyessy, P., Kulczynska-Przybik, A., Laplanche, J.L., Lewczuk, P., Li, Q.X., Lleó, A., Malaplate, C., Marquié, M., Masters, C.L., Mroczko, B., Nogueira, L., Orellana, A., Otto, M., Oudart, J.B., Paquet, C., Paoletti, F.P., Parnetti, L., Perret-Liaudet, A., Peoc'h, K., Poesen, K., Puig-Pijoan, A., Quadrio, I., Quillard-Muraine, M., Rucheton, B., Schraen, S., Schott, J.M., Shaw, L.M., Suárez-Calvet, M., Tsolaki, M., Tumani, H., Udeh-Momoh, C.T., Vaudran, L., Verbeek, M.M., Verde, F., Vermunt, L., Vogelgsang, J., Wiltfang, J., Zetterberg, H., Lehmann, S., Delaby, C., Teunissen, C.E., Blennow, K., Alcolea, D., Arisi, I., Amar, E.B., Beaume, A., Bedel, A., Bellomo, G., Bigot-Corbel, E., Bjerke, M., Blanc-Quintin, M.C., Boada, M., Bousiges, O., Chapman, M.D., DeMarco, M.L., D'Onofrio, M., Dumurgier, J., Dufour-Rainfray, D., Engelborghs, S., Esselmann, H., Fogli, A., Gabelle, A., Galloni, E., Gondolf, C., Grandhomme, F., Grau-Rivera, O., Hart, M., Ikeuchi, T., Jeromin, A., Kasuga, K., Keshavan, A., Khalil, M., Körtvelyessy, P., Kulczynska-Przybik, A., Laplanche, J.L., Lewczuk, P., Li, Q.X., Lleó, A., Malaplate, C., Marquié, M., Masters, C.L., Mroczko, B., Nogueira, L., Orellana, A., Otto, M., Oudart, J.B., Paquet, C., Paoletti, F.P., Parnetti, L., Perret-Liaudet, A., Peoc'h, K., Poesen, K., Puig-Pijoan, A., Quadrio, I., Quillard-Muraine, M., Rucheton, B., Schraen, S., Schott, J.M., Shaw, L.M., Suárez-Calvet, M., Tsolaki, M., Tumani, H., Udeh-Momoh, C.T., Vaudran, L., Verbeek, M.M., Verde, F., Vermunt, L., Vogelgsang, J., Wiltfang, J., Zetterberg, H., and Lehmann, S.

Abstract

Item does not contain fulltext, INTRODUCTION: The current practice of quantifying cerebrospinal fluid (CSF) biomarkers as an aid in the diagnosis of Alzheimer's disease (AD) varies from center to center. For a same biochemical profile, interpretation and reporting of results may differ, which can lead to misunderstandings and raises questions about the commutability of tests. METHODS: We obtained a description of (pre-)analytical protocols and sample reports from 40 centers worldwide. A consensus approach allowed us to propose harmonized comments corresponding to the different CSF biomarker profiles observed in patients. RESULTS: The (pre-)analytical procedures were similar between centers. There was considerable heterogeneity in cutoff definitions and report comments. We therefore identified and selected by consensus the most accurate and informative comments regarding the interpretation of CSF biomarkers in the context of AD diagnosis. DISCUSSION: This is the first time that harmonized reports are proposed across worldwide specialized laboratories involved in the biochemical diagnosis of AD.

Published
2022

15. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview

Author

Delaby, C, Teunissen, CE, Blennow, K, Alcolea, D, Arisi, I, Amar, EB, Beaume, A, Bedel, A, Bellomo, G, Bigot-Corbel, E, Bjerke, M, Blanc-Quintin, M-C, Boada, M, Bousiges, O, Chapman, MD, DeMarco, ML, D'Onofrio, M, Dumurgier, J, Dufour-Rainfray, D, Engelborghs, S, Esselmann, H, Fogli, A, Gabelle, A, Galloni, E, Gondolf, C, Grandhomme, F, Grau-Rivera, O, Hart, M, Ikeuchi, T, Jeromin, A, Kasuga, K, Keshavan, A, Khalil, M, Koertvelyessy, P, Kulczynska-Przybik, A, Laplanche, J-L, Lewczuk, P, Li, Q-X, Lleo, A, Malaplate, C, Marquie, M, Masters, CL, Mroczko, B, Nogueira, L, Orellana, A, Otto, M, Oudart, J-B, Paquet, C, Paoletti, FP, Parnetti, L, Perret-Liaudet, A, Peoc'h, K, Poesen, K, Puig-Pijoan, A, Quadrio, I, Quillard-Muraine, M, Rucheton, B, Schraen, S, Schott, JM, Shaw, LM, Suarez-Calvet, M, Tsolaki, M, Tumani, H, Udeh-Momoh, CT, Vaudran, L, Verbeek, MM, Verde, F, Vermunt, L, Vogelgsang, J, Wiltfang, J, Zetterberg, H, Lehmann, S, Delaby, C, Teunissen, CE, Blennow, K, Alcolea, D, Arisi, I, Amar, EB, Beaume, A, Bedel, A, Bellomo, G, Bigot-Corbel, E, Bjerke, M, Blanc-Quintin, M-C, Boada, M, Bousiges, O, Chapman, MD, DeMarco, ML, D'Onofrio, M, Dumurgier, J, Dufour-Rainfray, D, Engelborghs, S, Esselmann, H, Fogli, A, Gabelle, A, Galloni, E, Gondolf, C, Grandhomme, F, Grau-Rivera, O, Hart, M, Ikeuchi, T, Jeromin, A, Kasuga, K, Keshavan, A, Khalil, M, Koertvelyessy, P, Kulczynska-Przybik, A, Laplanche, J-L, Lewczuk, P, Li, Q-X, Lleo, A, Malaplate, C, Marquie, M, Masters, CL, Mroczko, B, Nogueira, L, Orellana, A, Otto, M, Oudart, J-B, Paquet, C, Paoletti, FP, Parnetti, L, Perret-Liaudet, A, Peoc'h, K, Poesen, K, Puig-Pijoan, A, Quadrio, I, Quillard-Muraine, M, Rucheton, B, Schraen, S, Schott, JM, Shaw, LM, Suarez-Calvet, M, Tsolaki, M, Tumani, H, Udeh-Momoh, CT, Vaudran, L, Verbeek, MM, Verde, F, Vermunt, L, Vogelgsang, J, Wiltfang, J, Zetterberg, H, and Lehmann, S

Abstract

INTRODUCTION: The current practice of quantifying cerebrospinal fluid (CSF) biomarkers as an aid in the diagnosis of Alzheimer's disease (AD) varies from center to center. For a same biochemical profile, interpretation and reporting of results may differ, which can lead to misunderstandings and raises questions about the commutability of tests. METHODS: We obtained a description of (pre-)analytical protocols and sample reports from 40 centers worldwide. A consensus approach allowed us to propose harmonized comments corresponding to the different CSF biomarker profiles observed in patients. RESULTS: The (pre-)analytical procedures were similar between centers. There was considerable heterogeneity in cutoff definitions and report comments. We therefore identified and selected by consensus the most accurate and informative comments regarding the interpretation of CSF biomarkers in the context of AD diagnosis. DISCUSSION: This is the first time that harmonized reports are proposed across worldwide specialized laboratories involved in the biochemical diagnosis of AD.

Published
2021

19. Association of cerebral amyloid-β Aggregation with cognitive functioning in persons without dementia

Author

Jansen, WJ, Ossenkoppele, R, Tijms, BM, Fagan, AM, Hansson, O, Klunk, WE, Van Der Flier, WM, Villemagne, VL, Frisoni, GB, Fleisher, AS, Lleó, A, Mintun, MA, Wallin, A, Engelborghs, S, Na, DL, Chételat, G, Molinuevo, JL, Landau, SM, Mattsson, N, Kornhuber, J, Sabri, O, Rowe, CC, Parnetti, L, Popp, J, Fladby, T, Jagust, WJ, Aalten, P, Lee, DY, Vandenberghe, R, De Oliveira, CR, Kapaki, E, Froelich, L, Ivanoiu, A, Gabryelewicz, T, Verbeek, MM, Sanchez-Juan, P, Hildebrandt, H, Camus, V, Zboch, M, Brooks, DJ, Drzezga, A, Rinne, JO, Newberg, A, De Mendonça, A, Sarazin, M, Rabinovici, GD, Madsen, K, Kramberger, MG, Nordberg, A, Mok, V, Mroczko, B, Wolk, DA, Meyer, PT, Tsolaki, M, Scheltens, P, Verhey, FRJ, Visser, PJ, Aarsland, D, Alcolea, D, Alexander, M, Almdahl, IS, Arnold, SE, Baldeiras, I, Barthel, H, Van Berckel, BNM, Blennow, K, Van Buchem, MA, Cavedo, E, Chen, K, Chipi, E, Cohen, AD, Förster, S, Fortea, J, Frederiksen, KS, Freund-Levi, Y, Gkatzima, O, Gordon, MF, Grimmer, T, Hampel, H, Hausner, L, Hellwig, S, Herukka, SK, Johannsen, P, Klimkowicz-Mrowiec, A, Köhler, S, and Koglin, N

Subjects
mental disorders
Abstract

IMPORTANCE Cerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials. OBJECTIVE To investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017. MAIN OUTCOMES AND MEASURES Global cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score≤27 or memory z score≤-1.28) and to assess whether this association was moderated by age, sex, educational level, or apolipoprotein E genotype. RESULTS Among 2908 persons with normal cognition (mean [SD] age, 67.4 [12.8] years), amyloid positivity was associated with low memory scores after age 70 years (mean difference in amyloid positive vs negative, 4%[95%CI, 0%-7%] at 72 years and 21% [95%CI, 10%-33%] at 90 years) but was not associated with low MMSE scores (mean difference, 3%[95%CI, -1%to 6%], P = .16). Among 4133 patients with MCI (mean [SD] age, 70.2 [8.5] years), amyloid positivity was associated with low memory (mean difference, 16%[95%CI, 12%-20%], P < .001) and low MMSE (mean difference, 14%[95%CI, 12%-17%], P < .001) scores, and this association decreased with age. Low cognitive scores had limited utility for screening of amyloid positivity in persons with normal cognition and those with MCI. In persons with normal cognition, the age-related increase in low memory score paralleled the age-related increase in amyloid positivity with an intervening period of 10 to 15 years. CONCLUSIONS AND RELEVANCE Although low memory scores are an early marker of amyloid positivity, their value as a screening measure for early AD among persons without dementia is limited.

Published
2018

20. Association of Cerebral Amyloid-beta Aggregation With Cognitive Functioning in Persons Without Dementia

Author

Jansen, WJ, Ossenkoppele, R, Tijms, BM, Fagan, AM, Hansson, O, Klunk, WE, van der Flier, WM, Villemagne, VL, Frisoni, GB, Fleisher, AS, Lleo, A, Mintun, MA, Wallin, A, Engelborghs, S, Na, DL, Chetelat, G, Molinuevo, JL, Landau, SM, Mattsson, N, Kornhuber, J, Sabri, O, Rowe, CC, Parnetti, L, Popp, J, Fladby, T, Jagust, WJ, Aalten, P, Lee, DY, Vandenberghe, R, de Oliveira, CR, Kapaki, E, Froelich, L, Ivanoiu, A, Gabryelewicz, T, Verbeek, MM, Sanchez-Juan, P, Hildebrandt, H, Camus, V, Zboch, M, Brooks, DJ, Drzezga, A, Rinne, JO, Newberg, A, de Mendonca, A, Sarazin, M, Rabinovici, GD, Madsen, K, Kramberger, MG, Nordberg, A, Mok, V, Mroczko, B, Wolk, DA, Meyer, PT, Tsolaki, M, Scheltens, P, Verhey, FRJ, Visser, PJ, and Amyloid Biomarker Study Grp

Subjects
mental disorders
Abstract

IMPORTANCE Cerebral amyloid-beta aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials. OBJECTIVE To investigate whether amyloid-beta aggregation is associated with cognitive functioning in persons without dementia. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017. MAIN OUTCOMES AND MEASURES Global cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score

Published
2018

21. Association of cerebral amyloid-β Aggregation with cognitive functioning in persons without dementia

Author

Jansen, W.J. Ossenkoppele, R. Tijms, B.M. Fagan, A.M. Hansson, O. Klunk, W.E. Van Der Flier, W.M. Villemagne, V.L. Frisoni, G.B. Fleisher, A.S. Lleó, A. Mintun, M.A. Wallin, A. Engelborghs, S. Na, D.L. Chételat, G. Molinuevo, J.L. Landau, S.M. Mattsson, N. Kornhuber, J. Sabri, O. Rowe, C.C. Parnetti, L. Popp, J. Fladby, T. Jagust, W.J. Aalten, P. Lee, D.Y. Vandenberghe, R. De Oliveira, C.R. Kapaki, E. Froelich, L. Ivanoiu, A. Gabryelewicz, T. Verbeek, M.M. Sanchez-Juan, P. Hildebrandt, H. Camus, V. Zboch, M. Brooks, D.J. Drzezga, A. Rinne, J.O. Newberg, A. De Mendonça, A. Sarazin, M. Rabinovici, G.D. Madsen, K. Kramberger, M.G. Nordberg, A. Mok, V. Mroczko, B. Wolk, D.A. Meyer, P.T. Tsolaki, M. Scheltens, P. Verhey, F.R.J. Visser, P.J. Aarsland, D. Alcolea, D. Alexander, M. Almdahl, I.S. Arnold, S.E. Baldeiras, I. Barthel, H. Van Berckel, B.N.M. Blennow, K. Van Buchem, M.A. Cavedo, E. Chen, K. Chipi, E. Cohen, A.D. Förster, S. Fortea, J. Frederiksen, K.S. Freund-Levi, Y. Gkatzima, O. Gordon, M.F. Grimmer, T. Hampel, H. Hausner, L. Hellwig, S. Herukka, S.-K. Johannsen, P. Klimkowicz-Mrowiec, A. Köhler, S. Koglin, N. Van Laere, K. De Leon, M. Lisetti, V. Maier, W. Marcusson, J. Meulenbroek, O. Møllergård, H.M. Morris, J.C. Nordlund, A. Novak, G.P. Paraskevas, G.P. Perera, G. Peters, O. Ramakers, I.H.G.B. Rami, L. Rodríguez-Rodríguez, E. Roe, C.M. Rot, U. Rüther, E. Santana, I. Schröder, J. Seo, S.W. Sorininen, H. Spiru, L. Stomrud, E. Struyfs, H. Teunissen, C.E. Vos, S.J.B. Van Waalwijk Van Doorn, L.J.C. Waldemar, G. Wallin, Å.K. Wiltfang, J. Zetterberg, H. Amyloid Biomarker Study Group

Subjects
mental disorders
Abstract

IMPORTANCE Cerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials. OBJECTIVE To investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017. MAIN OUTCOMES AND MEASURES Global cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score≤27 or memory z score≤-1.28) and to assess whether this association was moderated by age, sex, educational level, or apolipoprotein E genotype. RESULTS Among 2908 persons with normal cognition (mean [SD] age, 67.4 [12.8] years), amyloid positivity was associated with low memory scores after age 70 years (mean difference in amyloid positive vs negative, 4%[95%CI, 0%-7%] at 72 years and 21% [95%CI, 10%-33%] at 90 years) but was not associated with low MMSE scores (mean difference, 3%[95%CI, -1%to 6%], P = .16). Among 4133 patients with MCI (mean [SD] age, 70.2 [8.5] years), amyloid positivity was associated with low memory (mean difference, 16%[95%CI, 12%-20%], P < .001) and low MMSE (mean difference, 14%[95%CI, 12%-17%], P < .001) scores, and this association decreased with age. Low cognitive scores had limited utility for screening of amyloid positivity in persons with normal cognition and those with MCI. In persons with normal cognition, the age-related increase in low memory score paralleled the age-related increase in amyloid positivity with an intervening period of 10 to 15 years. CONCLUSIONS AND RELEVANCE Although low memory scores are an early marker of amyloid positivity, their value as a screening measure for early AD among persons without dementia is limited.

Published
2018

31. Prevalence of the apolipoprotein E epsilon4 allele in amyloid beta positive subjects across the spectrum of Alzheimer's disease

Author

Mattsson, N., Groot, C. de, Jansen, W.J., Landau, S.M., Villemagne, V.L., Engelborghs, S., Mintun, M.M., Lleo, A., Molinuevo, J.L., Jagust, W.J., Frisoni, G.B., Ivanoiu, A., Chetelat, G., Oliveira, C. de, Rodrigue, K.M., Kornhuber, J., Wallin, A., Klimkowicz-Mrowiec, A., Kandimalla, R., Popp, J., Aalten, P.P., Aarsland, D., Alcolea, D., Almdahl, I.S., Baldeiras, I., Buchem, M.A. van, Cavedo, E., Chen, K., Cohen, A.D., Forster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Gill, K.D., Gkatzima, O., Grimmer, T., Hampel, H., Herukka, S.K., Johannsen, P., Laere, K. Van, Leon, M.J. de, Maier, W., Marcusson, J., Meulenbroek, O.V., Mollergard, H.M., Morris, J.C., Mroczko, B., Nordlund, A., Prabhakar, S., Peters, O., Rami, L., Rodriguez-Rodriguez, E., Roe, C.M., Ruther, E., Santana, I., Schroder, J., Seo, S.W., Soininen, H., Spiru, L., Stomrud, E., Struyfs, H., Teunissen, C.E., Verhey, F.R.J., Vos, S.J.B., Waalwijk van Doorn, L.L.C. van, Waldemar, G., Wallin, A.K., Wiltfang, J., Vandenberghe, R., Brooks, D.J., Fladby, T., Rowe, C.C., Drzezga, A., Verbeek, M.M., Sarazin, M., Wolk, D.A., Fleisher, A.S., Klunk, W.E., Na, D.L., Sanchez-Juan, P., Lee, D.Y., Nordberg, A., Tsolaki, M., Camus, V., Rinne, J.O., Fagan, A.M., Zetterberg, H., Blennow, K., Rabinovici, G.D., Hansson, O., Berckel, B.N. van, Flier, W.M. van der, Scheltens, P., Visser, P.J., Ossenkoppele, R., Mattsson, N., Groot, C. de, Jansen, W.J., Landau, S.M., Villemagne, V.L., Engelborghs, S., Mintun, M.M., Lleo, A., Molinuevo, J.L., Jagust, W.J., Frisoni, G.B., Ivanoiu, A., Chetelat, G., Oliveira, C. de, Rodrigue, K.M., Kornhuber, J., Wallin, A., Klimkowicz-Mrowiec, A., Kandimalla, R., Popp, J., Aalten, P.P., Aarsland, D., Alcolea, D., Almdahl, I.S., Baldeiras, I., Buchem, M.A. van, Cavedo, E., Chen, K., Cohen, A.D., Forster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Gill, K.D., Gkatzima, O., Grimmer, T., Hampel, H., Herukka, S.K., Johannsen, P., Laere, K. Van, Leon, M.J. de, Maier, W., Marcusson, J., Meulenbroek, O.V., Mollergard, H.M., Morris, J.C., Mroczko, B., Nordlund, A., Prabhakar, S., Peters, O., Rami, L., Rodriguez-Rodriguez, E., Roe, C.M., Ruther, E., Santana, I., Schroder, J., Seo, S.W., Soininen, H., Spiru, L., Stomrud, E., Struyfs, H., Teunissen, C.E., Verhey, F.R.J., Vos, S.J.B., Waalwijk van Doorn, L.L.C. van, Waldemar, G., Wallin, A.K., Wiltfang, J., Vandenberghe, R., Brooks, D.J., Fladby, T., Rowe, C.C., Drzezga, A., Verbeek, M.M., Sarazin, M., Wolk, D.A., Fleisher, A.S., Klunk, W.E., Na, D.L., Sanchez-Juan, P., Lee, D.Y., Nordberg, A., Tsolaki, M., Camus, V., Rinne, J.O., Fagan, A.M., Zetterberg, H., Blennow, K., Rabinovici, G.D., Hansson, O., Berckel, B.N. van, Flier, W.M. van der, Scheltens, P., Visser, P.J., and Ossenkoppele, R.

Abstract

Item does not contain fulltext, INTRODUCTION: Apolipoprotein E (APOE) epsilon4 is the major genetic risk factor for Alzheimer's disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid beta (Abeta) pathology. METHODS: We included 3451 Abeta+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE epsilon4 prevalence in relation to age, sex, education, and geographical location. RESULTS: The APOE epsilon4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in Abeta+ cognitively normal and Abeta+ mild cognitive impairment (P < .05) but not in Abeta+ AD dementia (P = .66). The prevalence was highest in Northern Europe but did not vary by sex or education. DISCUSSION: The APOE epsilon4 prevalence in AD was higher than that in previous studies, which did not require presence of Abeta pathology. Furthermore, our results highlight disease heterogeneity related to age and geographical location.

Published
2018

32. Association of Cerebral Amyloid-beta Aggregation With Cognitive Functioning in Persons Without Dementia

Author

Jansen, W.J., Ossenkoppele, R., Tijms, B.M., Fagan, A.M., Hansson, O., Klunk, W.E., Flier, W.M. van der, Villemagne, V.L., Frisoni, G.B., Fleisher, A.S., Lleo, A., Mintun, M.A., Wallin, A., Engelborghs, S., Na, D.L., Chetelat, G., Molinuevo, J.L., Landau, S.M., Mattsson, N., Kornhuber, J., Sabri, O., Rowe, C.C., Parnetti, L., Popp, J., Fladby, T., Jagust, W.J., Aalten, P., Lee, D.Y., Vandenberghe, R., Oliveira, C. de, Kapaki, E., Froelich, L., Ivanoiu, A., Gabryelewicz, T., Verbeek, M.M., Sanchez-Juan, P., Hildebrandt, H., Camus, V., Zboch, M., Brooks, D.J., Drzezga, A., Rinne, J.O., Newberg, A., Mendonca, A. de, Sarazin, M., Rabinovici, G.D., Madsen, K., Kramberger, M.G., Nordberg, A., Mok, V., Mroczko, B., Wolk, D.A., Meyer, P.T., Tsolaki, M., Scheltens, P., Verhey, F.R.J., Visser, P.J., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I.S., Arnold, S.E., Baldeiras, I., Barthel, H., Berckel, B.N. van, Blennow, K., Buchem, M.A. van, Cavedo, E., Chen, K., Chipi, E., Cohen, A.D., Forster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Gkatzima, O., Gordon, M.F., Grimmer, T., Hampel, H., Hausner, L., Hellwig, S., Herukka, S.K., Johannsen, P., Klimkowicz-Mrowiec, A., Kohler, S., Koglin, N., Laere, K. Van, Leon, M., Lisetti, V., Maier, W., Marcusson, J., Meulenbroek, O., Mollergard, H.M., Morris, J.C., Nordlund, A., Novak, G.P., Paraskevas, G.P., Perera, G., Peters, O., Ramakers, I., et al., Jansen, W.J., Ossenkoppele, R., Tijms, B.M., Fagan, A.M., Hansson, O., Klunk, W.E., Flier, W.M. van der, Villemagne, V.L., Frisoni, G.B., Fleisher, A.S., Lleo, A., Mintun, M.A., Wallin, A., Engelborghs, S., Na, D.L., Chetelat, G., Molinuevo, J.L., Landau, S.M., Mattsson, N., Kornhuber, J., Sabri, O., Rowe, C.C., Parnetti, L., Popp, J., Fladby, T., Jagust, W.J., Aalten, P., Lee, D.Y., Vandenberghe, R., Oliveira, C. de, Kapaki, E., Froelich, L., Ivanoiu, A., Gabryelewicz, T., Verbeek, M.M., Sanchez-Juan, P., Hildebrandt, H., Camus, V., Zboch, M., Brooks, D.J., Drzezga, A., Rinne, J.O., Newberg, A., Mendonca, A. de, Sarazin, M., Rabinovici, G.D., Madsen, K., Kramberger, M.G., Nordberg, A., Mok, V., Mroczko, B., Wolk, D.A., Meyer, P.T., Tsolaki, M., Scheltens, P., Verhey, F.R.J., Visser, P.J., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I.S., Arnold, S.E., Baldeiras, I., Barthel, H., Berckel, B.N. van, Blennow, K., Buchem, M.A. van, Cavedo, E., Chen, K., Chipi, E., Cohen, A.D., Forster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Gkatzima, O., Gordon, M.F., Grimmer, T., Hampel, H., Hausner, L., Hellwig, S., Herukka, S.K., Johannsen, P., Klimkowicz-Mrowiec, A., Kohler, S., Koglin, N., Laere, K. Van, Leon, M., Lisetti, V., Maier, W., Marcusson, J., Meulenbroek, O., Mollergard, H.M., Morris, J.C., Nordlund, A., Novak, G.P., Paraskevas, G.P., Perera, G., Peters, O., and Ramakers, I., et al.

Abstract

Contains fulltext : 190311.pdf (Publisher’s version ) (Closed access), Importance: Cerebral amyloid-beta aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials. Objective: To investigate whether amyloid-beta aggregation is associated with cognitive functioning in persons without dementia. Design, Setting, and Participants: This cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017. Main Outcomes and Measures: Global cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score

Published
2018

33. Prevalence of cerebral amyloid pathology in persons without dementia: A meta-analysis

Author

Jansen, WJ, Ossenkoppele, R, Knol, DL, Tijms, BM, Scheltens, P, Verhey, FRJ, Visser, PJ, Aalten, P, Aarsland, D, Alcolea, D, Alexander, M, Almdahl, IS, Arnold, SE, Baldeiras, I, Barthel, H, Van Berckel, BNM, Bibeau, K, Blennow, K, Brooks, DJ, Van Buchem, MA, Camus, V, Cavedo, E, Chen, K, Chetelat, G, Cohen, AD, Drzezga, A, Engelborghs, S, Fagan, AM, Fladby, T, Fleisher, AS, Van Der Flier, WM, Ford, L, Forster, S, Fortea, J, Foskett, N, Frederiksen, KS, Freund-Levi, Y, Frisoni, GB, Froelich, L, Gabryelewicz, T, Gill, KD, Gkatzima, O, Gomez-Tortosa, E, Gordon, MF, Grimmer, T, Hampel, H, Hausner, L, Hellwig, S, Herukka, SK, Hildebrandt, H, Ishihara, L, Ivanoiu, A, Jagust, WJ, Johannsen, P, Kandimalla, R, Kapaki, E, Klimkowicz-Mrowiec, A, Klunk, WE, Kohler, S, Koglin, N, Kornhuber, J, Kramberger, MG, Van Laere, K, Landau, SM, Lee, DY, De Leon, M, Lisetti, V, Lleo, A, Madsen, K, Maier, W, Marcusson, J, Mattsson, N, De Mendonca, A, Meulenbroek, O, Meyer, PT, Mintun, MA, Mok, V, Molinuevo, JL, Mollergard, HM, Morris, JC, Mroczko, B, Van Der Mussele, S, Na, DL, Newberg, A, Nordberg, A, Nordlund, A, Novak, GP, Paraskevas, GP, and Parnetti, L

Subjects
mental disorders
Abstract

Copyright 2015 American Medical Association. All rights reserved. IMPORTANCE: Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies. OBJECTIVE To use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI). DATA SOURCES: Relevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE andWeb of Science databases and through personal communication with investigators. STUDY SELECTION: Studies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity. DATA EXTRACTION: AND SYNTHESIS: Individual recordswere provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies. MAIN OUTCOMES AND MEASURES: Prevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations. RESULTS The prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95%CI, 8%-13%) to 44%(95%CI, 37%-51%) among participants with normal cognition; from 12%(95%CI, 8%-18%) to 43%(95%CI, 32%-55%) among patients with SCI; and from 27%(95%CI, 23%-32%) to 71%(95%CI, 66%-76%) among patients with MCI. APOE-ϵ4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ϵ4ϵ4 carriers, 50 years for ϵ2ϵ4 carriers, 55 years for ϵ3ϵ4 carriers, 65 years for ϵ3ϵ3 carriers, and 95 years for ϵ2ϵ3 carriers. Amyloid positivity was more common in highly educated participants but not associated with sex or biomarker modality. CONCLUSIONS AND RELEVANCE: Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. These findings suggest a 20- to 30-year interval between first development of amyloid positivity and onset of dementia.

Published
2015

34. Cerebrospinal fluid biomarkers in trials for Alzheimer and Parkinson diseases

Author

Lleo, A, Cavedo, E, Parnetti, L, Vanderstichele, H, Herukka, SK, Andreasen, N, Ghidoni, R, Lewczuk, P, Jeromin, A, Winblad, B, Tsolaki, M, Mroczko, B, Visser, PJ, Santana, I, Svenningsson, P, Blennow, K, Aarsland, D, Molinuevo, JL, Zetterberg, H, and Mollenhauer, B

Abstract

Alzheimer disease (AD) and Parkinson disease (PD) are the most common neurodegenerative disorders. For both diseases, early intervention is thought to be essential to the success of disease-modifying treatments. Cerebrospinal fluid (CSF) can reflect some of the pathophysiological changes that occur in the brain, and the number of CSF biomarkers under investigation in neurodegenerative conditions has grown rapidly in the past 20 years. In AD, CSF biomarkers are increasingly being used in clinical practice, and have been incorporated into the majority of clinical trials to demonstrate target engagement, to enrich or stratify patient groups, and to find evidence of disease modification. In PD, CSF biomarkers have not yet reached the clinic, but are being studied in patients with parkinsonism, and are being used in clinical trials either to monitor progression or to demonstrate target engagement and downstream effects of drugs. CSF biomarkers might also serve as surrogate markers of clinical benefit after a specific therapeutic intervention, although additional data are required. It is anticipated that CSF biomarkers will have an important role in trials aimed at disease modification in the near future. In this Review, we provide an overview of CSF biomarkers in AD and PD, and discuss their role in clinical trials.

Published
2015

35. Prevalence of cerebral amyloid pathology in persons without dementia: A meta-analysis

Author

Jansen, W.J. Ossenkoppele, R. Knol, D.L. Tijms, B.M. Scheltens, P. Verhey, F.R.J. Visser, P.J. Aalten, P. Aarsland, D. Alcolea, D. Alexander, M. Almdahl, I.S. Arnold, S.E. Baldeiras, I. Barthel, H. Van Berckel, B.N.M. Bibeau, K. Blennow, K. Brooks, D.J. Van Buchem, M.A. Camus, V. Cavedo, E. Chen, K. Chetelat, G. Cohen, A.D. Drzezga, A. Engelborghs, S. Fagan, A.M. Fladby, T. Fleisher, A.S. Van Der Flier, W.M. Ford, L. Forster, S. Fortea, J. Foskett, N. Frederiksen, K.S. Freund-Levi, Y. Frisoni, G.B. Froelich, L. Gabryelewicz, T. Gill, K.D. Gkatzima, O. Gomez-Tortosa, E. Gordon, M.F. Grimmer, T. Hampel, H. Hausner, L. Hellwig, S. Herukka, S.-K. Hildebrandt, H. Ishihara, L. Ivanoiu, A. Jagust, W.J. Johannsen, P. Kandimalla, R. Kapaki, E. Klimkowicz-Mrowiec, A. Klunk, W.E. Kohler, S. Koglin, N. Kornhuber, J. Kramberger, M.G. Van Laere, K. Landau, S.M. Lee, D.Y. De Leon, M. Lisetti, V. Lleo, A. Madsen, K. Maier, W. Marcusson, J. Mattsson, N. De Mendonca, A. Meulenbroek, O. Meyer, P.T. Mintun, M.A. Mok, V. Molinuevo, J.L. Mollergard, H.M. Morris, J.C. Mroczko, B. Van Der Mussele, S. Na, D.L. Newberg, A. Nordberg, A. Nordlund, A. Novak, G.P. Paraskevas, G.P. Parnetti, L. Perera, G. Peters, O. Popp, J. Prabhakar, S. Rabinovici, G.D. Ramakers, I.H.G.B. Rami, L. De Oliveira, C.R. Rinne, J.O. Rodrigue, K.M. Rodriguez-Rodriguez, E. Roe, C.M. Rot, U. Rowe, C.C. Ruther, E. Sabri, O. Sanchez-Juan, P. Santana, I. Sarazin, M. Schroder, J. Schutte, C. Seo, S.W. Soetewey, F. Soininen, H. Spiru, L. Struyfs, H. Teunissen, C.E. Tsolaki, M. Vandenberghe, R. Verbeek, M.M. Villemagne, V.L. Vos, S.J.B. Van Waalwijk Van Doorn, L.J.C. Waldemar, G. Wallin, A. Wallin, A.K. Wiltfang, J. Wolk, D.A. Zboch, M. Zetterberg, H. the Amyloid Biomarker Study Group

Subjects
mental disorders
Abstract

IMPORTANCE: Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies. OBJECTIVE To use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI). DATA SOURCES: Relevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE andWeb of Science databases and through personal communication with investigators. STUDY SELECTION: Studies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity. DATA EXTRACTION: AND SYNTHESIS: Individual recordswere provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies. MAIN OUTCOMES AND MEASURES: Prevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations. RESULTS The prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95%CI, 8%-13%) to 44%(95%CI, 37%-51%) among participants with normal cognition; from 12%(95%CI, 8%-18%) to 43%(95%CI, 32%-55%) among patients with SCI; and from 27%(95%CI, 23%-32%) to 71%(95%CI, 66%-76%) among patients with MCI. APOE-ϵ4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ϵ4ϵ4 carriers, 50 years for ϵ2ϵ4 carriers, 55 years for ϵ3ϵ4 carriers, 65 years for ϵ3ϵ3 carriers, and 95 years for ϵ2ϵ3 carriers. Amyloid positivity was more common in highly educated participants but not associated with sex or biomarker modality. CONCLUSIONS AND RELEVANCE: Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. These findings suggest a 20- to 30-year interval between first development of amyloid positivity and onset of dementia. Copyright 2015 American Medical Association. All rights reserved.

Published
2015

36. Comparison of Different Matrices as Potential Quality Control Samples for Neurochemical Dementia Diagnostics

Author

Lelental, N., Brandner, S., Kofanova, O., Blennow, K., Zetterberg, H., Andreasson, U., Engelborghs, S., Mroczko, B., Gabryelewicz, T., Teunissen, C., Mollenhauer, B., Parnetti, L., Chiasserini, D., Molinuevo, J.L., Perret-Liaudet, A., Verbeek, M.M., Andreasen, N., Brosseron, F., Bahl, J.M., Herukka, S.K., Hausner, L., Frolich, L., Labonte, A., Poirier, J., Miller, A.M., Zilka, N., Kovacech, B., Urbani, A., Suardi, S., Oliveira, C. de, Baldeiras, I., Dubois, B., Rot, U., Lehmann, S., Skinningsrud, A., Betsou, F., Wiltfang, J., Gkatzima, O., Winblad, B., Buchfelder, M., Kornhuber, J., Lewczuk, P., Lelental, N., Brandner, S., Kofanova, O., Blennow, K., Zetterberg, H., Andreasson, U., Engelborghs, S., Mroczko, B., Gabryelewicz, T., Teunissen, C., Mollenhauer, B., Parnetti, L., Chiasserini, D., Molinuevo, J.L., Perret-Liaudet, A., Verbeek, M.M., Andreasen, N., Brosseron, F., Bahl, J.M., Herukka, S.K., Hausner, L., Frolich, L., Labonte, A., Poirier, J., Miller, A.M., Zilka, N., Kovacech, B., Urbani, A., Suardi, S., Oliveira, C. de, Baldeiras, I., Dubois, B., Rot, U., Lehmann, S., Skinningsrud, A., Betsou, F., Wiltfang, J., Gkatzima, O., Winblad, B., Buchfelder, M., Kornhuber, J., and Lewczuk, P.

Abstract

Item does not contain fulltext, BACKGROUND: Assay-vendor independent quality control (QC) samples for neurochemical dementia diagnostics (NDD) biomarkers are so far commercially unavailable. This requires that NDD laboratories prepare their own QC samples, for example by pooling leftover cerebrospinal fluid (CSF) samples. OBJECTIVE: To prepare and test alternative matrices for QC samples that could facilitate intra- and inter-laboratory QC of the NDD biomarkers. METHODS: Three matrices were validated in this study: (A) human pooled CSF, (B) Abeta peptides spiked into human prediluted plasma, and (C) Abeta peptides spiked into solution of bovine serum albumin in phosphate-buffered saline. All matrices were tested also after supplementation with an antibacterial agent (sodium azide). We analyzed short- and long-term stability of the biomarkers with ELISA and chemiluminescence (Fujirebio Europe, MSD, IBL International), and performed an inter-laboratory variability study. RESULTS: NDD biomarkers turned out to be stable in almost all samples stored at the tested conditions for up to 14 days as well as in samples stored deep-frozen (at - 80 degrees C) for up to one year. Sodium azide did not influence biomarker stability. Inter-center variability of the samples sent at room temperature (pooled CSF, freeze-dried CSF, and four artificial matrices) was comparable to the results obtained on deep-frozen samples in other large-scale projects. CONCLUSION: Our results suggest that it is possible to replace self-made, CSF-based QC samples with large-scale volumes of QC materials prepared with artificial peptides and matrices. This would greatly facilitate intra- and inter-laboratory QC schedules for NDD measurements.

Published
2016

37. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis

Author

Jansen, W.J., Ossenkoppele, R., Knol, D.L., Tijms, B.M., Scheltens, P.J., Verhey, F.R.J., Visser, P.J., Aalten, P., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I.S., Arnold, S.E., Baldeiras, I., Barthel, H., Berckel, B.N. van, Bibeau, K., Blennow, K., Brooks, D.J., Buchem, M.A. van, Camus, V., Cavedo, E., Chen, K., Chetelat, G., Cohen, A.D., Drzezga, A., Engelborghs, S., Fagan, A.M., Fladby, T., Fleisher, A.S., Flier, W.M. van der, Ford, L., Forster, S., Fortea, J., Foskett, N., Frederiksen, K.S., Freund-Levi, Y., Frisoni, G.B., Froelich, L., Gabryelewicz, T., Gill, K.D., Gkatzima, O., Gomez-Tortosa, E., Gordon, M.F., Grimmer, T., Hampel, H., Hausner, L., Hellwig, S., Herukka, S.K., Hildebrandt, H., Ishihara, L., Ivanoiu, A., Jagust, W.J., Johannsen, P., Kandimalla, R., Kapaki, E., Klimkowicz-Mrowiec, A., Klunk, W.E., Kohler, S., Koglin, N., Kornhuber, J., Kramberger, M.G., Laere, K. Van, Landau, S.M., Lee, D.Y., Leon, M., Lisetti, V., Lleo, A., Madsen, K., Maier, W., Marcusson, J., Mattsson, N., Mendonca, A. de, Meulenbroek, O.V., Meyer, P.T., Mintun, M.A., Mok, V., Molinuevo, J.L., Mollergard, H.M., Morris, J.C., Mroczko, B., Mussele, S. Van der, Na, D.L., Newberg, A., Nordberg, A., Nordlund, A., Novak, G.P., Paraskevas, G.P., Parnetti, L., Perera, G., Peters, O., Popp, J., Prabhakar, S., Rabinovici, G.D., Ramakers, I.H., Rami, L., Oliveira, C.R., Rinne, J.O., Rodrigue, K.M., Rodriguez-Rodriguez, E., Verbeek, M.M., et al., Jansen, W.J., Ossenkoppele, R., Knol, D.L., Tijms, B.M., Scheltens, P.J., Verhey, F.R.J., Visser, P.J., Aalten, P., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I.S., Arnold, S.E., Baldeiras, I., Barthel, H., Berckel, B.N. van, Bibeau, K., Blennow, K., Brooks, D.J., Buchem, M.A. van, Camus, V., Cavedo, E., Chen, K., Chetelat, G., Cohen, A.D., Drzezga, A., Engelborghs, S., Fagan, A.M., Fladby, T., Fleisher, A.S., Flier, W.M. van der, Ford, L., Forster, S., Fortea, J., Foskett, N., Frederiksen, K.S., Freund-Levi, Y., Frisoni, G.B., Froelich, L., Gabryelewicz, T., Gill, K.D., Gkatzima, O., Gomez-Tortosa, E., Gordon, M.F., Grimmer, T., Hampel, H., Hausner, L., Hellwig, S., Herukka, S.K., Hildebrandt, H., Ishihara, L., Ivanoiu, A., Jagust, W.J., Johannsen, P., Kandimalla, R., Kapaki, E., Klimkowicz-Mrowiec, A., Klunk, W.E., Kohler, S., Koglin, N., Kornhuber, J., Kramberger, M.G., Laere, K. Van, Landau, S.M., Lee, D.Y., Leon, M., Lisetti, V., Lleo, A., Madsen, K., Maier, W., Marcusson, J., Mattsson, N., Mendonca, A. de, Meulenbroek, O.V., Meyer, P.T., Mintun, M.A., Mok, V., Molinuevo, J.L., Mollergard, H.M., Morris, J.C., Mroczko, B., Mussele, S. Van der, Na, D.L., Newberg, A., Nordberg, A., Nordlund, A., Novak, G.P., Paraskevas, G.P., Parnetti, L., Perera, G., Peters, O., Popp, J., Prabhakar, S., Rabinovici, G.D., Ramakers, I.H., Rami, L., Oliveira, C.R., Rinne, J.O., Rodrigue, K.M., Rodriguez-Rodriguez, E., Verbeek, M.M., and et al.

Abstract

Item does not contain fulltext, IMPORTANCE: Cerebral amyloid-beta aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies. OBJECTIVE: To use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI). DATA SOURCES: Relevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE and Web of Science databases and through personal communication with investigators. STUDY SELECTION: Studies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity. DATA EXTRACTION AND SYNTHESIS: Individual records were provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies. MAIN OUTCOMES AND MEASURES: Prevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations. RESULTS: The prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95% CI, 8%-13%) to 44% (95% CI, 37%-51%) among participants with normal cognition; from 12% (95% CI, 8%-18%) to 43% (95% CI, 32%-55%) among patients with SCI; and from 27% (95% CI, 23%-32%) to 71% (95% CI, 66%-76%) among patients with MCI. APOE-epsilon4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE epsilon4epsilon4 carriers, 50 years for epsilon2epsilon4 carriers, 55 years for epsilon3epsilon4 c

Published
2015

38. A Practical Guide to Immunoassay Method Validation

Author

Andreasson, U., Perret-Liaudet, A., Waalwijk van Doorn, L.L.C. van, Blennow, K., Chiasserini, D., Engelborghs, S., Fladby, T., Genc, S., Kruse, N., Kuiperij, H.B., Kulic, L., Lewczuk, P., Mollenhauer, B., Mroczko, B., Parnetti, L., Vanmechelen, E., Verbeek, M.M., Winblad, B., Zetterberg, H., Koel-Simmelink, M., Teunissen, C.E., Andreasson, U., Perret-Liaudet, A., Waalwijk van Doorn, L.L.C. van, Blennow, K., Chiasserini, D., Engelborghs, S., Fladby, T., Genc, S., Kruse, N., Kuiperij, H.B., Kulic, L., Lewczuk, P., Mollenhauer, B., Mroczko, B., Parnetti, L., Vanmechelen, E., Verbeek, M.M., Winblad, B., Zetterberg, H., Koel-Simmelink, M., and Teunissen, C.E.

Abstract

Contains fulltext : 154779.pdf (publisher's version ) (Open Access), Biochemical markers have a central position in the diagnosis and management of patients in clinical medicine, and also in clinical research and drug development, also for brain disorders, such as Alzheimer's disease. The enzyme-linked immunosorbent assay (ELISA) is frequently used for measurement of low-abundance biomarkers. However, the quality of ELISA methods varies, which may introduce both systematic and random errors. This urges the need for more rigorous control of assay performance, regardless of its use in a research setting, in clinical routine, or drug development. The aim of a method validation is to present objective evidence that a method fulfills the requirements for its intended use. Although much has been published on which parameters to investigate in a method validation, less is available on a detailed level on how to perform the corresponding experiments. To remedy this, standard operating procedures (SOPs) with step-by-step instructions for a number of different validation parameters is included in the present work together with a validation report template, which allow for a well-ordered presentation of the results. Even though the SOPs were developed with the intended use for immunochemical methods and to be used for multicenter evaluations, most of them are generic and can be used for other technologies as well.

Published
2015

39. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis.

Author

Amyloid Biomarker Study Group, Jansen, W.J., Ossenkoppele, R., Knol, D.L., Tijms, B.M., Scheltens, P., Verhey, F.R., Visser, P.J., Aalten, P., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I.S., Arnold, S.E., Baldeiras, I., Barthel, H., van Berckel, B.N., Bibeau, K., Blennow, K., Brooks, D.J., van Buchem, M.A., Camus, V., Cavedo, E., Chen, K., Chetelat, G., Cohen, A.D., Drzezga, A., Engelborghs, S., Fagan, A.M., Fladby, T., Fleisher, A.S., van der Flier, W.M., Ford, L., Förster, S., Fortea, J., Foskett, N., Frederiksen, K.S., Freund-Levi, Y., Frisoni, G.B., Froelich, L., Gabryelewicz, T., Gill, K.D., Gkatzima, O., Gómez-Tortosa, E., Gordon, M.F., Grimmer, T., Hampel, H., Hausner, L., Hellwig, S., Herukka, S.K., Hildebrandt, H., Ishihara, L., Ivanoiu, A., Jagust, W.J., Johannsen, P., Kandimalla, R., Kapaki, E., Klimkowicz-Mrowiec, A., Klunk, W.E., Köhler, S., Koglin, N., Kornhuber, J., Kramberger, M.G., Van Laere, K., Landau, S.M., Lee, D.Y., de Leon, M., Lisetti, V., Lleó, A., Madsen, K., Maier, W., Marcusson, J., Mattsson, N., de Mendonça, A., Meulenbroek, O., Meyer, P.T., Mintun, M.A., Mok, V., Molinuevo, J.L., Møllergård, H.M., Morris, J.C., Mroczko, B., Van der Mussele, S., Na, D.L., Newberg, A., Nordberg, A., Nordlund, A., Novak, G.P., Paraskevas, G.P., Parnetti, L., Perera, G., Peters, O., Popp, J., Prabhakar, S., Rabinovici, G.D., Ramakers, I.H., Rami, L., Resende de Oliveira, C., Rinne, J.O., Rodrigue, K.M., Rodríguez-Rodríguez, E., Roe, C.M., Rot, U., Rowe, C.C., Rüther, E., Sabri, O., Sanchez-Juan, P., Santana, I., Sarazin, M., Schröder, J., Schütte, C., Seo, S.W., Soetewey, F., Soininen, H., Spiru, L., Struyfs, H., Teunissen, C.E., Tsolaki, M., Vandenberghe, R., Verbeek, M.M., Villemagne, V.L., Vos, S.J., van Waalwijk van Doorn, L.J., Waldemar, G., Wallin, A., Wallin, Å.K., Wiltfang, J., Wolk, D.A., Zboch, M., Zetterberg, H., Amyloid Biomarker Study Group, Jansen, W.J., Ossenkoppele, R., Knol, D.L., Tijms, B.M., Scheltens, P., Verhey, F.R., Visser, P.J., Aalten, P., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I.S., Arnold, S.E., Baldeiras, I., Barthel, H., van Berckel, B.N., Bibeau, K., Blennow, K., Brooks, D.J., van Buchem, M.A., Camus, V., Cavedo, E., Chen, K., Chetelat, G., Cohen, A.D., Drzezga, A., Engelborghs, S., Fagan, A.M., Fladby, T., Fleisher, A.S., van der Flier, W.M., Ford, L., Förster, S., Fortea, J., Foskett, N., Frederiksen, K.S., Freund-Levi, Y., Frisoni, G.B., Froelich, L., Gabryelewicz, T., Gill, K.D., Gkatzima, O., Gómez-Tortosa, E., Gordon, M.F., Grimmer, T., Hampel, H., Hausner, L., Hellwig, S., Herukka, S.K., Hildebrandt, H., Ishihara, L., Ivanoiu, A., Jagust, W.J., Johannsen, P., Kandimalla, R., Kapaki, E., Klimkowicz-Mrowiec, A., Klunk, W.E., Köhler, S., Koglin, N., Kornhuber, J., Kramberger, M.G., Van Laere, K., Landau, S.M., Lee, D.Y., de Leon, M., Lisetti, V., Lleó, A., Madsen, K., Maier, W., Marcusson, J., Mattsson, N., de Mendonça, A., Meulenbroek, O., Meyer, P.T., Mintun, M.A., Mok, V., Molinuevo, J.L., Møllergård, H.M., Morris, J.C., Mroczko, B., Van der Mussele, S., Na, D.L., Newberg, A., Nordberg, A., Nordlund, A., Novak, G.P., Paraskevas, G.P., Parnetti, L., Perera, G., Peters, O., Popp, J., Prabhakar, S., Rabinovici, G.D., Ramakers, I.H., Rami, L., Resende de Oliveira, C., Rinne, J.O., Rodrigue, K.M., Rodríguez-Rodríguez, E., Roe, C.M., Rot, U., Rowe, C.C., Rüther, E., Sabri, O., Sanchez-Juan, P., Santana, I., Sarazin, M., Schröder, J., Schütte, C., Seo, S.W., Soetewey, F., Soininen, H., Spiru, L., Struyfs, H., Teunissen, C.E., Tsolaki, M., Vandenberghe, R., Verbeek, M.M., Villemagne, V.L., Vos, S.J., van Waalwijk van Doorn, L.J., Waldemar, G., Wallin, A., Wallin, Å.K., Wiltfang, J., Wolk, D.A., Zboch, M., and Zetterberg, H.

Abstract

IMPORTANCE: Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies. OBJECTIVE: To use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI). DATA SOURCES: Relevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE and Web of Science databases and through personal communication with investigators. STUDY SELECTION: Studies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity. DATA EXTRACTION AND SYNTHESIS: Individual records were provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies. MAIN OUTCOMES AND MEASURES: Prevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations. RESULTS: The prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95% CI, 8%-13%) to 44% (95% CI, 37%-51%) among participants with normal cognition; from 12% (95% CI, 8%-18%) to 43% (95% CI, 32%-55%) among patients with SCI; and from 27% (95% CI, 23%-32%) to 71% (95% CI, 66%-76%) among patients with MCI. APOE-ε4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ε4ε4 carriers, 50 years for ε2ε4 carriers, 55 years for ε3ε4 carriers, 65 years for ε3ε3 carriers, and 95 y

Published
2015

42. Seroprevalence of Helicobacter pylori infection in Polish children and adults depending on socioeconomic status and living conditions

Author

Łaszewicz, Wiktor, primary, Iwańczak, Franciszek, additional, Iwańczak, Barbara, additional, Annabhani, A., additional, Bała, G., additional, Bąk-Romaniszyn, L., additional, Budzyńska, A., additional, Cader, J., additional, Celiński, K., additional, Cichy, W., additional, Czerwionka-Szaflarska, M., additional, Czkwianianc, E., additional, Czosnek, R., additional, Czykwin, M., additional, Daniluk, J., additional, Długosz, J., additional, Dzieniszewski, J., additional, Dzierżanowska, D., additional, Dzierżanowska-Fangrat, K., additional, Forencewicz, J., additional, Gościniak, G., additional, Ignyś, I., additional, Jarosz, M., additional, Jaroszewicz-Heidelmann, H., additional, Jędrychowski, W., additional, Kaczmarski, M., additional, Kemona, A., additional, Kiełtyka, A., additional, Klincewicz, B., additional, Kosidło, S., additional, Maciorkowska, E., additional, Marlicz, K., additional, Matusiewicz, K., additional, Mierzwa, G., additional, Mroczko, B., additional, Nowak, A., additional, Paradowski, L., additional, Płaneta-Małecka, I., additional, Pytrus, T., additional, Roszko, I., additional, Romańczuk, W., additional, Rożynek, E., additional, Rymarczyk, G., additional, Słomka, M., additional, Smereka, A., additional, Starzyńska, T., additional, Swincow, G., additional, Szaflarska, M., additional, Szaflarska-Popławska, A., additional, Szafraniec, K., additional, Szmitkowski, M., additional, Wasielica-Berger, J., additional, Wereszczyńska-Siemiątkowska, U., additional, Wogtt, E., additional, Wojda, U., additional, Wróblewski, E., additional, Zielińska, I., additional, and Zimnicki, P., additional

Published
2014
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44. Alzheimer’s Disease—Biochemical and Psychological Background for Diagnosis and Treatment

Author

Bocwinska-Kiluk Beata, Jelski Wojciech, Kornhuber Johannes, Lewczuk Piotr, and Mroczko Barbara

Subjects
Alzheimer’s disease, psychological intervention, diagnosis, treatment, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

There is a paucity of empirical research on the use of non-pharmacological interventions to both treat and curb the spread of Alzheimer’s disease (AD) across the globe. This paper examines the biochemical and clinical outlook and the social implications of the condition in relation to psychological aspects that may indicate a direction for further interventions. There is a scarcity of research on the effectiveness of using various psychological aspects of AD, a disease characterized by a process of transition from health and independence to a dependent state with a progressive loss of memory and functional skills. The paper investigates the biochemical and psychological aspects of AD and their significance for improving quality of life for patients with this disease. Psychological interventions based on, among other factors, biochemical studies, are conducted to improve the emotional wellbeing of AD patients and may assist in slowing down the progression of the disease. To date, however, no effective methods of AD treatment have been established.

Published
2023
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