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5 results on '"Mollergard, H.M."'

1. 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

2. 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

3. 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

4. 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

5. Validation of a quantitative cerebrospinal fluid alpha-synuclein assay in a European-wide interlaboratory study

Author

Kruse, N., Persson, S., Alcolea, D., Bahl, J.M., Baldeiras, I., Capello, E., Chiasserini, D., Bocchio Chiavetto, L., Emersic, A., Engelborghs, S., Eren, E., Fladby, T., Frisoni, G., Garcia-Ayllon, M.S., Genc, S., Gkatzima, O., Heegaard, N.H.H., Janeiro, A.M., Kovacech, B., Kuiperij, H.B., Leitao, M.J., Lleo, A., Martins, M., Matos, M., Mollergard, H.M., Nobili, F., Ohrfelt, A., Parnetti, L., Oliveira, C.R., Rot, U., Saez-Valero, J., Struyfs, H., Tanassi, J.T., Taylor, P., Tsolaki, M., Vanmechelen, E., Verbeek, M.M., Zilka, N., Blennow, K., Zetterberg, H., Mollenhauer, B., Kruse, N., Persson, S., Alcolea, D., Bahl, J.M., Baldeiras, I., Capello, E., Chiasserini, D., Bocchio Chiavetto, L., Emersic, A., Engelborghs, S., Eren, E., Fladby, T., Frisoni, G., Garcia-Ayllon, M.S., Genc, S., Gkatzima, O., Heegaard, N.H.H., Janeiro, A.M., Kovacech, B., Kuiperij, H.B., Leitao, M.J., Lleo, A., Martins, M., Matos, M., Mollergard, H.M., Nobili, F., Ohrfelt, A., Parnetti, L., Oliveira, C.R., Rot, U., Saez-Valero, J., Struyfs, H., Tanassi, J.T., Taylor, P., Tsolaki, M., Vanmechelen, E., Verbeek, M.M., Zilka, N., Blennow, K., Zetterberg, H., and Mollenhauer, B.

Abstract

Item does not contain fulltext, Decreased levels of alpha-synuclein (aSyn) in cerebrospinal fluid (CSF) in Parkinson's disease and related synucleinopathies have been reported, however, not consistently in all cross-sectional studies. To test the performance of one recently released human-specific enzyme-linked immunosorbent assay (ELISA) for the quantification of aSyn in CSF, we carried out a round robin trial with 18 participating laboratories trained in CSF ELISA analyses within the BIOMARKAPD project in the EU Joint Program - Neurodegenerative Disease Research. CSF samples (homogeneous aliquots from pools) and ELISA kits (one lot) were provided centrally and data reported back to one laboratory for data analysis. Our study showed that although factors such as preanalytical sample handling and lot-to-lot variability were minimized by our study design, we identified high variation in absolute values of CSF aSyn even when the same samples and same lots of assays were applied. We further demonstrate that although absolute concentrations differ between laboratories the quantitative results are comparable. With further standardization this assay may become an attractive tool for comparing aSyn measurements in diverse settings. Recommendations for further validation experiments and improvement of the interlaboratory results obtained are given.

Published
2015

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