Paraskevas, George P.
Mayo Clinic
National and Kapodistrian University of Athens
Citations 2
Depressive Symptoms and Amyloid Pathology
Oomens, Julie Elisabeth , Engelborghs, Sebastiaan , Arnim, Christine A. F. Von , Boada, Merçé , Didic, Mira , Dubois, Bruno, Fröhlich, Lutz, Gill, Kiran Dip, Grimmer, Timo, Hildebrandt, Helmut , Itoh, Yoshiaki , Lee, Dong Young , Lleó, Alberto, Meyer, Philipp T. , Kapaki, Elisabeth, Pardini, Matteo , Popp, Julius , Rami, Lorena , Reiman, Eric M. , Rinne, Juha O. , Sánchez‐Juan, Pascual, Sarazin, Marie , Scarmeas, Nikolaos , Villeneuve, Sylvia , Wallin, Anders, Vos, Stephanie J. B. , Jansen, Willemijn J. , group, Amyloid Biomarker Study, Altomare, Daniele , Baldeiras, Inês , Blennow, Kaj, Braber, Anouk den , Cerman, Jiří , Chipi, Elena , Eckerström, Marie , Ekblad, Laura L. , Förster, Stefan , Guedj, Éric , Hausner, Lucrezia , Huey, Edward D. , Jiménez‐Bonilla, J., Johnson, Keith A. , Juaristi, Arantxa, Kern, Silke , Kirsebom, Bjørn‐Eivind , Landau, Susan , Legdeur, Nienke , Guerra, Jorge J. Llibre, Maserejian, Nancy N., Marquié, Marta , Minatani, Shinobu, Olivieri, Pauline , Perrin, Richard J., Peters, Oliver , Prabhakar, Sudesh, Ramakers, Inez H., Rodríguez‐Rodríguez, Eloy , Ruiz, Agustín, Rüther, E., Selnes, Per , Spiru, Luiza , Takeda, Akitoshi , Teichmann, Marc , Thompson, Loisa I., Vogelgsangs, Jonathan, Wallin, Åsa K., Zettergren, Anna , Frisoni, Giovanni B. , Boada, Merce , Oomens, Julie E , Bottlaender, Michel , Wiels, Wietse A. , Baeken, Chris , Dubois, Bruno , Fladby, Tormod , Flier, Wiesje M. van der , Frisoni, Giovanni B. , Fröhlich, Lutz, Grimmer, Timo , Hort, Jakub , Iwatsubo, Takeshi , Klimkowicz‐Mrowiec, Aleksandra , Lleó, Alberto , Martínez‐Lage, Pablo , Mendonça, Alexandre de , Parchi, Piero , Parnetti, Lucilla , Rodrigue, Karen M. , Santana, Isabel , Skoog, Ingmar , Snyder, Peter J. , Sperling, Reisa Anne , Wiltfang, Jens , Zetterberg, Henrik , Ossenkoppele, Rik , Verhey, Frans R.J. , Visser, Pieter Jelle , Alcolea, Daniel , Baiardi, Simone , Bateman, Randall J. , Blennow, Kaj , Buchem, Mark A. van , Byun, Min Soo , Chen, Kewei , Day, Gregory S. , Drzezga, Alexander E. , Epelbaum, Stéphane , Fortea, Juan , Freund‐Levi, Yvonne , Frings, Lars , Hellwig, Sabine , Kandimalla, Ramesh , Paraskevas, George P. , Kornhuber, Johannes , Lagarde, Julien , Morbelli, Silvia , Mroczko, Barbara , Ntanasi, Eva , Oliveira, Catarina Resende , Olivieri, Pauline , Orellana, Adelina , Ruiz, Agustı́n , Silva, Dina , Soininen, Hilkka S. , Tijms, Betty M. , Teunissen, Charlotte E. , Vöglein, Jonathan , Waldemar, Gunhild , Yannakoulia, Mary , Yi, Dahyun
JAMA Psychiatry | January 22, 2025 | Volume: 82 | Issue: 3 | Pages: 296
10.1001/jamapsychiatry.2024.4305
Importance Depressive symptoms are associated with cognitive decline in older individuals. Uncertainty about underlying mechanisms hampers diagnostic and therapeutic efforts. This large-scale study aimed to elucidate the association between depressive symptoms and amyloid pathology. Objective To examine the association between depressive symptoms and amyloid pathology and its dependency on age, sex, education, and APOE genotype in older individuals without dementia. Design, Setting, and Participants Cross-sectional analyses were performed using data from the Amyloid Biomarker Study data pooling initiative. Data from 49 research, population-based, and memory clinic studies were pooled and harmonized. The Amyloid Biomarker Study has been collecting data since 2012 and data collection is ongoing. At the time of analysis, 95 centers were included in the Amyloid Biomarker Study. The study included 9746 individuals with normal cognition (NC) and 3023 participants with mild cognitive impairment (MCI) aged between 34 and 100 years for whom data on amyloid biomarkers, presence of depressive symptoms, and age were available. Data were analyzed from December 2022 to February 2024. Main Outcomes and Measures Amyloid-β1-42 levels in cerebrospinal fluid or amyloid positron emission tomography scans were used to determine presence or absence of amyloid pathology. Presence of depressive symptoms was determined on the basis of validated depression rating scale scores, evidence of a current clinical diagnosis of depression, or self-reported depressive symptoms. Results In individuals with NC (mean [SD] age, 68.6 [8.9] years; 5664 [58.2%] female; 3002 [34.0%] APOE ε4 carriers; 937 [9.6%] had depressive symptoms; 2648 [27.2%] had amyloid pathology), the presence of depressive symptoms was not associated with amyloid pathology (odds ratio [OR], 1.13; 95% CI, 0.90-1.40; P = .29). In individuals with MCI (mean [SD] age, 70.2 [8.7] years; 1481 [49.0%] female; 1046 [44.8%] APOE ε4 carriers; 824 [27.3%] had depressive symptoms; 1668 [55.8%] had amyloid pathology), the presence of depressive symptoms was associated with a lower likelihood of amyloid pathology (OR, 0.73; 95% CI 0.61-0.89; P = .001). When considering subgroup effects, in individuals with NC, the presence of depressive symptoms was associated with a higher frequency of amyloid pathology in APOE ε4 noncarriers (mean difference, 5.0%; 95% CI 1.0-9.0; P = .02) but not in APOE ε4 carriers. This was not the case in individuals with MCI. Conclusions and Relevance Depressive symptoms were not consistently associated with a higher frequency of amyloid pathology in participants with NC and were associated with a lower likelihood of amyloid pathology in participants with MCI. These findings were not influenced by age, sex, or education level. Mechanisms other than amyloid accumulation may commonly underlie depressive symptoms in late life.
The Alzheimer's Association external quality control program for cerebrospinal fluid biomarkers
Mattsson, Niklas , Andréasson, Ulf , Batish, Sat Dev, Bernardini, Sergio , Bocchio‐Chiavetto, Luisella , Blankenstein, Marinus A. , Carrillo, María C. , Chalbot, Sonia, Coart, Els, Chiasserini, Davide , Cutler, Neal E., Dahlfors, Gunilla, Duller, Stefan, Fagan, Anne M. , Frisoni, Giovanni B. , Galimberti, Daniela , Hampel, Harald , Handberg, Aase , Heneka, Michael T. , Herskovits, A. Zara , Herukka, Sanna‐Kaisa , Humpel, Christian , Iqbal, Khalid , Kaeser, Stephan A. , Kaiser, Elmar, Kapaki, Elisabeth, Kidd, Daniel, Klivènyi, Péter , Knudsen, Cindy Soendersoe, Kummer, Markus P. , Lui, James, Lladó, Albert , Li, Qiao‐Xin , Martins, Ralph N. , Masters, Colin L. , McAuliffe, John C., Mercken, Marc, Moghekar, Abhay , Molinuevo, José Luís , Montine, Thomas J. , Nowatzke, William, O’Brien, Richard , Otto, Markus , Parnetti, Lucilla , Petersen, Ronald C. , Prvulovic, David, Reus, Herman P.M. de, Scarpini, Elio , Stefani, Alessandro , Schröder, Johannes , Shaw, Leslie M. , Skinningsrud, Anders, Skrogstad, Brith, Spreer, Annette, Trojanowski, John Q. , Tumani, Hayrettin , Umek, Robert M., Broeck, Bianca Van, Vanderstichele, Hugo, Vécsei, László , Blennow, Kaj , Frisoni, Giovanni B. , Persson, Staffan , Arai, Hiroyuki N. , Forlenza, Orestes Vicente , Galasko, Douglas , Holtzman, David M. , Hyman, Bradley T. , Jucker, Mathias , Lewczuk, Piotr , Paraskevas, George P. , Rissman, Robert A. , Soininen, Hilkka S. , Talib, Leda Leme , Teunissen, Charlotte E. , Verbeek, Marcel M. , Windisch, Manfred , Zhang, Jing , Zetterberg, Henrik , Parnetti, Lucilla , Molinuevo, José Luis , Masters, Colin L , Otto, Markus , Galimberti, Daniela
Alzheimer's & Dementia | July 25, 2011 | Volume: 7 | Issue: 4 | Pages: 386
BackgroundThe cerebrospinal fluid (CSF) biomarkers amyloid β (Aβ)‐42, total‐tau (T‐tau), and phosphorylated‐tau (P‐tau) demonstrate good diagnostic accuracy for Alzheimer's disease (AD). However, there are large variations in biomarker measurements between studies, and between and within laboratories. The Alzheimer's Association has initiated a global quality control program to estimate and monitor variability of measurements, quantify batch‐to‐batch assay variations, and identify sources of variability. In this article, we present the results from the first two rounds of the program.MethodsThe program is open for laboratories using commercially available kits for Aβ, T‐tau, or P‐tau. CSF samples (aliquots of pooled CSF) are sent for analysis several times a year from the Clinical Neurochemistry Laboratory at the Mölndal campus of the University of Gothenburg, Sweden. Each round consists of three quality control samples.ResultsForty laboratories participated. Twenty‐six used INNOTEST enzyme‐linked immunosorbent assay kits, 14 used Luminex xMAP with the INNO‐BIA AlzBio3 kit (both measure Aβ‐(1‐42), P‐tau(181P), and T‐tau), and 5 used Meso Scale Discovery with the Aβ triplex (AβN‐42, AβN‐40, and AβN‐38) or T‐tau kits. The total coefficients of variation between the laboratories were 13% to 36%. Five laboratories analyzed the samples six times on different occasions. Within‐laboratory precisions differed considerably between biomarkers within individual laboratories.ConclusionsMeasurements of CSF AD biomarkers show large between‐laboratory variability, likely caused by factors related to analytical procedures and the analytical kits. Standardization of laboratory procedures and efforts by kit vendors to increase kit performance might lower variability, and will likely increase the usefulness of CSF AD biomarkers.