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10. Cerebrospinal Fluid Classical Biomarker Levels in Mixed vs. Pure A + T + (A + T 1 +) Alzheimer's Disease.

Author

Tsantzali, Ioanna, Athanasaki, Athanasia, Boufidou, Fotini, Constantinides, Vasilios C., Stefanou, Maria-Ioanna, Moschovos, Christos, Zompola, Christina, Paraskevas, Sotirios G., Bonakis, Anastasios, Giannopoulos, Sotirios, Tsivgoulis, Georgios, Kapaki, Elisabeth, and Paraskevas, George P.

Subjects
ALZHEIMER'S disease, TAU proteins, CEREBROSPINAL fluid, CEREBROVASCULAR disease, DISEASE duration
Abstract

Background: Alzheimer's disease (AD) may present with pure (typical or atypical) and mixed phenotypes, sometimes causing difficulties in (differential) diagnosis. In order to achieve a diagnostic accuracy as high as possible, the diagnosis of AD during life depends on various biomarkers, including the cerebrospinal fluid (CSF) biomarkers. Methods: Classical CSF AD biomarkers were determined in a total of 61 patients, classified as both beta amyloid- and tau-positive A+T+ (or A+T1+ according to the recently revised Alzheimer Association criteria for diagnosis and staging of AD). Twenty one of these patients fulfilled the criteria for mixed AD (mixed with Lewy bodies, cerebrovascular disease, or normal pressure hydrocephalus), whilst 40 had pure AD. Results: Patients did not differ with respect to gender, education, disease duration, and cognitive status. After controlling for confounding factors, no difference was observed between mixed and pure AD groups in Aβ42 or Aβ42/Aβ40 levels. Although by definition, patients of both groups had abnormal (increased) levels of phospho-tau181, the mixed AD group presented with lower (less abnormal) levels of phospho-tau181 and total tau as compared to the pure group. Conclusions: In patients with AD of comparable cognitive status, mixed AD cases may present with lower levels of tau proteins and, if close to the cut-off values, diagnostic uncertainty may be increased. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Symptomatic Unilateral Carotid Artery Disease

Author

Melanis, Konstantinos, primary, Athanasaki, Athanasia, additional, Bakola, Eleni, additional, Chondrogianni, Maria, additional, Lazaris, Andreas, additional, Akrivaki, Alexandra, additional, Triantafyllou, Alexandros Stavros, additional, Kotsali-Peteinelli, Vasiliki, additional, Bonakis, Anastasios, additional, Paraskevas, George P., additional, and Tsivgoulis, Georgios, additional

Published
2024
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12. SIMOA Diagnostics on Alzheimer’s Disease and Frontotemporal Dementia

Author

Chatziefstathiou, Athanasia, primary, Canaslan, Sezgi, additional, Kanata, Eirini, additional, Vekrellis, Kostas, additional, Constantinides, Vasilios C., additional, Paraskevas, George P., additional, Kapaki, Elisabeth, additional, Schmitz, Matthias, additional, Zerr, Inga, additional, Xanthopoulos, Konstantinos, additional, Sklaviadis, Theodoros, additional, and Dafou, Dimitra, additional

Published
2024
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13. Association of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia

Author

Jansen, Willemijn J, Ossenkoppele, Rik, Tijms, Betty M, Fagan, Anne M, Hansson, Oskar, Klunk, William E, van der Flier, Wiesje M, Villemagne, Victor L, Frisoni, Giovanni B, Fleisher, Adam S, Lleó, Alberto, Mintun, Mark A, Wallin, Anders, Engelborghs, Sebastiaan, Na, Duk L, Chételat, Gäel, Molinuevo, José Luis, Landau, Susan M, Mattsson, Niklas, Kornhuber, Johannes, Sabri, Osama, Rowe, Christopher C, Parnetti, Lucilla, Popp, Julius, Fladby, Tormod, Jagust, William J, Aalten, Pauline, Lee, Dong Young, Vandenberghe, Rik, de Oliveira, Catarina Resende, Kapaki, Elisabeth, Froelich, Lutz, Ivanoiu, Adrian, Gabryelewicz, Tomasz, Verbeek, Marcel M, Sanchez-Juan, Páscual, Hildebrandt, Helmut, Camus, Vincent, Zboch, Marzena, Brooks, David J, Drzezga, Alexander, Rinne, Juha O, Newberg, Andrew, de Mendonça, Alexandre, Sarazin, Marie, Rabinovici, Gil D, Madsen, Karine, Kramberger, Milica G, Nordberg, Agneta, Mok, Vincent, Mroczko, Barbara, Wolk, David A, Meyer, Philipp T, Tsolaki, Magda, Scheltens, Philip, Verhey, Frans RJ, Visser, Pieter Jelle, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S, Arnold, Steven E, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart NM, Blennow, Kaj, van Buchem, Mark A, Cavedo, Enrica, Chen, Kewei, Chipi, Elena, Cohen, Ann D, Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S, Freund-Levi, Yvonne, Gkatzima, Olymbia, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Johannsen, Peter, Klimkowicz-Mrowiec, Aleksandra, Köhler, Sebastian, Koglin, Norman, van Laere, Koen, de Leon, Mony, Lisetti, Viviana, Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M, Morris, John C, Nordlund, Arto, Novak, Gerald P, Paraskevas, George P, Perera, Gayan, Peters, Oliver, and Ramakers, Inez HGB

Subjects
Health Services and Systems, Health Sciences, Alzheimer's Disease Related Dementias (ADRD), Neurodegenerative, Dementia, Acquired Cognitive Impairment, Behavioral and Social Science, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Aging, Alzheimer's Disease, Neurosciences, Clinical Research, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Mental health, Neurological, Aged, Alzheimer Disease, Amyloid beta-Peptides, Brain, Cognition Disorders, Cognitive Dysfunction, Cross-Sectional Studies, Female, Humans, Male, Memory, Episodic, Mental Status and Dementia Tests, Middle Aged, Positron-Emission Tomography, Reference Values, Amyloid Biomarker Study Group, Other Medical and Health Sciences, Psychology, Cognitive Sciences, Clinical sciences, Clinical and health psychology
Abstract

ImportanceCerebral 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.ObjectiveTo investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia.Design, setting, and participantsThis 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 measuresGlobal 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.ResultsAmong 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

Published
2018

18. Waist Circumference and Body Mass Index as Predictors of Disability Progression in Multiple Sclerosis: A Systematic Review and Meta-Analysis

Author

Giannopapas, Vasileios, primary, Stefanou, Maria-Ioanna, additional, Smyrni, Vassiliki, additional, Kitsos, Dimitrios K., additional, Kosmidou, Maria, additional, Stasi, Sophia, additional, Chasiotis, Athanasios K., additional, Stavrogianni, Konstantina, additional, Papagiannopoulou, Georgia, additional, Tzartos, John S., additional, Paraskevas, George P., additional, Tsivgoulis, Georgios, additional, and Giannopoulos, Sotirios, additional

Published
2024
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23. Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia: A Meta-analysis

Author

Jansen, Willemijn J, Ossenkoppele, Rik, Knol, Dirk L, Tijms, Betty M, Scheltens, Philip, Verhey, Frans RJ, Visser, Pieter Jelle, Aalten, Pauline, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S, Arnold, Steven E, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart NM, Bibeau, Kristen, Blennow, Kaj, Brooks, David J, van Buchem, Mark A, Camus, Vincent, Cavedo, Enrica, Chen, Kewei, Chetelat, Gael, Cohen, Ann D, Drzezga, Alexander, Engelborghs, Sebastiaan, Fagan, Anne M, Fladby, Tormod, Fleisher, Adam S, van der Flier, Wiesje M, Ford, Lisa, Förster, Stefan, Fortea, Juan, Foskett, Nadia, Frederiksen, Kristian S, Freund-Levi, Yvonne, Frisoni, Giovanni B, Froelich, Lutz, Gabryelewicz, Tomasz, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Hildebrandt, Helmut, Ishihara, Lianna, Ivanoiu, Adrian, Jagust, William J, Johannsen, Peter, Kandimalla, Ramesh, Kapaki, Elisabeth, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E, Köhler, Sebastian, Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G, Van Laere, Koen, Landau, Susan M, Lee, Dong Young, de Leon, Mony, Lisetti, Viviana, Lleó, Alberto, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Mattsson, Niklas, de Mendonça, Alexandre, Meulenbroek, Olga, Meyer, Philipp T, Mintun, Mark A, Mok, Vincent, Molinuevo, José Luis, Møllergård, Hanne M, Morris, John C, Mroczko, Barbara, Van der Mussele, Stefan, Na, Duk L, Newberg, Andrew, Nordberg, Agneta, Nordlund, Arto, Novak, Gerald P, Paraskevas, George P, Parnetti, Lucilla, Perera, Gayan, Peters, Oliver, Popp, Julius, Prabhakar, Sudesh, Rabinovici, Gil D, Ramakers, Inez HGB, Rami, Lorena, de Oliveira, Catarina Resende, Rinne, Juha O, Rodrigue, Karen M, and Rodríguez-Rodríguez, Eloy

Subjects
Health Services and Systems, Health Sciences, Alzheimer's Disease, Clinical Research, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Vascular Cognitive Impairment/Dementia, Neurosciences, Dementia, Cerebrovascular, Acquired Cognitive Impairment, Brain Disorders, Prevention, Alzheimer's Disease Related Dementias (ADRD), Neurodegenerative, Aging, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, Neurological, Adult, Age Factors, Aged, Aged, 80 and over, Amyloid beta-Peptides, Apolipoprotein E4, Biomarkers, Brain, Cerebrospinal Fluid, Cognitive Dysfunction, Female, Genotype, Humans, Male, Middle Aged, Positron-Emission Tomography, Prevalence, Risk Factors, Amyloid Biomarker Study Group, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

ImportanceCerebral 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.ObjectiveTo 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 sourcesRelevant 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 selectionStudies 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 synthesisIndividual 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 measuresPrevalence 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.ResultsThe 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 relevanceAmong 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

28. Paraneoplastic Neurological Syndromes as Initial Presentation of Tumors: An Eight-Year Single-Center Experience

Author

Melanis, Konstantinos, primary, Stefanou, Maria-Ioanna, additional, Kitsos, Dimitrios K., additional, Athanasaki, Athanasia, additional, Theodorou, Aikaterini, additional, Koropouli, Eleftheria, additional, Keramida, Anna, additional, Dimitriadou, Evangelia Makrina, additional, Tzanetakos, Dimitrios, additional, Andreadou, Elizabeth, additional, Koutroulou, Ioanna, additional, Giannopoulos, Sotirios, additional, Paraskevas, George P., additional, Tsivgoulis, Georgios, additional, and Tzartos, John S., additional

Published
2024
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29. In Vivo Prevalence of Beta-Amyloid Pathology and Alzheimer's Disease Co-Pathology in Idiopathic Normal-Pressure Hydrocephalus—Association with Neuropsychological Features.

Author

Pyrgelis, Efstratios-Stylianos, Paraskevas, George P., Constantinides, Vasilios C., Boufidou, Fotini, Stefanis, Leonidas, and Kapaki, Elisabeth

Subjects
ALZHEIMER'S disease, TAU proteins, IDIOPATHIC diseases, NEUROPSYCHOLOGICAL tests, CEREBROSPINAL fluid
Abstract

Idiopathic normal-pressure hydrocephalus (iNPH) is a clinic-radiological neurological syndrome presenting with cognitive deficits, gait disturbances and urinary incontinence. It often coexists with Alzheimer's disease (AD). Due to the reversible nature of iNPH when promptly treated, a lot of studies have focused on possible biomarkers, among which are cerebrospinal fluid (CSF) biomarkers. The aim of the present study was to determine the rate of beta-amyloid pathology and AD co-pathology by measuring AD CSF biomarkers, namely, amyloid beta with 42 and 40 amino acids (Aβ42), the Aβ42/Aβ40 ratio, total Tau protein (t-Tau) and phosphorylated Tau protein at threonine 181 (p-Tau), in a cohort of iNPH patients, as well as to investigate the possible associations among CSF biomarkers and iNPH neuropsychological profiles. Fifty-three patients with iNPH were included in the present study. CSF Aβ42, Aβ40, t-Tau and p-Tau were measured in duplicate with double-sandwich ELISA assays. The neuropsychological evaluation consisted of the Mini-Mental State Examination, Frontal Assessment Battery, Five-Word Test and CLOX drawing tests 1 and 2. After statistical analysis, we found that amyloid pathology and AD co-pathology are rather common in iNPH patients and that higher values of t-Tau and p-Tau CSF levels, as well as the existence of the AD CSF profile, are associated with more severe memory impairment in the study patients. In conclusion, our study has confirmed that amyloid pathology and AD-co-pathology are rather common in iNPH patients and that CSF markers of AD pathology and t-Tau are associated with a worse memory decline in these patients. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Neuropsychological profiles comparison between Multiple Sclerosis patients and Multiple Sclerosis patients with overlapping features of systemic lupus erythematosus

Author

Stavrogianni, Konstantina, primary, Kitsos, Dimitrios K., additional, Giannopapas, Vasileios, additional, Chasiotis, Athanasios K., additional, Christouli, Niki, additional, Paraskevas, Panagiotis G., additional, Zompola, Christina, additional, Tsivgoulis, Georgios, additional, Paraskevas, George P., additional, and Giannopoulos, Sotirios, additional

Published
2023
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36. The impact of automated hippocampal volumetry on diagnostic confidence in patients with suspected Alzheimer's disease: A European Alzheimer's Disease Consortium study

Author

Bosco, Paolo, Redolfi, Alberto, Bocchetta, Martina, Ferrari, Clarissa, Mega, Anna, Galluzzi, Samantha, Austin, Mark, Chincarini, Andrea, Collins, D. Louis, Duchesne, Simon, Maréchal, Bénédicte, Roche, Alexis, Sensi, Francesco, Wolz, Robin, Alegret, Montserrat, Assal, Frederic, Balasa, Mircea, Bastin, Christine, Bougea, Anastasia, Emek-Savaş, Derya Durusu, Engelborghs, Sebastiaan, Grimmer, Timo, Grosu, Galina, Kramberger, Milica G., Lawlor, Brian, Mandic Stojmenovic, Gorana, Marinescu, Mihaela, Mecocci, Patrizia, Molinuevo, José Luis, Morais, Ricardo, Niemantsverdriet, Ellis, Nobili, Flavio, Ntovas, Konstantinos, O'Dwyer, Sarah, Paraskevas, George P., Pelini, Luca, Picco, Agnese, Salmon, Eric, Santana, Isabel, Sotolongo-Grau, Oscar, Spiru, Luiza, Stefanova, Elka, Popovic, Katarina Surlan, Tsolaki, Magda, Yener, Görsev G., Zekry, Dina, and Frisoni, Giovanni B.

Published
2017
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39. The Prevalence of Diabetes Mellitus Type II (DMII) in the Multiple Sclerosis Population: A Systematic Review and Meta-Analysis

Author

Giannopapas, Vasileios, primary, Palaiodimou, Lina, additional, Kitsos, Dimitrios, additional, Papagiannopoulou, Georgia, additional, Stavrogianni, Konstantina, additional, Chasiotis, Athanasios, additional, Kosmidou, Maria, additional, Tzartos, John S., additional, Paraskevas, George P., additional, Bakalidou, Daphne, additional, Tsivgoulis, Georgios, additional, and Giannopoulos, Sotirios, additional

Published
2023
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40. The Dynamic Relationship between the Glymphatic System, Aging, Memory, and Sleep

Author

Voumvourakis, Konstantinos I., primary, Sideri, Eleni, additional, Papadimitropoulos, Georgios N., additional, Tsantzali, Ioanna, additional, Hewlett, Paul, additional, Kitsos, Dimitrios, additional, Stefanou, Marianna, additional, Bonakis, Anastasios, additional, Giannopoulos, Sotirios, additional, Tsivgoulis, Giorgios, additional, and Paraskevas, George P., additional

Published
2023
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41. Assessment of Aggregated and Exosome-Associated α-Synuclein in Brain Tissue and Cerebrospinal Fluid Using Specific Immunoassays

Author

Anagnostou, Dimitrios, primary, Sfakianaki, Garifalia, additional, Melachroinou, Katerina, additional, Soutos, Miltiadis, additional, Constantinides, Vassilios, additional, Vaikath, Nishant, additional, Tsantzali, Ioanna, additional, Paraskevas, George P., additional, Agnaf, Omar El, additional, Vekrellis, Kostas, additional, and Emmanouilidou, Evangelia, additional

Published
2023
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44. CSF Aβ42 and Aβ42/Aβ40 Ratio in Alzheimer’s Disease and Frontotemporal Dementias

Author

Constantinides, Vasilios C., Paraskevas, George P., Boufidou, Fotini, Bourbouli, Mara, Pyrgelis, Efstratios-Stylianos, Stefanis, Leonidas, and Kapaki, Elisabeth

Subjects
amyloid beta with 42 amino acids, tau proteins, Alzheimer’s disease, frontotemporal dementia, cerebrospinal fluid
Abstract

Background: Alzheimer’s disease dementia (ADD) may manifest with atypical phenotypes, resembling behavioral variant frontotemporal dementia (bvFTD) and corticobasal syndrome (CBS), phenotypes which typically have an underlying frontotemporal lobar degeneration with tau proteinopathy (FTLD-tau), such as Pick’s disease, corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), or FTLD with TDP-43 proteinopathy (FTLD-TDP). CSF biomarkers total and phosphorylated tau (τT and τP-181), and amyloid beta with 42 and 40 amino acids (Aβ42 and Aβ40) are biomarkers of AD pathology. The primary aim of this study was to compare the diagnostic accuracy of Aβ42 to Aβ42/Aβ40 ratio in: (a) differentiating ADD vs. frontotemporal dementias; (b) patients with AD pathology vs. non-AD pathologies; (c) compare biomarker ratios and composite markers to single CSF biomarkers in the differentiation of AD from FTD; Methods: In total, 263 subjects were included (ADD: n = 98; bvFTD: n = 49; PSP: n = 50; CBD: n = 45; controls: n = 21). CSF biomarkers were measured by commercially available ELISAs (EUROIMMUN). Multiple biomarker ratios (Aβ42/Aβ40; τT/τP-181; τT/Aβ42; τP-181/Aβ42) and composite markers (t-tau: τT/(Aβ42/Aβ40); p-tau: τP-181/(Aβ42/Aβ40) were calculated. ROC curve analysis was performed to compare AUCs of Aβ42 and Aβ42/Aβ40 ratio and relevant composite markers between ADD and FTD, as defined clinically. BIOMARKAPD/ABSI criteria (abnormal τT, τP-181 Aβ42, and Aβ42/Aβ40 ratio) were used to re-classify all patients into AD pathology vs. non-AD pathologies, and ROC curve analysis was repeated to compare Aβ42 and Aβ42/Aβ40; Results: Aβ42 did not differ from Aβ42/Aβ40 ratio in the differentiation of ADD from FTD (AUCs 0.752 and 0.788 respectively; p = 0.212). The τT/Aβ42 ratio provided maximal discrimination between ADD and FTD (AUC:0.893; sensitivity 88.8%, specificity 80%). BIOMARKAPD/ABSI criteria classified 60 patients as having AD pathology and 211 as non-AD. A total of 22 had discrepant results and were excluded. Aβ42/Aβ40 ratio was superior to Aβ42 in the differentiation of AD pathology from non-AD pathology (AUCs: 0.939 and 0.831, respectively; p < 0.001). In general, biomarker ratios and composite markers were superior to single CSF biomarkers in both analyses. Conclusions: Aβ42/Aβ40 ratio is superior to Aβ42 in identifying AD pathology, irrespective of the clinical phenotype. CSF biomarker ratios and composite markers provide higher diagnostic accuracy compared to single CSF biomarkers.

Published
2023
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45. sj-docx-1-msj-10.1177_13524585221150881 – Supplemental material for Safety of COVID-19 vaccines in multiple sclerosis: A systematic review and meta-analysis

Author

Stefanou, Maria-Ioanna, Palaiodimou, Lina, Theodorou, Aikaterini, Christodoulou, Maria Veatriki, Tzartos, John S, Tzanetakos, Dimitrios, Kitsos, Dimitrios, Chondrogianni, Maria, Zouvelou, Vasiliki, Dardiotis, Efthimios, Tzavellas, Elias, Syrigou, Ekaterini, Benetou, Vassiliki, Paraskevas, George P, Tsiodras, Sotirios, Tsivgoulis, Georgios, and Giannopoulos, Sotirios

Subjects
FOS: Clinical medicine, 111702 Aged Health Care, FOS: Health sciences, 110904 Neurology and Neuromuscular Diseases
Abstract

Supplemental material, sj-docx-1-msj-10.1177_13524585221150881 for Safety of COVID-19 vaccines in multiple sclerosis: A systematic review and meta-analysis by Maria-Ioanna Stefanou, Lina Palaiodimou, Aikaterini Theodorou, Maria Veatriki Christodoulou, John S Tzartos, Dimitrios Tzanetakos, Dimitrios Kitsos, Maria Chondrogianni, Vasiliki Zouvelou, Efthimios Dardiotis, Elias Tzavellas, Ekaterini Syrigou, Vassiliki Benetou, George P Paraskevas, Sotirios Tsiodras, Georgios Tsivgoulis and Sotirios Giannopoulos in Multiple Sclerosis Journal

Published
2023
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46. Safety of COVID-19 vaccines in multiple sclerosis: A systematic review and meta-analysis

Author

Stefanou, Maria-Ioanna, primary, Palaiodimou, Lina, additional, Theodorou, Aikaterini, additional, Christodoulou, Maria Veatriki, additional, Tzartos, John S, additional, Tzanetakos, Dimitrios, additional, Kitsos, Dimitrios, additional, Chondrogianni, Maria, additional, Zouvelou, Vasiliki, additional, Dardiotis, Efthimios, additional, Tzavellas, Elias, additional, Syrigou, Ekaterini, additional, Benetou, Vassiliki, additional, Paraskevas, George P, additional, Tsiodras, Sotirios, additional, Tsivgoulis, Georgios, additional, and Giannopoulos, Sotirios, additional

Published
2023
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47. Application of the AT(N) and Other CSF Classification Systems in Behavioral Variant Frontotemporal Dementia

Author

Constantinides, Vasilios C., primary, Boufidou, Fotini, additional, Bourbouli, Mara, additional, Pyrgelis, Efstratios-Stylianos, additional, Ghika, Apostolia, additional, Koros, Christos, additional, Liakakis, George, additional, Papageorgiou, Sokratis, additional, Stefanis, Leonidas, additional, Paraskevas, George P., additional, and Kapaki, Elisabeth, additional

Published
2023
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48. Clinical, Neuroimaging, and Genetic Markers in Cerebral Amyloid Angiopathy-Related Inflammation: A Systematic Review and Meta-Analysis

Author

Theodorou, Aikaterini, primary, Palaiodimou, Lina, additional, Malhotra, Konark, additional, Zompola, Christina, additional, Katsanos, Aristeidis H., additional, Shoamanesh, Ashkan, additional, Boviatsis, Efstathios, additional, Dardiotis, Efthimios, additional, Spilioti, Martha, additional, Sacco, Simona, additional, Werring, David J., additional, Cordonnier, Charlotte, additional, Alexandrov, Andrei V., additional, Paraskevas, George P., additional, and Tsivgoulis, Georgios, additional

Published
2023
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49. Hippocampal subfield volumetry in corticobasal syndrome of diverse underlying pathologies

Author

Constantinides, Vasilios C., primary, Tentolouris-Piperas, Vasileios, additional, Paraskevas, George P., additional, Pyrgelis, Efstratios-Stylianos, additional, Velonakis, Georgios, additional, Karavasilis, Efstratios, additional, Toulas, Panagiotis, additional, Boufidou, Fotini, additional, Stefanis, Leonidas, additional, and Kapaki, Elisabeth, additional

Published
2022
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