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Start Over Author "De Deyn, Peter Paul" Journal journal of alzheimer's disease
28 results on '"De Deyn, Peter Paul"'

2. Improved Alzheimer’s Disease versus Frontotemporal Lobar Degeneration Differential Diagnosis Combining EEG and Neurochemical Biomarkers: A Pilot Study

Author

Laton, Jorne, primary, Van Schependom, Jeroen, additional, Goossens, Joery, additional, Wiels, Wietse, additional, Sieben, Anne, additional, De Deyn, Peter Paul, additional, Goeman, Johan, additional, Streffer, Johannes, additional, van der Zee, Julie, additional, Martin, Jean-Jacques, additional, Van Broeckhoven, Christine, additional, De Vos, Maarten, additional, Bjerke, Maria, additional, Nagels, Guy, additional, and Engelborghs, Sebastiaan, additional

Published
2022
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4. Diagnostic Performance of Automated MRI Volumetry by icobrain dm for Alzheimer’s Disease in a Clinical Setting: A REMEMBER Study

Author

Wittens, Mandy Melissa Jane, primary, Sima, Diana Maria, additional, Houbrechts, Ruben, additional, Ribbens, Annemie, additional, Niemantsverdriet, Ellis, additional, Fransen, Erik, additional, Bastin, Christine, additional, Benoit, Florence, additional, Bergmans, Bruno, additional, Bier, Jean-Christophe, additional, De Deyn, Peter Paul, additional, Deryck, Olivier, additional, Hanseeuw, Bernard, additional, Ivanoiu, Adrian, additional, Lemper, Jean-Claude, additional, Mormont, Eric, additional, Picard, Gaëtane, additional, de la Rosa, Ezequiel, additional, Salmon, Eric, additional, Segers, Kurt, additional, Sieben, Anne, additional, Smeets, Dirk, additional, Struyfs, Hanne, additional, Thiery, Evert, additional, Tournoy, Jos, additional, Triau, Eric, additional, Vanbinst, Anne-Marie, additional, Versijpt, Jan, additional, Bjerke, Maria, additional, and Engelborghs, Sebastiaan, additional

Published
2021
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5. Dementia, End of Life, and Euthanasia: A Survey Among Dementia Specialists Organized by the Belgian Dementia Council

Author

Picard, Gaëtane, primary, Bier, Jean-Christophe, additional, Capron, Isabelle, additional, De Deyn, Peter Paul, additional, Deryck, Olivier, additional, Engelborghs, Sebastiaan, additional, Hanseeuw, Bernard, additional, Lemper, Jean-Claude, additional, Mormont, Eric, additional, Petrovic, Mirko, additional, Salmon, Eric, additional, Segers, Kurt, additional, Sieben, Anne, additional, Thiery, Evert, additional, Ventura, Manfredi, additional, Versijpt, Jan, additional, and Ivanoiu, Adrian, additional

Published
2019
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6. Driving Difficulties Among Patients with Alzheimer’s Disease and Other Neurodegenerative Disorders

Author

Fuermaier, Anselm B.M., primary, Piersma, Dafne, additional, de Waard, Dick, additional, Davidse, Ragnhild J., additional, de Groot, Jolieke, additional, Doumen, Michelle J.A., additional, Bredewoud, Ruud A., additional, Claesen, René, additional, Lemstra, Afina W., additional, Scheltens, Philip, additional, Vermeeren, Annemiek, additional, Ponds, Rudolf, additional, Verhey, Frans, additional, De Deyn, Peter Paul, additional, Brouwer, Wiebo H., additional, and Tucha, Oliver, additional

Published
2019
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8. Anti-Tau Monoclonal Antibodies Derived from Soluble and Filamentous Tau Show Diverse Functional Properties in vitro and in vivo

Author

Vandermeeren, Marc, primary, Borgers, Marianne, additional, Van Kolen, Kristof, additional, Theunis, Clara, additional, Vasconcelos, Bruno, additional, Bottelbergs, Astrid, additional, Wintmolders, Cindy, additional, Daneels, Guy, additional, Willems, Roland, additional, Dockx, Koen, additional, Delbroek, Lore, additional, Marreiro, André, additional, Ver Donck, Luc, additional, Sousa, Cristiano, additional, Nanjunda, Rupesh, additional, Lacy, Eilyn, additional, Van De Casteele, Tom, additional, Van Dam, Debby, additional, De Deyn, Peter Paul, additional, Kemp, John A., additional, Malia, Thomas J., additional, and Mercken, Marc H., additional

Published
2018
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9. A Retrospective Belgian Multi-Center MRI Biomarker Study in Alzheimer’s Disease (REMEMBER)

Author

Niemantsverdriet, Ellis, primary, Ribbens, Annemie, additional, Bastin, Christine, additional, Benoit, Florence, additional, Bergmans, Bruno, additional, Bier, Jean-Christophe, additional, Bladt, Roxanne, additional, Claes, Lene, additional, De Deyn, Peter Paul, additional, Deryck, Olivier, additional, Hanseeuw, Bernard, additional, Ivanoiu, Adrian, additional, Lemper, Jean-Claude, additional, Mormont, Eric, additional, Picard, Gaëtane, additional, Salmon, Eric, additional, Segers, Kurt, additional, Sieben, Anne, additional, Smeets, Dirk, additional, Struyfs, Hanne, additional, Thiery, Evert, additional, Tournoy, Jos, additional, Triau, Eric, additional, Vanbinst, Anne-Marie, additional, Versijpt, Jan, additional, Bjerke, Maria, additional, and Engelborghs, Sebastiaan, additional

Published
2018
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11. The Cerebrospinal Fluid Aβ1–42/Aβ1–40 Ratio Improves Concordance with Amyloid-PET for Diagnosing Alzheimer’s Disease in a Clinical Setting

Author

Niemantsverdriet, Ellis, primary, Ottoy, Julie, additional, Somers, Charisse, additional, De Roeck, Ellen, additional, Struyfs, Hanne, additional, Soetewey, Femke, additional, Verhaeghe, Jeroen, additional, Van den Bossche, Tobi, additional, Van Mossevelde, Sara, additional, Goeman, Johan, additional, De Deyn, Peter Paul, additional, Mariën, Peter, additional, Versijpt, Jan, additional, Sleegers, Kristel, additional, Van Broeckhoven, Christine, additional, Wyffels, Leonie, additional, Albert, Adrien, additional, Ceyssens, Sarah, additional, Stroobants, Sigrid, additional, Staelens, Steven, additional, Bjerke, Maria, additional, and Engelborghs, Sebastiaan, additional

Published
2017
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12. EEG Dominant Frequency Peak Differentiates Between Alzheimer’s Disease and Frontotemporal Lobar Degeneration

Author

Goossens, Joery, primary, Laton, Jorne, additional, Van Schependom, Jeroen, additional, Gielen, Jeroen, additional, Struyfs, Hanne, additional, Van Mossevelde, Sara, additional, Van den Bossche, Tobi, additional, Goeman, Johan, additional, De Deyn, Peter Paul, additional, Sieben, Anne, additional, Martin, Jean-Jacques, additional, Van Broeckhoven, Christine, additional, van der Zee, Julie, additional, Engelborghs, Sebastiaan, additional, and Nagels, Guy, additional

Published
2016
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13. A Decade of Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease in Belgium

Author

Somers, Charisse, primary, Struyfs, Hanne, additional, Goossens, Joery, additional, Niemantsverdriet, Ellis, additional, Luyckx, Jill, additional, De Roeck, Naomi, additional, De Roeck, Ellen, additional, De Vil, Bart, additional, Cras, Patrick, additional, Martin, Jean-Jacques, additional, De Deyn, Peter-Paul, additional, Bjerke, Maria, additional, and Engelborghs, Sebastiaan, additional

Published
2016
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15. Association of Cerebrospinal Fluid (CSF) Insulin with Cognitive Performance and CSF Biomarkers of Alzheimer's Disease.

Author

Geijselaers, Stefan L. C., Aalten, Pauline, Ramakers, Inez H. G. B., De Deyn, Peter Paul, Heijboer, Annemieke C., Koek, Huiberdina L., OldeRikkert, Marcel G. M., Papma, Janne M., Reesink, Fransje E., Smits, Lieke L., Stehouwer, Coen D. A., Teunissen, Charlotte E., Verhey, Frans R. J., van der Flier, Wiesje M., Biessels, Geert Jan, and Parelsnoer Institute Neurodegenerative Diseases study group

Subjects
CEREBROSPINAL fluid, ALZHEIMER'S disease, MAGNETIC resonance imaging, MILD cognitive impairment, DEMENTIA, COGNITION disorders diagnosis, BRAIN metabolism, APOLIPOPROTEINS, BRAIN, CELLULAR signal transduction, COGNITION disorders, INSULIN, NEUROPSYCHOLOGICAL tests, NERVE tissue proteins, PEPTIDES, PSYCHOLOGICAL tests, DISEASE complications
Abstract

Background: Abnormal insulin signaling in the brain has been linked to Alzheimer's disease (AD).Objective: To evaluate whether cerebrospinal fluid (CSF) insulin levels are associated with cognitive performance and CSF amyloid-β and Tau. Additionally, we explore whether any such association differs by sex or APOE ɛ4 genotype.Methods: From 258 individuals participating in the Parelsnoer Institute Neurodegenerative Diseases, a nationwide multicenter memory clinic population, we selected 138 individuals (mean age 66±9 years, 65.2% male) diagnosed with subjective cognitive impairment (n = 45), amnestic mild cognitive impairment (n = 44), or AD (n = 49), who completed a neuropsychological assessment, including tests of global cognition and memory performance, and who underwent lumbar puncture. We measured CSF levels of insulin, amyloid-β1-42, total (t-)Tau, and phosphorylated (p-)Tau.Results: CSF insulin levels did not differ between the diagnostic groups (p = 0.136). Across the whole study population, CSF insulin was unrelated to cognitive performance and CSF biomarkers of AD, after adjustment for age, sex, body mass index, diabetes status, and clinic site (all p≥0.131). Importantly, however, we observed effect modification by sex and APOE ɛ4 genotype. Specifically, among women, higher insulin levels in the CSF were associated with worse global cognition (standardized regression coefficient -0.483; p = 0.008) and higher p-Tau levels (0.353; p = 0.040). Among non-carriers of the APOE ɛ4 allele, higher CSF insulin was associated with higher t-Tau (0.287; p = 0.008) and p-Tau (0.246; p = 0.029).Conclusion: Our findings provide further evidence for a relationship between brain insulin signaling and AD pathology. It also highlights the need to consider sex and APOE ɛ4 genotype when assessing the role of insulin. [ABSTRACT FROM AUTHOR]

Published
2018
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17. Region- and age-specific changes in glutamate transport in the <tex>A\beta PP23$</tex> mouse model for Alzheimers disease

Author

Schallier, Anneleen, Smolders, Ilse, Van Dam, Debby, Loyens, Ellen, De Deyn, Peter Paul, Michotte, Alex, Michotte, Yvette, and Massie, Ann

Subjects
Human medicine
Abstract

Using 8- and 18-month-old AβPP23 mice, we investigated the involvement of high-affinity glutamate transporters (GLAST, GLT-1, EAAC1), vesicular glutamate transporters (VGLUT1-3) and xCT, the specific subunit of system xc-, in Alzheimers disease (AD) pathogenesis. Transporter expression was studied in cortical and hippocampal tissue and linked to extracellular glutamate and glutamate reuptake activity as measured using in vivo microdialysis. In 8-month-old animals, we could not observe plaque formation or gliosis. Yet, in hippocampus as well as cortex GLAST and GLT-1 expression was decreased. Whereas in cortex this was accompanied by upregulated VGLUT1 expression, extracellular glutamate concentrations were decreased. Surprisingly, inhibiting glutamate reuptake with TBOA revealed increased glutamate reuptake activity in cortex of AβPP23 mice, despite decreased GLAST and GLT-1 expression, and resulted in status epilepticus in all AβPP23 mice, contrary to wildtype littermates. In hippocampus of 8-month-old AβPP23 mice, we observed increased EAAC1 expression besides the decrease in GLAST and GLT-1. Yet, glutamate reuptake activity was drastically decreased according to the decreased GLAST and GLT-1 expression. In 18-month-old AβPP23 mice, plaque formation and gliosis in cortex and hippocampus were accompanied by decreased GLT-1 expression. We also showed, for the first time, increased cortical expression of VGLUT3 and xCT together with a strong tendency towards increased cortical extracellular glutamate levels. VGLUT2 expression remained unaltered in all conditions. The present findings support the hypothesis that alterations in transport of glutamate, and more particular via GLT-1, may be involved in AD pathogenesis.

Published
2011

19. EEG Dominant Frequency Peak Differentiates Between Alzheimer's Disease and Frontotemporal Lobar Degeneration.

Author

Goossens, Joery, Laton, Jorne, Van Schependom, Jeroen, Gielen, Jeroen, Struyfs, Hanne, Van Mossevelde, Sara, den Bossche, Tobi Van, Goeman, Johan, De Deyn, Peter Paul, Sieben, Anne, Martin, Jean-Jacques, Van Broeckhoven, Christine, van der Zee, Julie, Engelborghs, Sebastiaan, Nagels, Guy, and Van den Bossche, Tobi

Subjects
ELECTROENCEPHALOGRAPHY, FRONTOTEMPORAL lobar degeneration, ALZHEIMER'S disease diagnosis, DIAGNOSIS of dementia, DIFFERENTIAL diagnosis, ALZHEIMER'S disease, BRAIN, LONGITUDINAL method, RECEIVER operating characteristic curves, DIAGNOSIS
Abstract

We investigated the power of EEG as biomarker in differential diagnosis of Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). EEG was recorded from 106 patients with AD or FTLD, of which 37 had a definite diagnosis, and 40 controls. Dominant frequency peaks were extracted for all 19 channels, for each subject. The average frequency of the largest dominant frequency peaks (maxpeak) was significantly lower in AD than FTLD patients and controls. Based on ROC analysis, classification could be made with diagnostic accuracy of 78.9%. Our findings show that quantitative analysis of EEG maxpeak frequency is an easy and useful measure for differential dementia diagnosis. [ABSTRACT FROM AUTHOR]

Published
2017
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24. A Decade of Cerebrospinal Fluid Biomarkers for Alzheimer's Disease in Belgium.

Author

Somersa, Charisse, Struyfs, Hanne, Goossens, Joery, Niemantsverdriet, Ellis, Luyckx, Jill, De Roeck, Naomi, De Roeck, Ellen, De Vil, Bart, Cras, Patrick, Martin, Jean-Jacques, De Deyn, Peter-Paul, Bjerke, Maria, Engelborghs, Sebastiaan, and Somers, Charisse

Subjects
CEREBROSPINAL fluid, BIOMARKERS, DEMENTIA, ALZHEIMER'S disease, ENZYME-linked immunosorbent assay
Abstract

During the past ten years, over 5,000 cerebrospinal fluid (CSF) samples were analyzed at the Reference Center for Biological Markers of Dementia (BIODEM), UAntwerp, for core Alzheimer's disease (AD) CSF biomarkers: amyloid-β peptide of 42 amino acids (Aβ1-42), total tau protein (T-tau), and tau phosphorylated at threonine 181 (P-tau181P). CSF biomarker analyses were performed using single-analyte ELISA kits. In-house validated cutoff values were applied: Aβ1-42 <638.5 pg/mL, T-tau >296.5 pg/mL, P-tau181P >56.5 pg/mL. A CSF biomarker profile was considered to be suggestive for AD if the CSF Aβ1-42 concentration was below the cutoff, in combination with T-tau and/or P-tau181P values above the cutoff (IWG2 criteria for AD). Biomarker analyses were requested for following clinical indications: 1) neurochemical confirmation of AD in case of clinical AD, 2) neurochemical confirmation of AD in case of doubt between AD and a non-AD dementia, 3) neurochemical diagnosis of prodromal AD in case of mild cognitive impairment, 4) neurochemical confirmation of AD in case of psychiatric symptoms (like depression, psychosis), or 5) other clinical indications. During these ten years, the number of yearly referred samples increased by 238% and clinical indications for referral showed a shift from neurochemical confirmation of AD in case of clinical AD to differential dementia diagnosis in case of doubt between AD and a non-AD dementia. Four percent of the patients also had a postmortem neuropathological examination. Together, these biomarker data were the basis for several research papers, and significantly contributed to the validation of these biomarkers in autopsy-confirmed subjects. [ABSTRACT FROM AUTHOR]

Published
2016
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27. Plasma Amyloid-β Forms in Alzheimer's Disease and Non-Alzheimer's Disease Patients.

Author

Le Bastard, Nathalie, Leurs, Judith, Blomme, Walter, De Deyn, Peter Paul, and Engelborghs, Sebastiaan

Subjects
AMYLOID beta-protein, ALZHEIMER'S patients, DEMENTIA, BIOMARKERS, NEUROBEHAVIORAL disorders
Abstract

The objective of this study was to evaluate the diagnostic performance of full-length and N-truncated plasma amyloid-β (Aβ) forms in patients with Alzheimer's disease (AD) and non-Alzheimer's disease dementia (non-AD) as compared to healthy control subjects. Plasma samples from 50 AD, 50 non-AD, and 47 control subjects were included and analyzed using a multiparameter fluorimetric bead-based immunoassay for the simultaneous quantification of different Aβ forms. No significant differences in Aβ isoforms were detected between dementia and controls; or AD, non-AD, and controls. Compared to control subjects, pooled dementia patients (AD and non-AD) and AD patients alone had significantly lower plasma Aβ1-42/AβN-42 ratios. In each diagnostic group, all plasma Aβ concentrations were significantly correlated. No significant correlations between plasma Aβ forms and age were found. The low diagnostic performance of cross-sectional plasma Aβ measurements hampers future application as diagnostic markers or screening tools for dementia. CSF biomarker analysis remains superior, although the possible application of longitudinal plasma Aβ measurements as screening tools for dementia remains to be elucidated. [ABSTRACT FROM AUTHOR]

Published
2010
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28. Effects of AZD3480 on cognition in patients with mild-to-moderate Alzheimers disease : a phase IIb dose-finding study

Author

Frölich, Lutz, Ashwood, Tim, Nilsson, Jonas, Eckerwall, Göran, De Deyn, Peter Paul, et al., and Sirocco Investigators

Subjects
mental disorders, Human medicine
Abstract

AZD3480 is a selective agonist of the central 42 and 22 neuronal icotinic cholinergic receptors (NNRs). Its effects on cognition were investigated in 567 patients with mild-to-moderate Alzheimers disease (AD) (Mini Mental State Examination [MMSE] 1226). Mean baseline MMSE was 21 (SD ± 3.7), with 61% of patients having mild disease (MMSE 2126). Mean age was 74 (range 5885) years. Patients were randomized to one of 5 treatment groups: AZD3480 5 mg, 20 mg or 35/100 mg, donepezil 10 mg (active comparator) or placebo, and treated once daily for 12 weeks. The primary outcome measure was change from baseline at Week 12 on the AD Assessment Scale-Cognitive Subscale (ADAS-Cog). Neither AZD3480 nor donepezil showed a statistically significant improvement versus placebo on ADAS-Cog. Improvements in a number of secondary outcome measures (MMSE, AD Cooperative Study-Clinical Global Impression of Change (ADCS-CGIC) and Disability Assessment for Dementia [DAD]) were observed for AZD3480 and for donepezil. A post-hoc analysis on ADAS-Cog, excluding patients with very mild AD (MMSE 2526) indicated improvement versus placebo for AZD3480 20 mg (−1.4, 95% CI: −3.0; 0.2) and donepezil (−1.0, 95% CI: −2.3; 0.3). AZD3480 was well tolerated. The study did not meet proof of concept criteria, since neither AZD3480 nor donepezil were statistically significantly superior to placebo on ADAS-Cog and was considered to be inconclusive. Further studies are required to determine the therapeutic potential of stimulating 42 receptors with NNRs in AD patients.

Published
2011

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