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6. The association between posterior resting-state EEG alpha rhythms and functional MRI connectivity in older adults with subjective memory complaint

Author

Lopez, Susanna, Hampel, Harald, Chiesa, Patrizia Andrea, Del Percio, Claudio, Noce, Giuseppe, Lizio, Roberta, Teipel, Stefan J., Dyrba, Martin, González-Escamilla, Gabriel, Bakardjian, Hovagim, Cavedo, Enrica, Lista, Simone, Vergallo, Andrea, Lemercier, Pablo, Spinelli, Giuseppe, Grothe, Michel J., Potier, Marie-Claude, Stocchi, Fabrizio, Ferri, Raffaele, Habert, Marie-Odile, Dubois, Bruno, and Babiloni, Claudio

Published
2024
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9. The β-Secretase BACE1 in Alzheimer’s Disease

Author

Hampel, Harald, Vassar, Robert, De Strooper, Bart, Hardy, John, Willem, Michael, Singh, Neeraj, Zhou, John, Yan, Riqiang, Vanmechelen, Eugeen, De Vos, Ann, Nisticò, Robert, Corbo, Massimo, Imbimbo, Bruno Pietro, Streffer, Johannes, Voytyuk, Iryna, Timmers, Maarten, Tahami Monfared, Amir Abbas, Irizarry, Michael, Albala, Bruce, Koyama, Akihiko, Watanabe, Naoto, Kimura, Teiji, Yarenis, Lisa, Lista, Simone, Kramer, Lynn, and Vergallo, Andrea

Subjects
Biochemistry and Cell Biology, Biological Sciences, Neurosciences, Acquired Cognitive Impairment, Aging, Alzheimer's Disease, Brain Disorders, Genetics, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, Neurodegenerative, Underpinning research, Aetiology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Neurological, Alzheimer Disease, Amyloid Precursor Protein Secretases, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Aspartic Acid Endopeptidases, Humans, Mice, Mice, Knockout, Alzheimer’s disease, BACE1 inhibitors, Biomarkers, Clinical trials, Soluble amyloid, Synaptic, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Biological sciences, Biomedical and clinical sciences, Psychology
Abstract

BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) was initially cloned and characterized in 1999. It is required for the generation of all monomeric forms of amyloid-β (Aβ), including Aβ42, which aggregates into bioactive conformational species and likely initiates toxicity in Alzheimer's disease (AD). BACE1 concentrations and rates of activity are increased in AD brains and body fluids, thereby supporting the hypothesis that BACE1 plays a critical role in AD pathophysiology. Therefore, BACE1 is a prime drug target for slowing down Aβ production in early AD. Besides the amyloidogenic pathway, BACE1 has other substrates that may be important for synaptic plasticity and synaptic homeostasis. Indeed, germline and adult conditional BACE1 knockout mice display complex neurological phenotypes. Despite BACE1 inhibitor clinical trials conducted so far being discontinued for futility or safety reasons, BACE1 remains a well-validated therapeutic target for AD. A safe and efficacious compound with high substrate selectivity as well as a more accurate dose regimen, patient population, and disease stage may yet be found. Further research should focus on the role of Aβ and BACE1 in physiological processes and key pathophysiological mechanisms of AD. The functions of BACE1 and the homologue BACE2, as well as the biology of Aβ in neurons and glia, deserve further investigation. Cellular and molecular studies of BACE1 and BACE2 knockout mice coupled with biomarker-based human research will help elucidate the biological functions of these important enzymes and identify their substrates and downstream effects. Such studies will have critical implications for BACE1 inhibition as a therapeutic approach for AD.

Published
2021

10. MiRNA-15b and miRNA-125b are associated with regional Aβ-PET and FDG-PET uptake in cognitively normal individuals with subjective memory complaints.

Author

Vergallo, Andrea, Lista, Simone, Zhao, Yuhai, Lemercier, Pablo, Teipel, Stefan J, Potier, Marie-Claude, Habert, Marie-Odile, Dubois, Bruno, Lukiw, Walter J, Hampel, Harald, INSIGHT-preAD study group, and Alzheimer Precision Medicine Initiative (APMI)

Subjects
INSIGHT-preAD study group, Alzheimer Precision Medicine Initiative, Clinical Sciences, Public Health and Health Services, Psychology
Abstract

There is substantial experimental evidence for dysregulation of several microRNA (miRNA) expression levels in Alzheimer's disease (AD). MiRNAs modulate critical brain intracellular signaling pathways and are associated with AD core pathophysiological mechanisms. First, we conducted a real-time quantitative PCR-based pilot study to identify a set of brain-enriched miRNAs in a monocentric cohort of cognitively normal individuals with subjective memory complaints, a condition associated with increased risk of AD. Second, we investigated the impact of age, sex, and the Apolipoprotein E ε4 (APOE ε4) allele, on the identified miRNA plasma concentrations. In addition, we explored the cross-sectional and longitudinal association of the miRNAs plasma concentrations with regional brain metabolic uptake using amyloid-β (Aβ)-positron emission tomography (Aβ-PET) and 18F-fluorodeoxyglucose-PET (18F-FDG-PET). We identified a set of six brain-enriched miRNAs-miRNA-125b, miRNA-146a, miRNA-15b, miRNA-148a, miRNA-26b, and miRNA-100. Age, sex, and APOE ε4 allele were not associated with individual miRNA abundance. MiRNA-15b concentrations were significantly lower in the Aβ-PET-positive compared to Aβ-PET-negative individuals. Furthermore, we found a positive effect of the miRNA-15b*time interaction on regional metabolic 18F-FDG-PET uptake in the left hippocampus. Plasma miRNA-125b concentrations, as well as the miRNA-125b*time interaction (over a 2-year follow-up), were negatively associated with regional Aβ-PET standard uptake value ratio in the right anterior cingulate cortex. At baseline, we found a significantly negative association between plasma miRNA-125b concentrations and 18F-FDG-PET uptake in specific brain regions. In an asymptomatic at-risk population for AD, we show significant associations between plasma concentrations of miRNA-125b and miRNA-15b with core neuroimaging biomarkers of AD pathophysiology. Our results, coupled with existing experimental evidence, suggest a potential protective anti-Aβ effect of miRNA-15b and a biological link between miRNA-125b and Aβ-independent neurotoxic pathways.

Published
2021

11. Aptamarker prediction of brain amyloid-β status in cognitively normal individuals at risk for Alzheimer's disease.

Author

Penner, Gregory, Lecocq, Soizic, Chopin, Anaëlle, Vedoya, Ximena, Lista, Simone, Vergallo, Andrea, Cavedo, Enrica, Lejeune, Francois-Xavier, Dubois, Bruno, Hampel, Harald, INSIGHT-preAD study group, and Alzheimer Precision Medicine Initiative (APMI)

Subjects
INSIGHT-preAD study group, Alzheimer Precision Medicine Initiative, Humans, Alzheimer Disease, Early Diagnosis, Case-Control Studies, Aged, Aged, 80 and over, Female, Male, SELEX Aptamer Technique, Amyloid beta-Peptides, Biomarkers, and over, General Science & Technology
Abstract

The traditional approach to biomarker discovery for any pathology has been through hypothesis-based research one candidate at a time. The objective of this study was to develop an agnostic approach for the simultaneous screening of plasma for consistent molecular differences between a group of individuals exhibiting a pathology and a group of healthy individuals. To achieve this, we focused on developing a predictive tool based on plasma for the amount of brain amyloid-β deposition as observed in PET scans. The accumulation of brain amyloid-β (Aβ) plaques is a key risk factor for the development of Alzheimer's disease. A contrast was established between cognitively normal individuals above the age of 70 that differed for the amount of brain amyloid-β observed in PET scans (INSIGHT study group). Positive selection was performed against a pool of plasma from individuals with high brain amyloid and negative selection against a pool of plasma from individuals with low brain amyloid This enriched, selected library was then applied to plasma samples from 11 individuals with high levels of brain amyloid and 11 individuals with low levels of brain Aβ accumulation. Each of these individually selected libraries was then characterized by next generation sequencing, and the relative frequency of 10,000 aptamer sequences that were observed in each selection was screened for ability to explain variation in brain amyloid using sparse partial least squares discriminant analysis. From this analysis a subset of 44 aptamers was defined, and the individual aptamers were synthesized. This subset was applied to plasma samples from 70 cognitively normal individuals all above the age of 70 that differed for brain amyloid deposition. 54 individuals were used as a training set, and 15 as a test set. Three of the 15 individuals in the test set were mis-classified resulting in an overall accuracy of 80% with 86% sensitivity and 75% specificity. The aptamers included in the subset serve directly as biomarkers, thus we have named them Aptamarkers. There are two potential applications of these results: extending the predictive capacity of these aptamers across a broader range of individuals, and/or using the individual aptamers to identify targets through covariance analysis and reverse omics approaches. We are currently expanding applications of the Aptamarker platform to other diseases and target matrices.

Published
2021

13. β-Secretase1 biological markers for Alzheimer’s disease: state-of-art of validation and qualification

Author

Hampel, Harald, Lista, Simone, Vanmechelen, Eugeen, Zetterberg, Henrik, Giorgi, Filippo Sean, Galgani, Alessandro, Blennow, Kaj, Caraci, Filippo, Das, Brati, Yan, Riqiang, and Vergallo, Andrea

Subjects
Biomedical and Clinical Sciences, Health Sciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Prevention, Alzheimer's Disease, Dementia, Brain Disorders, Aging, Clinical Research, Acquired Cognitive Impairment, Neurosciences, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Neurological, Good Health and Well Being, Alzheimer Disease, Amyloid Precursor Protein Secretases, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Biomarkers, Humans, Alzheimer’s Precision Medicine Initiative, Alzheimer’s disease, Amyloid-β pathway, Axonal damage, BACE1, Clinical trials, Context of use, Fluid biomarkers, Neurodegeneration, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

β-Secretase1 (BACE1) protein concentrations and rates of enzyme activity, analyzed in human bodily fluids, are promising candidate biological markers for guidance in clinical trials investigating BACE1 inhibitors to halt or delay the dysregulation of the amyloid-β pathway in Alzheimer's disease (AD). A robust body of evidence demonstrates an association between cerebrospinal fluid/blood BACE1 biomarkers and core pathophysiological mechanisms of AD, such as brain protein misfolding and aggregration, neurodegeneration, and synaptic dysfunction.In pharmacological trials, BACE1 candidate biomarkers may be applied to a wide set of contexts of use (CoU), including proof of mechanism, dose-finding, response and toxicity dose estimation. For clinical CoU, BACE1 biomarkers show good performance for prognosis and disease prediction.The roadmap toward validation and qualification of BACE1 biomarkers requires standardized pre-analytical and analytical protocols to reduce inter-site variance that may have contributed to inconsistent results.BACE1 biomarker-drug co-development programs, including biomarker-guided outcomes and endpoints, may support the identification of sub-populations with a higher probability to benefit from BACE1 inhibitors with a reduced risk of adverse effects, in line with the evolving precision medicine paradigm.

Published
2020

14. Integrative metabolomics science in Alzheimer’s disease: Relevance and future perspectives

Author

Lista, Simone, González-Domínguez, Raúl, López-Ortiz, Susana, González-Domínguez, Álvaro, Menéndez, Héctor, Martín-Hernández, Juan, Lucia, Alejandro, Emanuele, Enzo, Centonze, Diego, Imbimbo, Bruno P., Triaca, Viviana, Lionetto, Luana, Simmaco, Maurizio, Cuperlovic-Culf, Miroslava, Mill, Jericha, Li, Lingjun, Mapstone, Mark, Santos-Lozano, Alejandro, and Nisticò, Robert

Published
2023
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15. Age and sex impact plasma NFL and t-Tau trajectories in individuals with subjective memory complaints: a 3-year follow-up study.

Author

Baldacci, Filippo, Lista, Simone, Manca, Maria Laura, Chiesa, Patrizia A, Cavedo, Enrica, Lemercier, Pablo, Zetterberg, Henrik, Blennow, Kaj, Habert, Marie-Odile, Potier, Marie Claude, Dubois, Bruno, Vergallo, Andrea, Hampel, Harald, INSIGHT-preAD study group, and Alzheimer Precision Medicine Initiative (APMI)

Subjects
INSIGHT-preAD study group, Alzheimer Precision Medicine Initiative, Alzheimer’s disease, Biomarkers, Mild cognitive impairment, Neurofilament light chain, Subjective memory complainers, Tau, Medical and Health Sciences
Abstract

BackgroundPlasma neurofilament light (NFL) and total Tau (t-Tau) proteins are candidate biomarkers for early stages of Alzheimer's disease (AD). The impact of biological factors on their plasma concentrations in individuals with subjective memory complaints (SMC) has been poorly explored. We longitudinally investigate the effect of sex, age, APOE ε4 allele, comorbidities, brain amyloid-β (Aβ) burden, and cognitive scores on plasma NFL and t-Tau concentrations in cognitively healthy individuals with SMC, a condition associated with AD development.MethodsThree hundred sixteen and 79 individuals, respectively, have baseline and three-time point assessments (at baseline, 1-year, and 3-year follow-up) of the two biomarkers. Plasma biomarkers were measured with an ultrasensitive assay in a mono-center cohort (INSIGHT-preAD study).ResultsWe show an effect of age on plasma NFL, with women having a higher increase of plasma t-Tau concentrations compared to men, over time. The APOE ε4 allele does not affect the biomarker concentrations while plasma vitamin B12 deficiency is associated with higher plasma t-Tau concentrations. Both biomarkers are correlated and increase over time. Baseline NFL is related to the rate of Aβ deposition at 2-year follow-up in the left-posterior cingulate and the inferior parietal gyri. Baseline plasma NFL and the rate of change of plasma t-Tau are inversely associated with cognitive score.ConclusionWe find that plasma NFL and t-Tau longitudinal trajectories are affected by age and female sex, respectively, in SMC individuals. Exploring the influence of biological variables on AD biomarkers is crucial for their clinical validation in blood.

Published
2020

16. Blood-based systems biology biomarkers for next-generation clinical trials in Alzheimers disease
.

Author

Hampel, Harald, Vergallo, Andrea, Afshar, Mohammad, Akman-Anderson, Leyla, Arenas, Joaquín, Benda, Norbert, Batrla, Richard, Broich, Karl, Caraci, Filippo, Cuello, A, Emanuele, Enzo, Haberkamp, Marion, Kiddle, Steven, Lucía, Alejandro, Verdooner, Steven, Woodcock, Janet, Lista, Simone, and Mapstone, Mark

Subjects
Alzheimer’s disease, biomarker-drug codevelopment, blood-based biomarker, clinical trial, context of use, pathophysiology, precision medicine, predictive biomarker, systems biology, Alzheimer Disease, Biomarkers, Clinical Trials as Topic, Drug Development, Early Diagnosis, Eligibility Determination, Humans, Precision Medicine
Abstract

Alzheimers disease (AD)-a complex disease showing multiple pathomechanistic alterations-is triggered by nonlinear dynamic interactions of genetic/epigenetic and environmental risk factors, which, ultimately, converge into a biologically heterogeneous disease. To tackle the burden of AD during early preclinical stages, accessible blood-based biomarkers are currently being developed. Specifically, next-generation clinical trials are expected to integrate positive and negative predictive blood-based biomarkers into study designs to evaluate, at the individual level, target druggability and potential drug resistance mechanisms. In this scenario, systems biology holds promise to accelerate validation and qualification for clinical trial contexts of use-including proof-of-mechanism, patient selection, assessment of treatment efficacy and safety rates, and prognostic evaluation. Albeit in their infancy, systems biology-based approaches are poised to identify relevant AD signatures through multifactorial and interindividual variability, allowing us to decipher disease pathophysiology and etiology. Hopefully, innovative biomarker-drug codevelopment strategies will be the road ahead towards effective disease-modifying drugs.
.

Published
2019

17. Biomarker-Drug and Liquid Biopsy Co-development for Disease Staging and Targeted Therapy: Cornerstones for Alzheimer’s Precision Medicine and Pharmacology

Author

Hampel, Harald, Goetzl, Edward J, Kapogiannis, Dimitrios, Lista, Simone, and Vergallo, Andrea

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Dementia, Cancer, Acquired Cognitive Impairment, Neurodegenerative, Biotechnology, Neurosciences, Genetics, Brain Disorders, Clinical Research, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Alzheimer's disease, liquid biopsy, exosomes, systems pharmacology, precision medicine, Alzheimer’s disease, Pharmacology and Pharmaceutical Sciences, Pharmacology and pharmaceutical sciences
Abstract

Systems biology studies have demonstrated that different (epi)genetic and pathophysiological alterations may be mapped onto a single tumor's clinical phenotype thereby revealing commonalities shared by cancers with divergent phenotypes. The success of this approach in cancer based on analyses of traditional and emerging body fluid-based biomarkers has given rise to the concept of liquid biopsy enabling a non-invasive and widely accessible precision medicine approach and a significant paradigm shift in the management of cancer. Serial liquid biopsies offer clues about the evolution of cancer in individual patients across disease stages enabling the application of individualized genetically and biologically guided therapies. Moreover, liquid biopsy is contributing to the transformation of drug research and development strategies as well as supporting clinical practice allowing identification of subsets of patients who may enter pathway-based targeted therapies not dictated by clinical phenotypes alone. A similar liquid biopsy concept is emerging for Alzheimer's disease, in which blood-based biomarkers adaptable to each patient and stage of disease, may be used for positive and negative patient selection to facilitate establishment of high-value drug targets and counter-measures for drug resistance. Going beyond the "one marker, one drug" model, integrated applications of genomics, transcriptomics, proteomics, receptor expression and receptor cell biology and conformational status assessments during biomarker-drug co-development may lead to a new successful era for Alzheimer's disease therapeutics. We argue that the time is now for implementing a liquid biopsy-guided strategy for the development of drugs that precisely target Alzheimer's disease pathophysiology in individual patients.

Published
2019

19. Precision pharmacology for Alzheimer’s disease

Author

Hampel, Harald, Vergallo, Andrea, Aguilar, Lisi Flores, Benda, Norbert, Broich, Karl, Cuello, A Claudio, Cummings, Jeffrey, Dubois, Bruno, Federoff, Howard J, Fiandaca, Massimo, Genthon, Remy, Haberkamp, Marion, Karran, Eric, Mapstone, Mark, Perry, George, Schneider, Lon S, Welikovitch, Lindsay A, Woodcock, Janet, Baldacci, Filippo, Lista, Simone, and Initiative, for the Alzheimer Precision Medicine

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Neurosciences, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Alzheimer's Disease, Acquired Cognitive Impairment, Neurodegenerative, Brain Disorders, Aging, 2.1 Biological and endogenous factors, Aetiology, Neurological, Good Health and Well Being, Alzheimer Disease, Amyloid beta-Peptides, Animals, Biomarkers, Drug Discovery, Humans, Precision Medicine, tau Proteins, Alzheimer's disease, Precision pharmacology, Precision medicine, Pathway-based therapy, Pathophysiology, Clinical trials, Alzheimer Precision Medicine Initiative, Alzheimer’s disease, Pharmacology & Pharmacy, Pharmacology and pharmaceutical sciences
Abstract

The complex multifactorial nature of polygenic Alzheimer's disease (AD) presents significant challenges for drug development. AD pathophysiology is progressing in a non-linear dynamic fashion across multiple systems levels - from molecules to organ systems - and through adaptation, to compensation, and decompensation to systems failure. Adaptation and compensation maintain homeostasis: a dynamic equilibrium resulting from the dynamic non-linear interaction between genome, epigenome, and environment. An individual vulnerability to stressors exists on the basis of individual triggers, drivers, and thresholds accounting for the initiation and failure of adaptive and compensatory responses. Consequently, the distinct pattern of AD pathophysiology in space and time must be investigated on the basis of the individual biological makeup. This requires the implementation of systems biology and neurophysiology to facilitate Precision Medicine (PM) and Precision Pharmacology (PP). The regulation of several processes at multiple levels of complexity from gene expression to cellular cycle to tissue repair and system-wide network activation has different time delays (temporal scale) according to the affected systems (spatial scale). The initial failure might originate and occur at every level potentially affecting the whole dynamic interrelated systems within an organism. Unraveling the spatial and temporal dynamics of non-linear pathophysiological mechanisms across the continuum of hierarchical self-organized systems levels and from systems homeostasis to systems failure is key to understand AD. Measuring and, possibly, controlling space- and time-scaled adaptive and compensatory responses occurring during AD will represent a crucial step to achieve the capacity to substantially modify the disease course and progression at the best suitable timepoints, thus counteracting disrupting critical pathophysiological inputs. This approach will provide the conceptual basis for effective disease-modifying pathway-based targeted therapies. PP is based on an exploratory and integrative strategy to complex diseases such as brain proteinopathies including AD, aimed at identifying simultaneous aberrant molecular pathways and predicting their temporal impact on the systems levels. The depiction of pathway-based molecular signatures of complex diseases contributes to the accurate and mechanistic stratification of distinct subcohorts of individuals at the earliest compensatory stage when treatment intervention may reverse, stop, or delay the disease. In addition, individualized drug selection may optimize treatment safety by decreasing risk and amplitude of side effects and adverse reactions. From a methodological point of view, comprehensive "omics"-based biomarkers will guide the exploration of spatio-temporal systems-wide morpho-functional shifts along the continuum of AD pathophysiology, from adaptation to irreversible failure. The Alzheimer Precision Medicine Initiative (APMI) and the APMI cohort program (APMI-CP) have commenced to facilitate a paradigm shift towards effective drug discovery and development in AD.

Published
2018

20. Basal Forebrain Volume, but Not Hippocampal Volume, Is a Predictor of Global Cognitive Decline in Patients With Alzheimer's Disease Treated With Cholinesterase Inhibitors

Author

Teipel, Stefan J, Cavedo, Enrica, Hampel, Harald, Grothe, Michel J, Initiative, Alzheimer's Disease Neuroimaging, Initiative, Alzheimer Precision Medicine, Aguilar, Lisi Flores, Babiloni, Claudio, Baldacci, Filippo, Benda, Norbert, Black, Keith L, Bokde, Arun LW, Bonuccelli, Ubaldo, Broich, Karl, Bun, René S, Cacciola, Francesco, Castrillo, Juan, Ceravolo, Roberto, chiesa, Patrizia A, Colliot, Olivier, Coman, Cristina-Maria, Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L, Depypere, Herman, Dubois, Bruno, Duggento, Andrea, Durrleman, Stanley, Escott-price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A, Garaci, Francesco, Genthon, Remy, George, Nathalie, Giorgi, Filippo S, Graziani, Manuela, Haberkamp, Marion, Habert, Marie-Odile, Herholz, Karl, Karran, Eric, Seung, H KIM, Koronyo, Yosef, Koronyo-Hamaoui, Maya, Lamari, Foudil, Langevin, Todd, Lehéricy, Stéphane, Lista, Simone, Lorenceau, Jean, Mapstone, Mark, Neri, Christian, Nisticò, Robert, Nyasse-Messene, Francis, O'Bryant, Sid E, Perry, George, Ritchie, Craig, Rojkova, Katrine, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S, Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R, Vergallo, Andrea, Villain, Nicolas, Welikovitch, Lindsay A, Woodcock, Janet, and Younesi, Erfan

Subjects
Biological Psychology, Psychology, Neurosciences, Brain Disorders, Dementia, Neurodegenerative, Clinical Research, Acquired Cognitive Impairment, Behavioral and Social Science, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Neurological, Alzheimer's Disease Neuroimaging Initiative, Alzheimer Precision Medicine Initiative, MRI, basal forebrain, cholinergic treatment, executive function, hippocampus, memory, prediction, Clinical Sciences, Clinical sciences, Biological psychology
Abstract

Background: Predicting the progression of cognitive decline in Alzheimer's disease (AD) is important for treatment selection and patient counseling. Structural MRI markers such as hippocampus or basal forebrain volumes might represent useful instruments for the prediction of cognitive decline. The primary objective was to determine the predictive value of hippocampus and basal forebrain volumes for global and domain specific cognitive decline in AD dementia during cholinergic treatment. Methods: We used MRI and cognitive data from 124 patients with the clinical diagnosis of AD dementia, derived from the ADNI-1 cohort, who were on standard of care cholinesterase inhibitor treatment during a follow-up period between 0.4 and 3.1 years. We used linear mixed effects models with cognitive function as outcome to assess the main effects as well as two-way interactions between baseline volumes and time controlling for age, sex, and total intracranial volume. This model accounts for individual variation in follow-up times. Results: Basal forebrain volume, but not hippocampus volume, was a significant predictor of rates of global cognitive decline. Larger volumes were associated with smaller rates of cognitive decline. Left hippocampus volume had a modest association with rates of episodic memory decline. Baseline performance in global cognition and memory was significantly associated with hippocampus and basal forebrain volumes; in addition, basal forebrain volume was associated with baseline performance in executive function. Conclusions: Our findings indicate that in AD dementia patients, basal forebrain volume may be a useful marker to predict subsequent cognitive decline during cholinergic treatment.

Published
2018

24. Blood‐based biomarkers in Alzheimer disease: Current state of the science and a novel collaborative paradigm for advancing from discovery to clinic

Author

O'Bryant, Sid E, Mielke, Michelle M, Rissman, Robert A, Lista, Simone, Vanderstichele, Hugo, Zetterberg, Henrik, Lewczuk, Piotr, Posner, Holly, Hall, James, Johnson, Leigh, Fong, Yiu‐Lian, Luthman, Johan, Jeromin, Andreas, Batrla‐Utermann, Richard, Villarreal, Alcibiades, Britton, Gabrielle, Snyder, Peter J, Henriksen, Kim, Grammas, Paula, Gupta, Veer, Martins, Ralph, Hampel, Harald, and Area, Biofluid Based Biomarker Professional Interest

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Dementia, Aging, Neurodegenerative, Brain Disorders, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Clinical Research, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Neurological, Alzheimer Disease, Biomarkers, Cooperative Behavior, Female, Humans, Male, Public-Private Sector Partnerships, Reproducibility of Results, Alzheimer's disease, Biomarker, Blood, Diagnosis, Cerebrospinal fluid, Imaging, Context of use, Biofluid Based Biomarker Professional Interest Area, Geriatrics, Clinical sciences, Biological psychology
Abstract

The last decade has seen a substantial increase in research focused on the identification of blood-based biomarkers that have utility in Alzheimer's disease (AD). Blood-based biomarkers have significant advantages of being time- and cost-efficient as well as reduced invasiveness and increased patient acceptance. Despite these advantages and increased research efforts, the field has been hampered by lack of reproducibility and an unclear path for moving basic discovery toward clinical utilization. Here we reviewed the recent literature on blood-based biomarkers in AD to provide a current state of the art. In addition, a collaborative model is proposed that leverages academic and industry strengths to facilitate the field in moving past discovery only work and toward clinical use. Key resources are provided. This new public-private partnership model is intended to circumvent the traditional handoff model and provide a clear and useful paradigm for the advancement of biomarker science in AD and other neurodegenerative diseases.

Published
2017

25. Association of plasma YKL-40 with brain amyloid-β levels, memory performance, and sex in subjective memory complainers

Author

Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Lista, Simone, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, de Schotten, Michel Thiebaut, Vergallo, Andrea, Younsi, Nadjia, Afshar, Mohammad, Aguilar, Lisi Flores, Akman-Anderson, Leyla, Arenas, Joaquín, Ávila, Jesús, Babiloni, Claudio, Baldacci, Filippo, Batrla, Richard, Benda, Norbert, Black, Keith L., Bokde, Arun L.W., Bonuccelli, Ubaldo, Broich, Karl, Cacciola, Francesco, Caraci, Filippo, Caruso, Giuseppe, Castrillo†, Juan, Ceravolo, Roberto, Chiesa, Patrizia A., Corbo, Massimo, Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L., Depypere, Herman, Duggento, Andrea, Emanuele, Enzo, Escott-Price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, Geerts, Hugo, Giacobini, Ezio, Giorgi, Filippo S., Goetzl, Edward J., Graziani, Manuela, Haberkamp, Marion, Hänisch, Britta, Herholz, Karl, Hernandez, Felix, Imbimbo, Bruno P., Kapogiannis, Dimitrios, Karran, Eric, Kiddle, Steven J., Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehéricy, Stéphane, Lemercier, Pablo, Llavero, Francisco, Lorenceau, Jean, Lucía, Alejandro, Mango, Dalila, Mapstone, Mark, Neri, Christian, Nisticò, Robert, O’bryant, Sid E., Palermo, Giovanni, Perry, George, Ritchie, Craig, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Valenzuela, Pedro L., Vellas, Bruno, Verdooner, Steven R., Villain, Nicolas, Giudici, Kelly Virecoulon, Watling, Mark, Welikovitch, Lindsay A., Woodcock, Janet, Younesi, Erfan, Zugaza, José L., Zetterberg, Henrik, and Blennow, Kaj

Published
2020
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27. Resting-state posterior alpha rhythms are abnormal in subjective memory complaint seniors with preclinical Alzheimer's neuropathology and high education level: the INSIGHT-preAD study

Author

Babiloni, Claudio, Lopez, Susanna, Del Percio, Claudio, Noce, Giuseppe, Pascarelli, Maria Teresa, Lizio, Roberta, Teipel, Stefan J., González-Escamilla, Gabriel, Bakardjian, Hovagim, George, Nathalie, Cavedo, Enrica, Lista, Simone, Chiesa, Patrizia Andrea, Vergallo, Andrea, Lemercier, Pablo, Spinelli, Giuseppe, Grothe, Michel J., Potier, Marie-Claude, Stocchi, Fabrizio, Ferri, Raffaele, Habert, Marie-Odile, Fraga, Francisco J., Dubois, Bruno, and Hampel, Harald

Published
2020
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30. Preclinical Alzheimer's disease: Definition, natural history, and diagnostic criteria.

Author

Dubois, Bruno, Hampel, Harald, Feldman, Howard H, Scheltens, Philip, Aisen, Paul, Andrieu, Sandrine, Bakardjian, Hovagim, Benali, Habib, Bertram, Lars, Blennow, Kaj, Broich, Karl, Cavedo, Enrica, Crutch, Sebastian, Dartigues, Jean-François, Duyckaerts, Charles, Epelbaum, Stéphane, Frisoni, Giovanni B, Gauthier, Serge, Genthon, Remy, Gouw, Alida A, Habert, Marie-Odile, Holtzman, David M, Kivipelto, Miia, Lista, Simone, Molinuevo, José-Luis, O'Bryant, Sid E, Rabinovici, Gil D, Rowe, Christopher, Salloway, Stephen, Schneider, Lon S, Sperling, Reisa, Teichmann, Marc, Carrillo, Maria C, Cummings, Jeffrey, Jack, Cliff R, Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, July 23, 2015, and Washington DC, USA

Subjects
Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, July 23, 2015, Washington DC, USA, Brain, Animals, Humans, Alzheimer Disease, Disease Progression, Alzheimer's disease, Amyloid PET, Asymptomatic, Biomarkers, Blood biomarkers, CSF biomarkers, Diagnostic criteria, Genetics, MRI, Pathophysiology, Preclinical, Tau PET, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Neurodegenerative, Dementia, Alzheimer's Disease, Brain Disorders, Acquired Cognitive Impairment, Human Genome, Neurosciences, Neurological, Clinical Sciences, Geriatrics
Abstract

During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum. Thanks to evolving biomarker research and substantial discoveries, it is now possible to identify the disease even at the preclinical stage before the occurrence of the first clinical symptoms. This preclinical stage of AD has become a major research focus as the field postulates that early intervention may offer the best chance of therapeutic success. To date, very little evidence is established on this "silent" stage of the disease. A clarification is needed about the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage. This article is aimed at addressing all the different issues by providing for each of them an updated review of the literature and evidence, with practical recommendations.

Published
2016

31. Comparing biological markers of Alzheimer's disease across blood fraction and platforms: Comparing apples to oranges

Author

O'Bryant, Sid E, Lista, Simone, Rissman, Robert A, Edwards, Melissa, Zhang, Fan, Hall, James, Zetterberg, Henrik, Lovestone, Simon, Gupta, Veer, Graff‐Radford, Neill, Martins, Ralph, Jeromin, Andreas, Waring, Stephen, Oh, Esther, Kling, Mitchel, Baker, Laura D, Hampel, Harald, and Area, ISTAART Blood Based Biomarker Professional Interest

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Alzheimer's Disease, Aging, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, Acquired Cognitive Impairment, Clinical Research, Brain Disorders, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Alzheimer's disease, Biomarker discovery, Blood, Diagnostics, Meso Scale Discovery, Multiplex assay platform, Plasma, Preanalytic processing, Proteins, Rules Based Medicine, Serum, Standardization, Genetics, Biological psychology
Abstract

IntroductionThis study investigated the comparability of potential Alzheimer's disease (AD) biomarkers across blood fractions and assay platforms.MethodsNonfasting serum and plasma samples from 300 participants (150 AD patients and 150 controls) were analyzed. Proteomic markers were obtained via electrochemiluminescence or Luminex technology. Comparisons were conducted via Pearson correlations. The relative importance of proteins within an AD diagnostic profile was examined using random forest importance plots.ResultsOn the Meso Scale Discovery multiplex platform, 10 of the 21 markers shared >50% of the variance across blood fractions (serum amyloid A R(2) = 0.99, interleukin (IL)10 R(2) = 0.95, fatty acid-binding protein (FABP) R(2) = 0.94, I309 R(2) = 0.94, IL-5 R(2) = 0.94, IL-6 R(2) = 0.94, eotaxin3 R(2) = 0.91, IL-18 R(2) = 0.87, soluble tumor necrosis factor receptor 1 R(2) = 0.85, and pancreatic polypeptide R(2) = 0.81). When examining protein concentrations across platforms, only five markers shared >50% of the variance (beta 2 microglobulin R(2) = 0.92, IL-18 R(2) = 0.80, factor VII R(2) = 0.78, CRP R(2) = 0.74, and FABP R(2) = 0.70).DiscussionThe current findings highlight the importance of considering blood fractions and assay platforms when searching for AD relevant biomarkers.

Published
2016

32. Education and amyloid load affect posterior lobe function in subjective memory complainers: an EEG‐fMRI study

Author

Lopez, Susanna, primary, Hampel, Harald, additional, Chiesa, Patrizia Andrea, additional, Percio, Claudio Del, additional, Lizio, Roberta, additional, Noce, Giuseppe, additional, Teipel, Stefan, additional, González‐Escamilla, Gabriel, additional, Cavedo, Enrica, additional, Lista, Simone, additional, Vergallo, Andrea, additional, Lemercier, Pablo, additional, Spinelli, Giuseppe, additional, Grothe, Michel J., additional, and Babiloni, Claudio, additional

Published
2023
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34. Guidelines for the standardization of preanalytic variables for blood‐based biomarker studies in Alzheimer's disease research

Author

O'Bryant, Sid E, Gupta, Veer, Henriksen, Kim, Edwards, Melissa, Jeromin, Andreas, Lista, Simone, Bazenet, Chantal, Soares, Holly, Lovestone, Simon, Hampel, Harald, Montine, Thomas, Blennow, Kaj, Foroud, Tatiana, Carrillo, Maria, Graff-Radford, Neill, Laske, Christoph, Breteler, Monique, Shaw, Leslie, Trojanowski, John Q, Schupf, Nicole, Rissman, Robert A, Fagan, Anne M, Oberoi, Pankaj, Umek, Robert, Weiner, Michael W, Grammas, Paula, Posner, Holly, Martins, Ralph, and groups, STAR-B and BBBIG working

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Aging, Acquired Cognitive Impairment, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Neurodegenerative, Alzheimer's Disease, Clinical Research, Neurological, Alzheimer Disease, Biomarkers, Guidelines as Topic, Humans, Blood, Serum, Plasma, Alzheimer's disease, Diagnosis, Treatment, STAR-B and BBBIG working groups, Geriatrics, Clinical sciences, Biological psychology
Abstract

The lack of readily available biomarkers is a significant hindrance toward progressing to effective therapeutic and preventative strategies for Alzheimer's disease (AD). Blood-based biomarkers have potential to overcome access and cost barriers and greatly facilitate advanced neuroimaging and cerebrospinal fluid biomarker approaches. Despite the fact that preanalytical processing is the largest source of variability in laboratory testing, there are no currently available standardized preanalytical guidelines. The current international working group provides the initial starting point for such guidelines for standardized operating procedures (SOPs). It is anticipated that these guidelines will be updated as additional research findings become available. The statement provides (1) a synopsis of selected preanalytical methods utilized in many international AD cohort studies, (2) initial draft guidelines/SOPs for preanalytical methods, and (3) a list of required methodological information and protocols to be made available for publications in the field to foster cross-validation across cohorts and laboratories.

Published
2015

35. Biomarker-guided clustering of Alzheimer's disease clinical syndromes

Author

Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Lista, Simone, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, Thiebaut de Schotten, Michel, Vergallo, Andrea, Younsi, Nadjia, Toschi, Nicola, Baldacci, Filippo, Zetterberg, Henrik, Blennow, Kaj, Kilimann, Ingo, Teipel, Stefan J., Melo dos Santos, Antonio, Floris, Roberto, and Garaci, Francesco

Published
2019
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36. Brain Aβ load association and sexual dimorphism of plasma BACE1 concentrations in cognitively normal individuals at risk for AD

Author

Bakardjian, H., Benali, H., Bertin, H., Bonheur, J., Boukadida, L., Boukerrou, N., Cavedo, E., Chiesa, P., Colliot, O., Dubois, B., Dubois, M., Epelbaum, S., Gagliardi, G., Genthon, R., Habert, M.O., Hampel, H., Houot, M., Kas, A., Lamari, F., Levy, M., Lista, S., Metzinger, C., Mochel, F., Nyasse, F., Poisson, C., Potier, M.C., Revillon, M., Santos, A., Andrade, K.S., Sole, M., Surtee, M., Thiebaud de Schotten, M., Vergallo, A., Younsi, N., Afshar, Mohammad, Flores Aguilar, Lisi, Akman-Anderson, Leyla, Arenas, Joaquín, Avila, Jesus, Babiloni, Claudio, Baldacci, Filippo, Batrla, Richard, Benda, Norbert, Black, Keith L., Bokde, Arun L.W., Bonuccelli, Ubaldo, Broich, Karl, Cacciola, Francesco, Caraci, Filippo, Castrillo, Juan, Cavedo, Enrica, Ceravolo, Roberto, Chiesa, Patrizia A., Corvol, Jean-Christophe, Claudio Cuello, Augusto, Cummings, Jeffrey L., Depypere, Herman, Dubois, Bruno, Duggento, Andrea, Emanuele, Enzo, Escott-Price, Valentina, Federoff, Howard, Teresa Ferretti, Maria, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, Geerts, Hugo, Giorgi, Filippo S., Goetzl, Edward J., Graziani, Manuela, Haberkamp, Marion, Marie-Odile, Habert, Hampel, Harald, Herholz, Karl, Hernandez, Felix, Kapogiannis, Dimitrios, Karran, Eric, Kiddle, Steven J., Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehéricy, Stéphane, Lucía, Alejandro, Lista, Simone, Lorenceau, Jean, Mango, Dalila, Mapstone, Mark, Neri, Christian, Nisticò, Robert, O'Bryant, Sid E., Palermo, Giovanni, Perry, George, Ritchie, Craig, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R., Vergallo, Andrea, Villain, Nicolas, Welikovitch, Lindsay A., Woodcock, Janet, Younesi, Erfan, Houot, Marion, Lemercier, Pablo, Vanmechelen, Eugeen, De Vos, Ann, Habert, Marie-Odile, and Potier, Marie-Claude

Published
2019
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37. Differential default mode network trajectories in asymptomatic individuals at risk for Alzheimer's disease

Author

Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Lista, Simone, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, de Schotten, Michel Thiebaud, Vergallo, Andrea, Younsi, Nadjia, Afshar, Mohammad, Aguilar, Lisi Flores, Akman-Anderson, Leyla, Arenas, Joaquín, Avila, Jesus, Babiloni, Claudio, Baldacci, Filippo, Batrla, Richard, Benda, Norbert, Black, Keith L., Bokde, Arun L.W., Bonuccelli, Ubaldo, Broich, Karl, Cacciola, Francesco, Caraci, Filippo, Castrillo, Juan, Ceravolo, Roberto, Chiesa, Patrizia A., Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L., Depypere, Herman, Duggento, Andrea, Emanuele, Enzo, Escott-Price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, Geerts, Hugo, Giorgi, Filippo S., Goetzl, Edward J., Graziani, Manuela, Haberkamp, Marion, Herholz, Karl, Hernandez, Felix, Kapogiannis, Dimitrios, Karran, Eric, Kiddle, Steven J., Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehéricy, Stéphane, Lucía, Alejandro, Lorenceau, Jean, Mango, Dalila, Mapstone, Mark, Neri, Christian, Nisticó, Robert, O’Bryant, Sid E., Palermo, Giovanni, Perry, George, Ritchie, Craig, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R., Villain, Nicolas, Welikovitch, Lindsay A., Woodcock, Janet, Younesi, Erfan, and Thiebaut de Schotten, Michel

Published
2019
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38. Plasma amyloid β 40/42 ratio predicts cerebral amyloidosis in cognitively normal individuals at risk for Alzheimer's disease

Author

Bakardjian, H., Benali, H., Bertin, H., Bonheur, J., Boukadida, L., Boukerrou, N., Cavedo, E., Chiesa, P., Colliot, O., Dubois, B., Dubois, M., Epelbaum, S., Gagliardi, G., Genthon, R., Habert, M.O., Hampel, H., Houot, M., Kas, A., Lamari, F., Levy, M., Lista, S., Metzinger, C., Mochel, F., Nyasse, F., Poisson, C., Potier, M.C., Revillon, M., Santos, A., Andrade, K.S., Sole, M., Surtee, M., de Schotten M, Thiebaud, Vergallo, A., Younsi, N., Aguilar, Lisi Flores, Babiloni, Claudio, Baldacci, Filippo, Benda, Norbert, Black, Keith L., Bokde, Arun L.W., Bonuccelli, Ubaldo, Broich, Karl, Cacciola, Francesco, Castrillo, Juan, Cavedo, Enrica, Ceravolo, Roberto, Chiesa, Patrizia A., Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L., Depypere, Herman, Dubois, Bruno, Duggento, Andrea, Escott-Price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, Geerts, Hugo, Giorgi, Filippo S., Graziani, Manuela, Haberkamp, Marion, Habert, Marie-Odile, Hampel, Harald, Herholz, Karl, Karran, Eric, Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Lamari, Foudil, Langevin, Todd, Lehéricy, Stéphane, Lista, Simone, Lorenceau, Jean, Mango, Dalila, Mapstone, Mark, Neri, Christian, Nisticò, Robert, O'Bryant, Sid E., Perry, George, Ritchie, Craig, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R., Vergallo, Andrea, Villain, Nicolas, Welikovitch, Lindsay A., Woodcock, Janet, Younesi, Erfan, Mégret, Lucile, Zetterberg, Henrik, Blennow, Kaj, Vanmechelen, Eugeen, De Vos, Ann, and Potier, Marie-Claude

Published
2019
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39. Subjective cognitive decline and rates of incident Alzheimer's disease and non–Alzheimer's disease dementia

Author

Boada, Mercè, de Deyn, Peter Paul, Jones, Roy, Frisoni, Giovanni, Spiru, Luiza, Nobili, Flavio, Freund-Levi, Yvonne, Soininen, Hilkka, Verhey, Frans, Wallin, Åsa K., Touchon, Jacques, Rikkert, Marcel Olde, Rigaud, Anne-Sophie, Bullock, Roger, Tsolaki, Magda, Vellas, Bruno, Wilcock, Gordon, Hampel, Harald, Froelich, Lutz, Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Lista, Simone, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, Thiebaud de Schotten, Michel, Vergallo, Andrea, Younsi, Nadjia, Slot, Rosalinde E.R., Sikkes, Sietske A.M., Berkhof, Johannes, Brodaty, Henry, Buckley, Rachel, Dardiotis, Efthimios, Guillo-Benarous, Francoise, Kochan, Nicole A., Luck, Tobias, Maruff, Paul, Molinuevo, José Luis, Kornhuber, Johannes, Reisberg, Barry, Riedel-Heller, Steffi G., Risacher, Shannon L., Roehr, Susanne, Sachdev, Perminder S., Scarmeas, Nikolaos, Scheltens, Philip, Shulman, Melanie B., Saykin, Andrew J., Verfaillie, Sander C.J., Visser, Pieter Jelle, Vos, Stephanie J.B., Wagner, Michael, Wolfsgruber, Steffen, Jessen, Frank, and van der Flier, Wiesje M.

Published
2019
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40. Latent class analysis identifies functional decline with Amsterdam IADL in preclinical Alzheimer's disease

Author

Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, LaurieBoukadida, Joel Bonheur, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Lista, Simone, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, Thiebaud de Schotten, Michel, Vergallo, Andrea, Younsi, Nadjia, Villeneuve, Sarah-Christine, Cacciamani, Federica, Verrijp, Merike, and Sikkes, Sietske

Published
2019
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41. Association of cerebrospinal fluid α-synuclein with total and phospho-tau181 protein concentrations and brain amyloid load in cognitively normal subjective memory complainers stratified by Alzheimer's disease biomarkers

Author

Audrain, C., Auffret, A., Bakardjian, H., Baldacci, F., Batrancourt, B., Benakki, I., Benali, H., Bertin, H., Bertrand, A., Boukadida, L., Cacciamani, F., Causse, V., Cavedo, E., Cherif Touil, S., Chiesa, P.A., Colliot, O., Dalla Barba, G., Depaulis, M., Dos Santos, A., Dubois, B., Dubois, M., Epelbaum, S., Fontaine, B., Francisque, H., Gagliardi, G., Genin, A., Genthon, R., Glasman, P., Gombert, F., Habert, M.O., Hampel, H., Hewa, H., Houot, M., Jungalee, N., Kas, A., Kilani, M., La Corte, V., Le Roy, F., Lehericy, S., Letondor, C., Levy, M., Lista, S., Lowrey, M., Ly, J., Makiese, O., Masetti, I., Mendes, A., Metzinger, C., Michon, A., Mochel, F., Nait Arab, R., Nyasse, F., Perrin, C., Poirier, F., Poisson, C., Potier, M.C., Ratovohery, S., Revillon, M., Rojkova, K., Santos-Andrade, K., Schindler, R., Servera, M.C., Seux, L., Simon, V., Skovronsky, D., Thiebaut, M., Uspenskaya, O., Vlaincu, M., Aguilar, L.F., Babiloni, C., Benda, N., Black, K.L., Bokde, A.L.W., Bonuccelli, U., Broich, K., Bun, R.S., Cacciola, F., Castrillo, J., Ceravolo, R., Coman, C.M., Corvol, J.C., Cuello, A.C., Cummings, J.L., Depypere, H., Duggento, A., Durrleman, S., Escott-Price, V., Federoff, H., Ferretti, M.T., Fiandaca, M., Frank, R.A., Garaci, F., George, N., Giorgi, F.S., Graziani, M., Haberkamp, M., Herholz, K., Karran, E., Kim, S.H., Koronyo, Y., Koronyo-Hamaoui, M., Lamari, F., Langevin, T., Lehéricy, S., Lorenceau, J., Mapstone, M., Neri, C., Nisticò, R., Nyasse-Messene, F., O'Bryant, S.E., Perry, G., Ritchie, C., Rossi, S., Santarnecchi, E., Schneider, L.S., Sporns, O., Toschi, N., Verdooner, S.R., Vergallo, A., Villain, N., Welikovitch, L., Woodcock, J., Younesi, E., Vergallo, Andrea, Bun, René-Sosata, Toschi, Nicola, Baldacci, Filippo, Zetterberg, Henrik, Blennow, Kaj, Cavedo, Enrica, Lamari, Foudil, Habert, Marie-Odile, Dubois, Bruno, Floris, Roberto, Garaci, Francesco, Lista, Simone, and Hampel, Harald

Published
2018
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44. Effect of Alzheimer's disease risk and protective factors on cognitive trajectories in subjective memory complainers: An INSIGHT-preAD study

Author

Audrain, C., Auffret, A., Bakardjian, H., Baldacci, F., Batrancourt, B., Benakki, I., Benali, H., Bertin, H., Bertrand, A., Boukadida, L., Cacciamani, F., Causse, V., Cavedo, E., Cherif Touil, S., Chiesa, P.A., Colliot, O., Dalla Barba, G., Depaulis, M., Dos Santos, A., Dubois, B., Dubois, M., Epelbaum, S., Fontaine, B., Francisque, H., Gagliardi, G., Genin, A., Genthon, R., Glasman, P., Gombert, F., Habert, M.O., Hampel, H., Hewa, H., Houot, M., Jungalee, N., Kas, A., Kilani, M., La Corte, V., Le Roy, F., Lehericy, S., Letondor, C., Levy, M., Lista, S., Lowrey, M., Ly, J., Makiese, O., Masetti, I., Mendes, A., Metzinger, C., Michon, A., Mochel, F., Nait Arab, R., Nyasse, F., Perrin, C., Poirier, F., Poisson, C., Potier, M.C., Ratovohery, S., Revillon, M., Rojkova, K., Santos-Andrade, K., Schindler, R., Servera, M.C., Seux, L., Simon, V., Skovronsky, D., Thiebaut, M., Uspenskaya, O., Vlaincu, M., Teipel, Stefan J., Cavedo, Enrica, Lista, Simone, Habert, Marie-Odile, Potier, Marie-Claude, Grothe, Michel J., Epelbaum, Stephane, Sambati, Luisa, Gagliardi, Geoffroy, Toschi, Nicola, Greicius, Michael D., Dubois, Bruno, and Hampel, Harald

Published
2018
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45. Sex differences in functional and molecular neuroimaging biomarkers of Alzheimer's disease in cognitively normal older adults with subjective memory complaints

Author

Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Lista, Simone, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, de Schotten, Michel Thiebaud, Vergallo, Andrea, Younsi, Nadjia, Aguilar, Lisi Flores, Babiloni, Claudio, Baldacci, Filippo, Benda, Norbert, Black, Keith L., Bokde, Arun L.W., Bonuccelli, Ubaldo, Broich, Karl, Bun, René S., Cacciola, Francesco, Castrillo, Juan, Ceravolo, Roberto, Chiesa, Patrizia A., Coman, Cristina-Maria, Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L., Depypere, Herman, Duggento, Andrea, Durrleman, Stanley, Escott-Price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, George, Nathalie, Giorgi, Filippo S., Graziani, Manuela, Haberkamp, Marion, Herholz, Karl, Karran, Eric, Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehéricy, Stéphane, Lorenceau, Jean, Mapstone, Mark, Neri, Christian, Nisticò, Robert, Nyasse-Messene, Francis, O'bryant, Sid E., Perry, George, Ritchie, Craig, Rojkova, Katrine, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R., Villain, Nicolas, Welikovitch, Lindsay A., Woodcock, Janet, Younesi, Erfan, Grothe, Michel J., and Teipel, Stefan J.

Published
2018
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46. Alzheimer's disease biomarker-guided diagnostic workflow using the added value of six combined cerebrospinal fluid candidates: Aβ1–42, total-tau, phosphorylated-tau, NFL, neurogranin, and YKL-40

Author

Hampel, Harald, Toschi, Nicola, Baldacci, Filippo, Zetterberg, Henrik, Blennow, Kaj, Kilimann, Ingo, Teipel, Stefan J., Cavedo, Enrica, Melo dos Santos, Antonio, Epelbaum, Stéphane, Lamari, Foudil, Genthon, Remy, Dubois, Bruno, Floris, Roberto, Garaci, Francesco, and Lista, Simone

Published
2018
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47. Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study

Author

Audrain, Christelle, Auffret, Alexandra, Baldacci, Filippo, Benakki, Ismahane, Bertin, Hugo, Boukadida, Laurie, Cavedo, Enrica, Chiesa, Patrizia, Dauphinot, Luce, Dos Santos, Antonio, Dubois, Marion, Durrleman, Stanley, Fontaine, Gaëlle, Genin, Alexis, Glasman, Pauline, Jungalee, Navichka, Kas, Aurélie, Kilani, Maya, La Corte, Valentina, Lehericy, Stephane, Letondor, Claire, Levy, Marcel, Lowrey, Mark, Ly, Juliette, Makiese, Ornella, Metzinger, Christiane, Michon, Agnès, Mochel, Fanny, Poisson, Catherine, Ratovohery, Stephie, Revillon, Marie, Rojkova, Katrine, Roy, Perrine, Santos-Andrade, Katia, Schindler, Rachel, Seux, Laure, Simon, Valérie, Sole, Marine, Tandetnik, Caroline, Teichmann, Marc, Thiebaut de Shotten, Michel, Younsi, Nadjia, Dubois, Bruno, Epelbaum, Stephane, Nyasse, Francis, Bakardjian, Hovagim, Gagliardi, Geoffroy, Uspenskaya, Olga, Houot, Marion, Lista, Simone, Cacciamani, Federica, Potier, Marie-Claude, Bertrand, Anne, Lamari, Foudil, Benali, Habib, Mangin, Jean-François, Colliot, Olivier, Genthon, Remy, Habert, Marie-Odile, and Hampel, Harald

Published
2018
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49. N°7 – Education and amyloid load affect posterior lobe function in subjective memory complainers: An EEG-fMRI study

Author

Lopez, Susanna, primary, Hampel, Harald, additional, Chiesa, Patrizia Andrea, additional, del Percio, Claudio, additional, Lizio, Roberta, additional, Noce, Giuseppe, additional, Teipel, Stefan, additional, Cavedo, Enrica, additional, Lista, Simone, additional, Vergallo, Andrea, additional, Lemercier, Pablo, additional, and Babiloni, Claudio, additional

Published
2023
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