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5. Relationship between astrocyte reactivity, using novel 11C-BU99008 PET, and glucose metabolism, grey matter volume and amyloid load in cognitively impaired individuals

Author

Livingston, Nicholas R., Calsolaro, Valeria, Hinz, Rainer, Nowell, Joseph, Raza, Sanara, Gentleman, Steve, Tyacke, Robin J., Myers, Jim, Venkataraman, Ashwin V., Perneczky, Robert, Gunn, Roger N., Rabiner, Eugenii A., Parker, Christine A., Murphy, Philip S., Wren, Paul B., Nutt, David J., Matthews, Paul M., and Edison, Paul

Published
2022
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6. Incretin Mimetics as Potential Disease Modifying Treatment for Alzheimer's Disease.

Author

Crook, Harry and Edison, Paul

Subjects
*DISEASE risk factors, *TYPE 2 diabetes, *ALZHEIMER'S disease, *GASTRIC inhibitory polypeptide, *PATHOLOGY
Abstract

Alzheimer's disease is a devastating neurodegenerative condition that exerts a significant global burden. Despite recent efforts, disease modifying therapies remain extremely limited, with a tremendous proportion of patients having to rely on symptomatic treatment only. Epidemiological and pathological overlaps exist between Alzheimer's disease and diabetes mellitus type 2, with people with diabetes mellitus type 2 at a significantly increased risk of developing Alzheimer's disease in the future. Incretin mimetics, also known as GLP-1/GIP receptor agonists, are useful tools licensed for the treatment of diabetes mellitus type 2 which have recently been the subject of news coverage for their off-label use as weight loss medications. Emerging evidence highlights the possible neuroprotective function of incretin mimetics in models of Alzheimer's disease as well as in clinical studies. This review details the pre-clinical and clinical studies that have explored the effectiveness of incretin mimetics to alleviate Alzheimer's disease associated pathology and cognitive impairment, while also highlighting the progress made to examine the effectiveness of these molecules in Parkinson's disease. Should clinical trials prove effective, incretin mimetics may be able to be repurposed and become useful novel tools as disease-modifying treatments for Alzheimer's disease and other neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Do Tau Deposition and Glucose Metabolism Dissociate in Alzheimer's Disease Trajectory?

Author

Nowell, Joseph, Raza, Sanara, Livingston, Nicholas R., Sivanathan, Shayndhan, Gentleman, Steve, and Edison, Paul

Subjects
ALZHEIMER'S disease, TAU proteins, GLUCOSE metabolism, MILD cognitive impairment, FLUORODEOXYGLUCOSE F18
Abstract

Background: Tau aggregation demonstrates close associations with hypometabolism in Alzheimer's disease (AD), although differing pathophysiological processes may underlie their development. Objective: To establish whether tau deposition and glucose metabolism have different trajectories in AD progression and evaluate the utility of global measures of these pathological hallmarks in predicting cognitive deficits. Methods: 279 participants with amyloid-β (Aβ) status, and T1-weighted MRI scans, were selected from the Alzheimer's Disease Neuroimaging Initiative (). We created the standard uptake value ratio images using Statistical Parametric Mapping 12 for [18F]AV1451-PET (tau) and [18F]FDG-PET (glucose metabolism) scans. Voxel-wise group and single-subject level SPM analysis evaluated the relationship between global [18F]FDG-PET and [18F]AV1451-PET depending on the Aβ status. Linear models assessed whether tau deposition or glucose metabolism better predicted clinical progression. Results: There was a dissociation between global cerebral glucose hypometabolism and global tau load in amyloid-positive AD and amyloid-negative mild cognitive impairment (MCI) (p > 0.05). Global hypometabolism was only associated with global cortical tau in amyloid-positive MCI. Voxel-level single subject tau load better predicted neuropsychological performance, Alzheimer's disease assessment scale-cognitive (ADAS-Cog) 13 score, and one-year change compared with regional and global hypometabolism. Conclusions: A dissociation between tau pathology and glucose metabolism at a global level in AD could imply that other pathological processes influence glucose metabolism. Furthermore, as tau is a better predictor of clinical progression, these processes may have independent trajectories and require independent consideration in the context of therapeutic interventions. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Astrocyte reactivity with late-onset cognitive impairment assessed in vivo using 11C-BU99008 PET and its relationship with amyloid load

Author

Calsolaro, Valeria, Matthews, Paul M., Donat, Cornelius K., Livingston, Nicholas R., Femminella, Grazia D., Guedes, Sandra Silva, Myers, Jim, Fan, Zhen, Tyacke, Robin J., Venkataraman, Ashwin V., Perneczky, Robert, Gunn, Roger, Rabiner, Eugenii A., Gentleman, Steve, Parker, Christine A., Murphy, Philip S., Wren, Paul B., Hinz, Rainer, Sastre, Magdalena, Nutt, David J., and Edison, Paul

Published
2021
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10. Microglial activation and tau propagate jointly across Braak stages

Author

Pascoal, Tharick A., Benedet, Andrea L., Ashton, Nicholas J., Kang, Min Su, Therriault, Joseph, Chamoun, Mira, Savard, Melissa, Lussier, Firoza Z., Tissot, Cécile, Karikari, Thomas K., Ottoy, Julie, Mathotaarachchi, Sulantha, Stevenson, Jenna, Massarweh, Gassan, Schöll, Michael, de Leon, Mony J., Soucy, Jean-Paul, Edison, Paul, Blennow, Kaj, Zetterberg, Henrik, Gauthier, Serge, and Rosa-Neto, Pedro

Published
2021
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11. Combined Neuroinflammation and Amyloid PET Markers in Predicting Disease Progression in Cognitively Impaired Subjects.

Author

Leng, Fangda, Hinz, Rainer, Gentleman, Steve, Dani, Melanie, Brooks, David J., and Edison, Paul

Subjects
POSITRON emission tomography, MILD cognitive impairment, ALZHEIMER'S disease, PROGNOSIS, DISEASE progression
Abstract

Background: Neuroinflammation in Alzheimer's disease is known as an important process in the disease, yet how microglial activation affects disease progression remains unclear. Objective: The current study aims to interrogate the predictive value of neuroinflammation biomarker (11C-PBR28 PET), together with A/T/N imaging markers on disease deterioration in a cognitively impaired patient cohort. Methods: The study included 6 AD and 27 MCI patients, who had MRI, 11C-PBR28, 18F-flutemetamol (amyloid marker), 18F-AV1451 (tau marker) PET scans, and were followed up with multiple neuropsychological assessments for at least one year (1.6 and 2.8 years on average for AD and MCI). The predictive values of imaging biomarkers on baseline and longitudinal cognition were interrogated using linear regression to identify the biomarkers that could explain disease progression. Results: Linear mixed models found the average intercepts (baseline) MMSE were 23.5 for AD and 28.2 for MCI patients, and the slope of MMSE (annual change) were –0.74 for AD and –0.52 for MCI patients. White matter microstructural integrity was predictive of baseline cognition, while PET markers of amyloid, tau and neuroinflammation were predictive of longitudinal cognitive decline. Both amyloid and neuroinflammation PET markers were predictors independent of each other. And a sub-group analysis showed the predictive effect of neuroinflammation on cognitive decline is independent of amyloid and tau. Conclusions: Our study highlights the prognostic value of disease specific markers (amyloid, tau and neuroinflammation) in clinically diagnosed AD and MCI patients and suggests that the effects of these molecular markers are mediated by structural damage to the brain. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Does insulin resistance influence neurodegeneration in non-diabetic Alzheimer’s subjects?

Author

Femminella, Grazia Daniela, Livingston, Nicholas R., Raza, Sanara, van der Doef, Thalia, Frangou, Eleni, Love, Sharon, Busza, Gail, Calsolaro, Valeria, Carver, Stefan, Holmes, Clive, Ritchie, Craig W., Lawrence, Robert M., McFarlane, Brady, Tadros, George, Ridha, Basil H., Bannister, Carol, Walker, Zuzana, Archer, Hilary, Coulthard, Elizabeth, Underwood, Ben, Prasanna, Aparna, Koranteng, Paul, Karim, Salman, Junaid, Kehinde, McGuinness, Bernadette, Passmore, Anthony Peter, Nilforooshan, Ramin, Macharouthu, Ajayverma, Donaldson, Andrew, Thacker, Simon, Russell, Gregor, Malik, Naghma, Mate, Vandana, Knight, Lucy, Kshemendran, Sajeev, Tan, Tricia, Holscher, Christian, Harrison, John, Brooks, David J., Ballard, Clive, and Edison, Paul

Published
2021
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14. A new perspective for advanced positron emission tomography–based molecular imaging in neurodegenerative proteinopathies

Author

Bottlaender, Michel, Brooks, David, Carroll, Michael A., Chalon, Sylvie, Gee, Anthony, Gerhard, Alexander, Halldin, Christer, Herholz, Karl, Herth, Matthias M., Hinz, Rainer, Knudsen, Gitte M., Kuhnast, Bertrand, López-Picón, Francisco, Moresco, Rosa Maria, Pappata, Sabina, Rinne, Juha O., Rodriguez-Vieitez, Elena, Santiago-Ribeiro, Marie Joao, Turkheimer, Federico E., Van Laere, Koen, Varrone, Andrea, Vercouillie, Johnny, Winkeler, Alexandra, Perani, Daniela, Iaccarino, Leonardo, Lammertsma, Adriaan A., Windhorst, Albert D., Edison, Paul, Boellaard, Ronald, Hansson, Oskar, Nordberg, Agneta, and Jacobs, Andreas H.

Published
2019
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16. Impact of serum leptin and adiponectin levels on brain infarcts in patients with mild cognitive impairment and Alzheimer’s disease: a longitudinal analysis.

Author

Carbone, Giovanni, Bencivenga, Leonardo, Santoro, Maria Angela, De Lucia, Natascia, Palaia, Maria Emiliana, Ercolano, Erica, Scognamiglio, Francesco, Edison, Paul, Ferrara, Nicola, Vitale, Dino Franco, Rengo, Giuseppe, and Femminella, Grazia Daniela

Subjects
LEPTIN, ALZHEIMER'S disease, MILD cognitive impairment, ADIPONECTIN, CEREBRAL infarction, ADIPOKINES, NEUROPSYCHOLOGY, MYOCARDIAL reperfusion
Abstract

Introduction: The adipokines leptin and adiponectin have been associated with atherosclerosis and the risk of cerebral infarcts. Pre-clinical studies, however, suggest a protective role against ischemic brain damage. In this study we analyzed the relationship between serum leptin and adiponectin levels and the onset or progression of brain infarcts in subjects with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). Methods: All data were extracted from the ADNI database. The final population included 566 subjects, with 58 healthy controls, 396 MCI and 112 AD. All patients with available serum leptin and adiponectin levels at baseline were selected. Demographics, neuropsychological test results, CSF biomarkers, regional brain metabolism with FDG-PET data and the number of brain infarcts on longitudinal MRI scans were extracted. Results: Leptin levels were significantly lower in patients with MCI than controls at baseline, while adiponectin levels were not different between the groups. Multivariate logistic regression analysis at baseline for the presence of brain infarcts showed a predictive value for leptin but not for adiponectin. Multivariate longitudinal analysis showed that age was the only significant predictor of brain infarcts development at 15-year follow-up, while serum leptin and adiponectin levels did not play a role in this population. Discussion: The evidence on the pathogenetic or protective role of adipokines on ischemic brain damage is mixed. In this MCI and AD population, serum leptin and adiponectin were not associated with the development of brain infarcts; therefore, these results do not support the use of adipokines as biomarkers of cerebrovascular pathology in this population. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Astroglial activation: Current concepts and future directions.

Author

Edison, Paul

Abstract

Astrocytes are abundantly and ubiquitously expressed cell types with diverse functions throughout the central nervous system. Astrocytes show remarkable plasticity and exhibit morphological, molecular, and functional remodeling in response to injury, disease, or infection of the central nervous system, as evident in neurodegenerative diseases. Astroglial mediated inflammation plays a prominent role in the pathogenesis of neurodegenerative diseases. This review focus on the role of astrocytes as essential players in neuroinflammation and discuss their morphological and functional heterogeneity in the normal central nervous system and explore the spatial and temporal variations in astroglial phenotypes observed under different disease conditions. This review discusses the intimate relationship of astrocytes to pathological hallmarks of neurodegenerative diseases. Finally, this review considers the putative therapeutic strategies that can be deployed to modulate the astroglial functions in neurodegenerative diseases. Highlights: Astroglia mediated neuroinflammation plays a key role in the pathogenesis of neurodegenerative diseases.Activated astrocytes exhibit diverse phenotypes in a region‐specific manner in brain and interact with β‐amyloid, tau, and α‐synuclein species as well as with microglia and neuronal circuits.Activated astrocytes are likely to influence the trajectory of disease progression of neurodegenerative diseases, as determined by the stage of disease, individual susceptibility, and state of astroglial priming.Modulation of astroglial activation may be a therapeutic strategy at various stages in the trajectory of neurodegenerative diseases to modify the disease course. [ABSTRACT FROM AUTHOR]

Published
2024
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19. Publisher Correction: Microglial activation and tau propagate jointly across Braak stages

Author

Pascoal, Tharick A., Benedet, Andrea L., Ashton, Nicholas J., Kang, Min Su, Therriault, Joseph, Chamoun, Mira, Savard, Melissa, Lussier, Firoza Z., Tissot, Cécile, Karikari, Thomas K., Ottoy, Julie, Mathotaarachchi, Sulantha, Stevenson, Jenna, Massarweh, Gassan, Schöll, Michael, de Leon, Mony J., Soucy, Jean-Paul, Edison, Paul, Blennow, Kaj, Zetterberg, Henrik, Gauthier, Serge, and Rosa-Neto, Pedro

Published
2021
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21. Correction to: Evaluating the effects of the novel GLP-1 analogue liraglutide in Alzheimer’s disease: study protocol for a randomised controlled trial (ELAD study)

Author

Femminella, Grazia Daniela, Frangou, Eleni, Love, Sharon B., Busza, Gail, Holmes, Clive, Ritchie, Craig, Lawrence, Robert, McFarlane, Brady, Tadros, George, Ridha, Basil H., Bannister, Carol, Walker, Zuzana, Archer, Hilary, Coulthard, Elizabeth, Underwood, Ben R., Prasanna, Aparna, Koranteng, Paul, Karim, Salman, Junaid, Kehinde, McGuinness, Bernadette, Nilforooshan, Ramin, Macharouthu, Ajay, Donaldson, Andrew, Thacker, Simon, Russell, Gregor, Malik, Naghma, Mate, Vandana, Knight, Lucy, Kshemendran, Sajeev, Harrison, John, Hölscher, Christian, Brooks, David J., Passmore, Anthony Peter, Ballard, Clive, and Edison, Paul

Published
2020
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22. Analysis of Psychological Symptoms Following Disclosure of Amyloid-Positron Emission Tomography Imaging Results to Adults With Subjective Cognitive Decline

Author

Caprioglio, Camilla, Ribaldi, Federica, Visser, Leonie N. C., Minguillon, Carolina, Collij, Lyduine E., Grau-Rivera, Oriol, Zeyen, Philip, Molinuevo, José Luis, Gispert, Juan Domingo, Garibotto, Valentina, Moro, Christian, Walker, Zuzana, Edison, Paul, Demonet, Jean-François, Barkhof, Frederik, Scheltens, Philip, Alves, Isadora Lopes, Gismondi, Rossella, Farrar, Gill, Stephens, Andrew W., Jessen, Frank, Frisoni, Giovanni B., Altomare, Daniele, Abdelnour, Carla, Aguilera, Nuria, Aksman, Leon, Alarcón-Martín, Emilio, Alegret, Montse, Alonso-Lana, Silvia, Andersen, Pia, Arab, Majd, Aspö, Malin, Bader, Ilona, Bader, Ilse, Banton, Nigel, Barnes, Rodrigo, Barrie, Dawn, Battle, Mark, Belén Collado, Ana, Bellet, Julie, Berkhof, Johannes, Biger, Marine, Birck, Cindy, Bischof, Gerard, Boada, Mercè, Boellaard, Ronald, Bogdanovic, Nenad, Bollack, Ariane, Bombois, Stéphanie, Borg, Stefan, Borjesson-Hanson, Anne, Boskov, Vladimir, Boutantin, Justine, Boutoleau-Bretonniere, Claire, Bouwman, Femke, Breuilh, Laetitia, Bringman, Eva, Brunel, Baptiste, Bucci, Marco, Buckley, Chris, Buendía, Mar, Bullich, Santi, Calvet, Anna, Cañada, Laia, Cañada, Marta, Cardoso, Jorge, Carlier, Jasmine, Carre, Elise, Carrie, Isabelle, Cassagnaud, Pascaline, Cassol, Emmanuelle, Castilla-Martí, Miguel, Cazalon, Elodie, Chaarriau, Tiphaine, Chaigeau, Rachel, Chalmers, Taylor, Clerc, Marie-Thérèse, Clerigue, Montserrat, Cognat, Emmanuel, Coll, Nina, Collij, Lyduine E, Connely, Peter, Cordier, Elodie, Costes, Corine, Coulange, Camille, Courtemanche, Hélène, Creisson, Eric, Crinquette, Charlotte, Cuevas, Rosario, Cufi, Marie-Noëlle, Dardenne, Sophie, de Arriba, Maria, de Costa Luis, Casper, de Gier, Yvonne, de Verbizier Lonjon, Delphine, Dekker, Veronique, Dekyndt, Bérengère, Delbeuck, Xavier, Delrieu, Julien, Deramecourt, Vincent, Desclaux, Françoise, Diaz, Carlos, Diego, Susana, Djafar, Mehdi, Dölle, Britta, Doull, Laura, Dricot, Laurence, Drzezga, Alexander, Dubois, Bruno, Dumont, Julien, Dumur, Jean, Dumurgier, Julien, Dvorak, Martin, Ecay, Mirian, Escher, Claus, Estanga, Ainara, Esteban, Ester, Fanjaud, Guy, Fauria, Karine, Felez Sanchez, Marta, Feukam Talla, Patrick, Ford, Lisa, Frisoni, Giovanni B, Fuster, David, Gabelle, Audrey, Gaubert, Sinead, Gauci, Cédric, Geldhof, Christine, Georges, Jean, Ghika, Joseph, González, Elena, Goovaerts, Valerie, Goulart, Denis Mariano, Grasselli, Caroline, Gray, Katherine, Greensmith, Martin, Grozn, Laure, Guillemaud, Céline, Gunn, Fiona, Guntur Ramkumar, Prasad, Hagman, Göran, Hansseuw, Bernard, Heeman, Fiona, Hendriks, Janine, Himmelmann, Jakob, Hitzel, Anne, Hives, Florent, Hoenig, Merle, Hourrègue, Claire, Hudson, Justine, Huguet, Jordi, Ibarria, Marta, Iidow, Ifrah, Indart, Sandrine, Ingala, Silvia, Ivanoiu, Adrian, Jacquemont, Charlotte, Jelic, Vesna, Jiao, Jieqing, Jofresa, Sara, Jonsson, Cathrine, Kaliukhovich, Dzmitry, Kern, Silke, Kivipelto, Miia, Knezevic, Iva, Kuchcinski, Grégory, Laforce, Manon, Lafuente, Asunción, Lala, Françoise, Lammertsma, Adriaan, Lax, Michelle, Lebouvier, Thibaud, Lee, Ho-Yun, Lee, Lean, Leeuwis, Annebet, Lefort, Amandine, Legrand, Jean-François, Leroy, Mélanie, Lesoil Markowski, Constance, Levy, Marcel, Lhommel , Renaud, Lopes, Renaud, Lopes Alves, Isadora, Lorenzini, Luigi, Lorette, Adrien, Luckett, Emma, Lundin, Marie, Mackowiak, Marie-Anne, Malotaux, Vincent, Manber, Richard, Manyakov, Nikolay, Markiewicz, Pawel, Marne, Paula, Marquié, Marta, Martín, Elvira, Martínez, Joan, Martinez Lage, Pablo, Mastenbroek, Sophie E, Maureille, Aurélien, Meersmans, Karen, Mett, Anja, Milne, Joseph, Minguillón, Carolina, Modat, Marc, Montrreal, Laura, Müller, Theresa, Muniz, Graciela, Mutsarts, Henk Jan, Nilsson, Ted, Ninerola, Aida, Nordberg, Agneta, Novaes, Wilse, Nuno Carmelo Pires Silva, Joao, Operto, Greg, Orellana, Adela, Ousset, Pierre-Jean, Outteryck, Olivier, Pallardy, Amandine, Palombit, Alessandro, Pancho, Ana, Pappon, Martin, Paquet, Claire, Pariente, Jérémie, Pasquier, Florence, Payoux, Pierre, Peaker, Harry, Pelejà, Esther, Pennetier, Delphine, Pérez-Cordón, Alba, Perissinotti, Andrés, Perrenoud, Matthieu Paul, Petit, Sandrine, Petyt, Grégory, Pfeil, Julia, Pirotte, Blanche, Pla, Sandra, Plaza Wuthrich, Sonia, Poitrine, Lea, Pollet, Marianne, Poncelet, Jean-Benoit, Prior, John, Pruvo, Jean-Pierre, Putallaz, Pauline, Queneau, Mathieu, Quenon , Lisa, Rădoi, Andreea, Rafiq, Marie, Ramage, Fiona, Ramis, Maribel, Reinwald, Michael, Rios, Gonzalo, Ritchie, Craig, Rodriguez, Elena, Rollin, Adeline, Rouaud, Olivier, Sacuiu, Simona, Saint-Aubert, Laure, Sala, Arianna, Salabert, Anne-Sophie, Saldias, Jon, Salvadó, Gemma, Sanabria, Angela, Sannemann, Lena, Sastre, Nathalie, Savina, Daniela, Savitcheva, Irina, Schaeverbeke, Jolien, Schildermans, Carine, Schmidt, Mark, Schöll, Michael, Schuermans, Jeroen, Semah, Franck, Shekari, Mahnaz, Skoog, Ingmar, Sotolongo-Grau, Oscar, Stephens, Andrew, Stewart, Tiffany, Stutzmann, Jennyfer, Tait, Murray, Tárraga, Lluis, Tartari, Juan Pablo, Tysen-backstrom, Ann-christine, Valero, Sergi, Vallez Garcia, David, van Berckel, Bart N M, van Essen, Martijn, Van Laere, Koen, van Leur, Jeroen, van Maurik, Ingrid S, Vandenberghe, Rik, Vellas, Bruno, Virolinen, Jukka, Visser, Pieter Jelle, Walles, Håkan, Wallin, Emilia, Whitelaw, Grant, Wimberley, Catriona, Win , Zarni, Wink, Alle Meije, Wolz, Robin, Woodside, John, Yaqub, Maqsood, Zettergren, Anna, Medical Psychology, APH - Personalized Medicine, APH - Quality of Care, Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Neuroinfection & -inflammation, CCA - Cancer Treatment and quality of life, CCA - Imaging and biomarkers, Neurology, Dekyndt, Bérengère, Delbeuck, Xavier, Delrieu, Julien, Demonet, Jean-François, Deramecourt, Vincent, Desclaux, Françoise, Diaz, Carlos, Diego, Susana, Djafar, Mehdi, Dölle, Britta, Doull, Laura, Dricot, Laurence, Drzezga, Alexander, Dubois, Bruno, Dumont, Julien, Dumur, Jean, Dumurgier, Julien, Dvorak, Martin, Ecay, Mirian, Edison, Paul, Escher, Claus, Estanga, Ainara, Esteban, Ester, Fanjaud, Guy, Farrar, Gill, Fauria, Karine, Felez Sanchez, Marta, Feukam Talla, Patrick, Ford, Lisa, Frisoni, Giovanni B, Fuster, David, Gabelle, Audrey, Garibotto, Valentina, Gaubert, Sinead, Gauci, Cédric, Geldhof, Christine, Georges, Jean, Ghika, Joseph, Gismondi, Rossella, Gispert, Juan Domingo, González, Elena, Goovaerts, Valerie, Goulart, Denis Mariano, Grasselli, Caroline, Grau-Rivera, Oriol, Gray, Katherine, Greensmith, Martin, Grozn, Laure, Guillemaud, Céline, Gunn, Fiona, Guntur Ramkumar, Prasad, Hagman, Göran, Hansseuw, Bernard, Heeman, Fiona, Hendriks, Janine, Himmelmann, Jakob, Hitzel, Anne, Hives, Florent, Hoenig, Merle, Hourrègue, Claire, Hudson, Justine, Huguet, Jordi, Ibarria, Marta, Iidow, Ifrah, Indart, Sandrine, Ingala, Silvia, Ivanoiu, Adrian, Jacquemont, Charlotte, Jelic, Vesna, Jessen, Frank, Jiao, Jieqing, Jofresa, Sara, Jonsson, Cathrine, Kaliukhovich, Dzmitry, Kern, Silke, Kivipelto, Miia, Knezevic, Iva, Kuchcinski, Grégory, Laforce, Manon, Lafuente, Asunción, Lala, Françoise, Lammertsma, Adriaan, Lax, Michelle, Lebouvier, Thibaud, Lee, Ho-Yun, Lee, Lean, Leeuwis, Annebet, Lefort, Amandine, Legrand, Jean-François, Leroy, Mélanie, Lesoil Markowski, Constance, Levy, Marcel, Lhommel, Renaud, Lopes, Renaud, Lopes Alves, Isadora, Lorenzini, Luigi, Lorette, Adrien, Luckett, Emma, Lundin, Marie, Mackowiak, Marie-Anne, Malotaux, Vincent, Manber, Richard, Manyakov, Nikolay, Markiewicz, Pawel, Marne, Paula, Marquié, Marta, Martín, Elvira, Martínez, Joan, Martinez Lage, Pablo, Mastenbroek, Sophie E, Maureille, Aurélien, Meersmans, Karen, Mett, Anja, Milne, Joseph, Minguillón, Carolina, Modat, Marc, Molinuevo, José Luis, Montrreal, Laura, Moro, Christian, Müller, Theresa, Muniz, Graciela, Mutsarts, Henk Jan, Nilsson, Ted, Ninerola, Aida, Nordberg, Agneta, Novaes, Wilse, Nuno Carmelo Pires Silva, Joao, Operto, Greg, Orellana, Adela, Ousset, Pierre-Jean, Outteryck, Olivier, Pallardy, Amandine, Palombit, Alessandro, Pancho, Ana, Pappon, Martin, Paquet, Claire, Pariente, Jérémie, Pasquier, Florence, Payoux, Pierre, Peaker, Harry, Abdelnour, Carla, Pelejà, Esther, Pennetier, Delphine, Pérez-Cordón, Alba, Perissinotti, Andrés, Perrenoud, Matthieu Paul, Petit, Sandrine, Petyt, Grégory, Pfeil, Julia, Pirotte, Blanche, Pla, Sandra, Aguilera, Nuria, Plaza Wuthrich, Sonia, Poitrine, Lea, Pollet, Marianne, Poncelet, Jean-Benoit, Prior, John, Pruvo, Jean-Pierre, Putallaz, Pauline, Queneau, Mathieu, Quenon, Lisa, Rădoi, Andreea, Aksman, Leon, Rafiq, Marie, Ramage, Fiona, Ramis, Maribel, Reinwald, Michael, Rios, Gonzalo, Ritchie, Craig, Rodriguez, Elena, Rollin, Adeline, Rouaud, Olivier, Sacuiu, Simona, Alarcón-Martín, Emilio, Saint-Aubert, Laure, Sala, Arianna, Salabert, Anne-Sophie, Saldias, Jon, Salvadó, Gemma, Sanabria, Angela, Sannemann, Lena, Sastre, Nathalie, Savina, Daniela, Savitcheva, Irina, Alegret, Montse, Schaeverbeke, Jolien, Scheltens, Philip, Schildermans, Carine, Schmidt, Mark, Schöll, Michael, Schuermans, Jeroen, Semah, Franck, Shekari, Mahnaz, Skoog, Ingmar, Sotolongo-Grau, Oscar, Alonso-Lana, Silvia, Stephens, Andrew, Stewart, Tiffany, Stutzmann, Jennyfer, Tait, Murray, Tárraga, Lluis, Tartari, Juan Pablo, Tysen-Backstrom, Ann-Christine, Valero, Sergi, Vallez Garcia, David, van Berckel, Bart N M, Altomare, Daniele, van Essen, Martijn, Van Laere, Koen, van Leur, Jeroen, van Maurik, Ingrid S, Vandenberghe, Rik, Vellas, Bruno, Virolinen, Jukka, Visser, Pieter Jelle, Walker, Zuzana, Walles, Håkan, Andersen, Pia, Wallin, Emilia, Whitelaw, Grant, Wimberley, Catriona, Win, Zarni, Wink, Alle Meije, Wolz, Robin, Woodside, John, Yaqub, Maqsood, Zettergren, Anna, Zeyen, Philip, Arab, Majd, Aspö, Malin, Bader, Ilona, Bader, Ilse, Banton, Nigel, Barkhof, Frederik, Barnes, Rodrigo, Barrie, Dawn, Battle, Mark, Belén Collado, Ana, Bellet, Julie, Berkhof, Johannes, Biger, Marine, Birck, Cindy, Bischof, Gerard, Boada, Mercè, Boellaard, Ronald, Bogdanovic, Nenad, Bollack, Ariane, Bombois, Stéphanie, Borg, Stefan, Borjesson-Hanson, Anne, Boskov, Vladimir, Boutantin, Justine, Boutoleau-Bretonniere, Claire, Bouwman, Femke, Breuilh, Laetitia, Bringman, Eva, Brunel, Baptiste, Bucci, Marco, Buckley, Chris, Buendía, Mar, Bullich, Santi, Calvet, Anna, Cañada, Laia, Cañada, Marta, Caprioglio, Camilla, Cardoso, Jorge, Carlier, Jasmine, Carre, Elise, Carrie, Isabelle, Cassagnaud, Pascaline, Cassol, Emmanuelle, Castilla-Martí, Miguel, Cazalon, Elodie, Chaarriau, Tiphaine, Chaigeau, Rachel, Chalmers, Taylor, Clerc, Marie-Thérèse, Clerigue, Montserrat, Cognat, Emmanuel, Coll, Nina, Collij, Lyduine E, Connely, Peter, Cordier, Elodie, Costes, Corine, Coulange, Camille, Courtemanche, Hélène, Creisson, Eric, Crinquette, Charlotte, Cuevas, Rosario, Cufi, Marie-Noëlle, Dardenne, Sophie, de Arriba, Maria, de Costa Luis, Casper, de Gier, Yvonne, de Verbizier Lonjon, Delphine, and Dekker, Veronique

Subjects
Male, Adult, metabolism [Brain], Positron-Emission Tomography, diagnosis [Alzheimer Disease], diagnostic imaging [Cognitive Dysfunction], Humans, metabolism [Amyloid beta-Peptides], ddc:610, Prospective Studies, Disclosure, General Medicine, Aged
Abstract

ImportanceIndividuals who are amyloid-positive with subjective cognitive decline and clinical features increasing the likelihood of preclinical Alzheimer disease (SCD+) are at higher risk of developing dementia. Some individuals with SCD+ undergo amyloid-positron emission tomography (PET) as part of research studies and frequently wish to know their amyloid status; however, the disclosure of a positive amyloid-PET result might have psychological risks.ObjectiveTo assess the psychological outcomes of the amyloid-PET result disclosure in individuals with SCD+ and explore which variables are associated with a safer disclosure in individuals who are amyloid positive.Design, Setting, and ParticipantsThis prospective, multicenter study was conducted as part of The Amyloid Imaging to Prevent Alzheimer Disease Diagnostic and Patient Management Study (AMYPAD-DPMS) (recruitment period: from April 2018 to October 2020). The setting was 5 European memory clinics, and participants included patients with SCD+ who underwent amyloid-PET. Statistical analysis was performed from July to October 2022.ExposuresDisclosure of amyloid-PET result.Main Outcomes and MeasuresPsychological outcomes were defined as (1) disclosure related distress, assessed using the Impact of Event Scale–Revised (IES-R; scores of at least 33 indicate probable presence of posttraumatic stress disorder [PTSD]); and (2) anxiety and depression, assessed using the Hospital Anxiety and Depression scale (HADS; scores of at least 15 indicate probable presence of severe mood disorder symptoms).ResultsAfter disclosure, 27 patients with amyloid-positive SCD+ (median [IQR] age, 70 [66-74] years; gender: 14 men [52%]; median [IQR] education: 15 [13 to 17] years, median [IQR] Mini-Mental State Examination [MMSE] score, 29 [28 to 30]) had higher median (IQR) IES-R total score (10 [2 to 14] vs 0 [0 to 2]; P P P P P = .06) and Depression (–1.0 [–2.0 to 0.0] vs –1.0 [–3.0 to 0.0]; P = .46) deltas (score after disclosure – scores at baseline). In patients with amyloid-positive SCD+, despite the small sample size, higher education was associated with lower disclosure-related distress (ρ = –0.43; P = .02) whereas the presence of study partner was associated with higher disclosure-related distress (W = 7.5; P = .03). No participants with amyloid-positive SCD+ showed probable presence of PTSD or severe anxiety or depression symptoms at follow-up.Conclusions and RelevanceThe disclosure of a positive amyloid-PET result to patients with SCD+ was associated with a bigger psychological change, yet such change did not reach the threshold for clinical concern.

Published
2023
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23. Clinical Effect of Early vs Late Amyloid Positron Emission Tomography in Memory Clinic Patients: The AMYPAD-DPMS Randomized Clinical Trial

Author

Altomare, Daniele, Barkhof, Frederik, Moro, Christian, Delrieu, Julien, Payoux, Pierre, Saint-Aubert, Laure, Hitzel, Anne, Molinuevo, José Luis, Grau-Rivera, Oriol, Gispert, Juan Domingo, Drzezga, Alexander, Jessen, Frank, Caprioglio, Camilla, Zeyen, Philip, Nordberg, Agneta, Savitcheva, Irina, Jelic, Vesna, Walker, Zuzana, Edison, Paul, Demonet, Jean-François, Gismondi, Rossella, Farrar, Gill, Stephens, Andrew W, Collij, Lyduine E, Frisoni, Giovanni B, Disease, Amyloid Imaging to Prevent Alzheimer’s, Scheltens, Philip, Lopes Alves, Isadora, Bouwman, Femke, Berkhof, Johannes, van Maurik, Ingrid S, Garibotto, Valentina, Cuevas, Rosario, Cufi, Marie-Noëlle, Dardenne, Sophie, de Arriba, Maria, de Costa Luis, Casper, de Gier, Yvonne, de Verbizier Lonjon, Delphine, Dekker, Veronique, Dekyndt, Bérengère, Delbeuck, Xavier, Delrieu, Julien, Demonet, Jean-François, Deramecourt, Vincent, Desclaux, Françoise, Diaz, Carlos, Diego, Susana, Djafar, Mehdi, Dölle, Britta, Doull, Laura, Dricot, Laurence, Drzezga, Alexander, Dubois, Bruno, Dumont, Julien, Dumur, Jean, Dumurgier, Julien, Dvorak, Martin, Ecay, Mirian, Edison, Paul, Escher, Claus, Estanga, Ainara, Esteban, Ester, Fanjaud, Guy, Farrar, Gill, Fauria, Karine, Felez Sanchez, Marta, Feukam Talla, Patrick, Ford, Lisa, Frisoni, Giovanni B, Fuster, David, Gabelle, Audrey, Garibotto, Valentina, Gaubert, Sinead, Gauci, Cédric, Geldhof, Christine, Georges, Jean, Ghika, Joseph, Gismondi, Rossella, Gispert, Juan Domingo, González, Elena, Goovaerts, Valerie, Goulart, Denis Mariano, Grasselli, Caroline, Grau-Rivera, Oriol, Gray, Katherine, Greensmith, Martin, Grozn, Laure, Guillemaud, Céline, Gunn, Fiona, Guntur Ramkumar, Prasad, Hagman, Göran, Hansseuw, Bernard, Heeman, Fiona, Hendriks, Janine, Himmelmann, Jakob, Hitzel, Anne, Hives, Florent, Hoenig, Merle, Hourrègue, Claire, Hudson, Justine, Huguet, Jordi, Ibarria, Marta, Iidow, Ifrah, Indart, Sandrine, Ingala, Silvia, Ivanoiu, Adrian, Jacquemont, Charlotte, Jelic, Vesna, Jessen, Frank, Jiao, Jieqing, Jofresa, Sara, Jonsson, Cathrine, Kaliukhovich, Dzmitry, Kern, Silke, Kivipelto, Miia, Knezevic, Iva, Kuchcinski, Grégory, Laforce, Manon, Lafuente, Asunción, Lala, Françoise, Lammertsma, Adriaan, Lax, Michelle, Lebouvier, Thibaud, Lee, Ho-Yun, Lee, Lean, Leeuwis, Annebet, Lefort, Amandine, Legrand, Jean-François, Leroy, Mélanie, Lesoil Markowski, Constance, Levy, Marcel, Lhommel, Renaud, Lopes, Renaud, Lopes Alves, Isadora, Lorenzini, Luigi, Lorette, Adrien, Luckett, Emma, Lundin, Marie, Mackowiak, Marie-Anne, Malotaux, Vincent, Manber, Richard, Manyakov, Nikolay, Markiewicz, Pawel, Marne, Paula, Marquié, Marta, Martín, Elvira, Martínez, Joan, Martinez Lage, Pablo, Mastenbroek, Sophie E, Maureille, Aurélien, Meersmans, Karen, Mett, Anja, Milne, Joseph, Minguillón, Carolina, Modat, Marc, Molinuevo, José Luis, Montrreal, Laura, Moro, Christian, Müller, Theresa, Muniz, Graciela, Mutsarts, Henk Jan, Nilsson, Ted, Ninerola, Aida, Nordberg, Agneta, Novaes, Wilse, Nuno Carmelo Pires Silva, Joao, Operto, Greg, Orellana, Adela, Ousset, Pierre-Jean, Outteryck, Olivier, Pallardy, Amandine, Palombit, Alessandro, Pancho, Ana, Pappon, Martin, Paquet, Claire, Pariente, Jérémie, Pasquier, Florence, Payoux, Pierre, Peaker, Harry, Pelejà, Esther, Pennetier, Delphine, Pérez-Cordón, Alba, Perissinotti, Andrés, Perrenoud, Matthieu Paul, Petit, Sandrine, Petyt, Grégory, Pfeil, Julia, Pirotte, Blanche, Pla, Sandra, Plaza Wuthrich, Sonia, Poitrine, Lea, Pollet, Marianne, Poncelet, Jean-Benoit, Prior, John, Pruvo, Jean-Pierre, Putallaz, Pauline, Queneau, Mathieu, Quenon, Lisa, Rădoi, Andreea, Rafiq, Marie, Ramage, Fiona, Ramis, Maribel, Reinwald, Michael, Rios, Gonzalo, Ritchie, Craig, Rodriguez, Elena, Rollin, Adeline, Rouaud, Olivier, Sacuiu, Simona, Saint-Aubert, Laure, Sala, Arianna, Salabert, Anne-Sophie, Saldias, Jon, Salvadó, Gemma, Sanabria, Angela, Sannemann, Lena, Sastre, Nathalie, Savina, Daniela, Savitcheva, Irina, Schaeverbeke, Jolien, Scheltens, Philip, Schildermans, Carine, Schmidt, Mark, Schöll, Michael, Schuermans, Jeroen, Semah, Franck, Shekari, Mahnaz, Skoog, Ingmar, Sotolongo-Grau, Oscar, Stephens, Andrew, Stewart, Tiffany, Stutzmann, Jennyfer, Tait, Murray, Tárraga, Lluis, Tartari, Juan Pablo, Tysen-Backstrom, Ann-Christine, Valero, Sergi, Vallez Garcia, David, van Berckel, Bart N M, van Essen, Martijn, Van Laere, Koen, van Leur, Jeroen, van Maurik, Ingrid S, Vandenberghe, Rik, Vellas, Bruno, Virolinen, Jukka, Visser, Pieter Jelle, Walker, Zuzana, Walles, Håkan, Wallin, Emilia, Whitelaw, Grant, Abdelnour, Carla, Wimberley, Catriona, Win, Zarni, Wink, Alle Meije, Wolz, Robin, Woodside, John, Yaqub, Maqsood, Zettergren, Anna, Zeyen, Philip, Aguilera, Nuria, Aksman, Leon, Alarcón-Martín, Emilio, Alegret, Montse, Alonso-Lana, Silvia, Altomare, Daniele, Andersen, Pia, Arab, Majd, Aspö, Malin, Bader, Ilona, Bader, Ilse, Banton, Nigel, Barkhof, Frederik, Barnes, Rodrigo, Barrie, Dawn, Battle, Mark, Belén Collado, Ana, Bellet, Julie, Berkhof, Johannes, Biger, Marine, Birck, Cindy, Bischof, Gerard, Boada, Mercè, Boellaard, Ronald, Bogdanovic, Nenad, Bollack, Ariane, Bombois, Stéphanie, Borg, Stefan, Borjesson-Hanson, Anne, Boskov, Vladimir, Boutantin, Justine, Boutoleau-Bretonniere, Claire, Bouwman, Femke, Breuilh, Laetitia, Bringman, Eva, Brunel, Baptiste, Bucci, Marco, Buckley, Chris, Buendía, Mar, Bullich, Santi, Calvet, Anna, Cañada, Laia, Cañada, Marta, Caprioglio, Camilla, Cardoso, Jorge, Carlier, Jasmine, Carre, Elise, Carrie, Isabelle, Cassagnaud, Pascaline, Cassol, Emmanuelle, Castilla-Martí, Miguel, Cazalon, Elodie, Chaarriau, Tiphaine, Chaigeau, Rachel, Chalmers, Taylor, Clerc, Marie-Thérèse, Clerigue, Montserrat, Cognat, Emmanuel, Coll, Nina, Collij, Lyduine E, Connely, Peter, Cordier, Elodie, Costes, Corine, Coulange, Camille, Courtemanche, Hélène, Creisson, Eric, and Crinquette, Charlotte

Subjects
Male, Amyloid, psychology [Alzheimer Disease], Amyloid beta-Peptides, metabolism [Amyloid beta-Peptides], Amyloidogenic Proteins, metabolism [Brain], Positron-Emission Tomography, Humans, Female, Cognitive Dysfunction, ddc:610, Prospective Studies, 3-(3,5-dichlorophenyl)-1-methyl-2,5-pyrrolidinedione, Aged, metabolism [Amyloid]
Abstract

Amyloid positron emission tomography (PET) allows the direct assessment of amyloid deposition, one of the main hallmarks of Alzheimer disease. However, this technique is currently not widely reimbursed because of the lack of appropriately designed studies demonstrating its clinical effect.To assess the clinical effect of amyloid PET in memory clinic patients.The AMYPAD-DPMS is a prospective randomized clinical trial in 8 European memory clinics. Participants were allocated (using a minimization method) to 3 study groups based on the performance of amyloid PET: arm 1, early in the diagnostic workup (within 1 month); arm 2, late in the diagnostic workup (after a mean [SD] 8 [2] months); or arm 3, if and when the managing physician chose. Participants were patients with subjective cognitive decline plus (SCD+; SCD plus clinical features increasing the likelihood of preclinical Alzheimer disease), mild cognitive impairment (MCI), or dementia; they were assessed at baseline and after 3 months. Recruitment took place between April 16, 2018, and October 30, 2020. Data analysis was performed from July 2022 to January 2023.Amyloid PET.The main outcome was the difference between arm 1 and arm 2 in the proportion of participants receiving an etiological diagnosis with a very high confidence (ie, ≥90% on a 50%-100% visual numeric scale) after 3 months.A total of 844 participants were screened, and 840 were enrolled (291 in arm 1, 271 in arm 2, 278 in arm 3). Baseline and 3-month visit data were available for 272 participants in arm 1 and 260 in arm 2 (median [IQR] age: 71 [65-77] and 71 [65-77] years; 150/272 male [55%] and 135/260 male [52%]; 122/272 female [45%] and 125/260 female [48%]; median [IQR] education: 12 [10-15] and 13 [10-16] years, respectively). After 3 months, 109 of 272 participants (40%) in arm 1 had a diagnosis with very high confidence vs 30 of 260 (11%) in arm 2 (P < .001). This was consistent across cognitive stages (SCD+: 25/84 [30%] vs 5/78 [6%]; P < .001; MCI: 45/108 [42%] vs 9/102 [9%]; P < .001; dementia: 39/80 [49%] vs 16/80 [20%]; P < .001).In this study, early amyloid PET allowed memory clinic patients to receive an etiological diagnosis with very high confidence after only 3 months compared with patients who had not undergone amyloid PET. These findings support the implementation of amyloid PET early in the diagnostic workup of memory clinic patients.EudraCT Number: 2017-002527-21.

Published
2023
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27. Evaluating the effects of the novel GLP-1 analogue liraglutide in Alzheimer’s disease: study protocol for a randomised controlled trial (ELAD study)

Author

Femminella, Grazia Daniela, Frangou, Eleni, Love, Sharon B., Busza, Gail, Holmes, Clive, Ritchie, Craig, Lawrence, Robert, McFarlane, Brady, Tadros, George, Ridha, Basil H., Bannister, Carol, Walker, Zuzana, Archer, Hilary, Coulthard, Elizabeth, Underwood, Ben R., Prasanna, Aparna, Koranteng, Paul, Karim, Salman, Junaid, Kehinde, McGuinness, Bernadette, Nilforooshan, Ramin, Macharouthu, Ajay, Donaldson, Andrew, Thacker, Simon, Russell, Gregor, Malik, Naghma, Mate, Vandana, Knight, Lucy, Kshemendran, Sajeev, Harrison, John, Brooks, David J., Passmore, Anthony Peter, Ballard, Clive, and Edison, Paul

Published
2019
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34. Covid-19: virology, variants, and vaccines

Author

Young, Megan, Crook, Harry, Scott, Janet, and Edison, Paul

Abstract

As of 25 January 2022, over 349 million individuals have received a confirmed diagnosis of covid-19, with over 5.59 million confirmed deaths associated with the SARS-CoV-2 virus. The covid-19 pandemic has prompted an extensive global effort to study the molecular evolution of the virus and develop vaccines to prevent its spread. Although rigorous determination of SARS-CoV-2 infectivity remains elusive, owing to the continuous evolution of the virus, steps have been made to understand its genome, structure, and emerging genetic mutations. The SARS-CoV-2 genome is composed of several open reading frames and structural proteins, including the spike protein, which is essential for entry into host cells. As of 25 January 2022, the World Health Organization has reported five variants of concern, two variants of interest, and three variants under monitoring. Additional sublineages have since been identified, and are being monitored. The mutations harboured in these variants confer an increased transmissibility, severity of disease, and escape from neutralising antibodies compared with the primary strain. The current vaccine strategy, including booster doses, provides protection from severe disease. As of 24 January 2022, 33 vaccines have been approved for use in 197 countries. In this review, we discuss the genetics, structure, and transmission methods of SARS-CoV-2 and its variants, highlighting how mutations provide enhanced abilities to spread and inflict disease. This review also outlines the vaccines currently in use around the world, providing evidence for every vaccine's immunogenicity and effectiveness.

Published
2022

42. A European multicentre PET study of fibrillar amyloid in Alzheimer’s disease

Author

Nordberg, Agneta, Carter, Stephen F., Rinne, Juha, Drzezga, Alexander, Brooks, David J., Vandenberghe, Rik, Perani, Daniela, Forsberg, Anton, Långström, Bengt, Scheinin, Noora, Karrasch, Mira, Någren, Kjell, Grimmer, Timo, Miederer, Isabelle, Edison, Paul, Okello, Aren, Van Laere, Koen, Nelissen, Natalie, Vandenbulcke, Mathieu, Garibotto, Valentina, Almkvist, Ove, Kalbe, Elke, Hinz, Rainer, and Herholz, Karl

Published
2013
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43. Prevalence of Depressive Symptoms in a Memory Clinic Cohort: A Retrospective Study.

Author

Loreto, Flavia, Fitzgerald, Anna, Golemme, Mara, Gunning, Stephen, Win, Zarni, Patel, Neva, Carswell, Christopher, Perry, Richard, Kennedy, Angus, Edison, Paul, and Malhotra, Paresh

Abstract

Background: Depression has been suggested to be a cause of reversible cognitive impairment but also a risk factor for neurodegenerative disease. Studies suggest that depression prevalence may be high in early onset dementia, particularly Alzheimer's disease, but this has not been systematically assessed in a biomarker-validated clinical dementia cohort to date.Objective: To examine the prevalence, features, and association with amyloid pathology of lifetime depressive symptoms in a memory clinic cohort meeting appropriate use criteria for amyloid PET imaging.Methods: We included 300 patients from a single-center memory clinic cohort that received diagnostic biomarker evaluation with amyloid PET imaging according to appropriate use criteria. History of lifetime depressive symptoms was retrospectively assessed through structured review of clinical correspondence.Results: One hundred forty-two (47%) patients had a history of significant depressive symptoms ('D+'). Of these, 89% had ongoing symptoms and 60% were on antidepressants at the time of presentation to our Clinic. Depressive symptoms were equally highly prevalent in the amyloid-positive and the heterogeneous group of amyloid-negative patients.Conclusion: Approximately half of patients who meet appropriate use criteria for amyloid PET have a history of depressive symptoms. We suggest that depression is an important feature of both neurodegenerative and non-neurodegenerative cognitive impairment and may contribute to the diagnostic uncertainty behind referral to amyloid PET. [ABSTRACT FROM AUTHOR]

Published
2022
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45. Cerebrospinal Fluid sTREM2 Has Paradoxical Association with Brain Structural Damage Rate in Early- and Late-Stage Alzheimer's Disease.

Author

Leng, Fangda, Zhan, Zhenying, Sun, Yunchuang, Liu, Fang, Edison, Paul, Sun, Yongan, Wang, Zhaoxia, and Alzheimer’s Disease Neuroimaging Initiative

Subjects
ALZHEIMER'S disease, CEREBROSPINAL fluid, BRAIN damage, DIFFUSION tensor imaging, WHITE matter (Nerve tissue), BRAIN, NERVE tissue proteins, MAGNETIC resonance imaging, BRAIN injuries, PEPTIDES
Abstract

Background: Recently it has been proposed that microglial response has a stage-dependent effect on the progression of Alzheimer's disease (AD). Cerebrospinal fluid (CSF) sTREM2 has emerged as a promising microglial activation marker.Objective: To test the stage-dependent role of microglia by studying the association between baseline sTREM2 and dynamic brain structural changes in AD and mild cognitive impairment (MCI) patients.Methods: 22 amyloid-β-positive (A+) and tau-positive (T+) AD and 24 A+T+MCI patients were identified from the Alzheimer's Disease Neuroimaging Initiative. The patients had baseline CSF amyloid-β, phosphorylated-tau, and sTREM2, and were followed up for at least one year by T1-weighted and diffusion tensor imaging scans. Gray matter volumes and white matter microstructural integrity were evaluated. Linear mixed models were applied to analyze how baseline sTREM2 may influence the rate of brain structural changes while adjusting for the effects of age, APOE4 status, and the CSF core markers.Results: In A+T+AD patients, baseline CSF sTREM2 was associated with faster mean diffusivity increase in the bilateral posterior corona radiata and right superior longitudinal fasciculus. In A+T+MCI patients, baseline CSF sTREM2 was associated slower gray matter volumetric loss in parahippocampal gyrus, left fusiform cortex, left middle temporal gyrus, and left lateral occipital cortex. Baseline CSF sTREM2 also had a protective effect against mean diffusivity increase in right inferior fronto-occipital fasciculus, left superior longitudinal fasciculus, left forceps minor, and left uncinate fasciculus.Conclusion: Microglial activation at early stage might have a protective effect against neurodegeneration, while at late stage it might facilitate AD. Future efforts on modulating microglial activation could be promising, given a carefully selected time window for intervention. [ABSTRACT FROM AUTHOR]

Published
2022
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46. Correction to:Evaluating the effects of the novel GLP-1 analogue liraglutide in Alzheimer's disease: Study protocol for a randomised controlled trial (ELAD study) (Trials. (2019) 20 (191) DOI: 10.1186/s13063-019-3259-x)

Author

Femminella, Grazia Daniela, Frangou, Eleni, Love, Sharon B., Busza, Gail, Holmes, Clive, Ritchie, Craig, Lawrence, Robert, McFarlane, Brady, Tadros, George, Ridha, Basil H., Bannister, Carol, Walker, Zuzana, Archer, Hilary, Coulthard, Elizabeth, Underwood, Ben R., Prasanna, Aparna, Koranteng, Paul, Karim, Salman, Junaid, Kehinde, McGuinness, Bernadette, Nilforooshan, Ramin, Macharouthu, Ajay, Donaldson, Andrew, Thacker, Simon, Russell, Gregor, Malik, Naghma, Mate, Vandana, Knight, Lucy, Kshemendran, Sajeev, Harrison, John, Hölscher, Christian, Brooks, David J., Passmore, Anthony Peter, Ballard, Clive, and Edison, Paul

Abstract

After publication of our article [1] the authors have notified us that the name of Prof. Christian Hölscher had been inadvertently forgotten when compiling the list of authors. Dr. Hölscher developed the concept of testing liraglutide in Alzheimer’s mouse model, has done the preclinical experiments, and is a co-applicant of the Alzheimer ociety UK grant that partially funds the study.

Published
2020
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48. Conquest unrequited: French expeditionary science in Mexico, 1864-1867

Author

Edison, Paul N.

Subjects
France -- History, History, Regional focus/area studies
Abstract

When Napoleon III created the Scientific Commission of Mexico in 1864 to study the occupied country and promote France's civilizing mission, participants expected a scientific conquest on the scale of Bonaparte's Egyptian campaign of 1798. However, the commission's work was not only cut short by the withdrawal of French troops in 1867, it was also contested by Mexican agents who resented French scientific hegemony. As illustrated by the archeological mission of Leon Mehedin, the unilateral and extractive science practiced by the commission served to widen the gulf between Parisian knowledge and the complex local setting, standing in stark contrast to the more collaborative version of colonial science simultaneously pursued by the French army in Mexico. Whereas French science in Egypt was translated into an enduring national achievement, controversy and dejection surrounded the considerable results of the Commission of Mexico and its problematic display at the Universal Exposition of 1867.

Published
2003

50. Application of advanced brain positron emission tomography–based molecular imaging for a biological framework in neurodegenerative proteinopathies

Author

Lammertsma, Adriaan A., Nordberg, Agneta, Windhorst, Albert D., Gerhard, Alexander, Winkeler, Alexandra, Jacobs, Andreas H., Gee, Anthony, Kuhnast, Bertrand, Halldin, Christer, Perani, Daniela, Brooks, David, Rodriguez-Vieitez, Elena, Turkheimer, Federico E., López-Picón, Francisco, Knudsen, Gitte M., Vercouillie, Johnny, Rinne, Juha O., Herholz, Karl, Van Laere, Koen, Varrone, Andrea, Santiago-Ribeiro, Marie Joao, Herth, Matthias M., Carroll, Michael A., Chalon, Sylvie, Bottlaender, Michel, Hansson, Oskar, Edison, Paul, Hinz, Rainer, Boellaard, Ronald, Moresco, Rosa Maria, Pappata, Sabina, and Iaccarino, Leonardo

Published
2019
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