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{userid:"siroos.mirzaei", "articletype":"article","pages":"312-319","author":"E Dimou, J Booij, M Rodrigues, H Prosch, J Attems, P Knoll, B Zajicek, R Dudczak, G Mostbeck, C Kuntner, O Langer, T Bruecke, S Mirzaei","year":"2009","title":"Amyloid PET and MRI in Alzheimer's disease and mild cognitive impairment.","month":"Jun","journal":"Curr Alzheimer Res","publisher":"","volume":"6","number":"3","note":"","tags":"Alzheimer Disease,Amyloid beta-Peptides,Benzothiazoles,Brain Mapping,Cognition Disorders,Fluorodeoxyglucose F18,Humans,Magnetic Resonance Imaging,Positron-Emission Tomography","booktitle":"","editor":"","abstract":"The neurodegenerative disorder Alzheimer's disease (AD) is the most common form of dementia. It is characterized by progressive impairment of cognitive functions and behavior. To distinguish clinically AD from other forms of dementia is an ongoing challenge. In addition, although mild cognitive impairment (MCI) is recognized as a risk factor for dementia, it remains a challenge to predict on an individual level who will convert to become demented. Amyloid beta (Abeta) is one of the crucial pathological findings in AD. Recently, amyloid tracers for PET imaging have been developed successfully which may offer the unique possibility for measuring fibrillar Abeta load in the living brain. Therefore, in the near future positron emission tomography (PET) may become an important tool for in vivo amyloid imaging contributing to early (differential) diagnosis as well as evaluation of treatment response in AD. Moreover, Abeta may play a role in prediction the conversion of MCI to AD. In this paper we review the recent development of the molecular imaging technique PET and its different radiopharmaceuticals on the trail for imaging amyloid in AD and the conversion of MCI to AD.","address":"","school":"","issn":"1875-5828","doi":"","isi":"","pubmed":"19519314","key":"Dimou2009","howpublished":"","urllink":"","refid":5}
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{userid:"tobias.nef", "refid":"413","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Analysis of primary visual cortex in dementia with Lewy bodies indicates GABAergic involvement associated with recurrent complex visual hallucinations.","year":"2016","author":"Ahmad A Khundakar, Peter S Hanson, Daniel Erskine, Nichola Z Lax, Joseph Roscamp, Evangelia Karyka, Eliona Tsefou, Preeti Singh, Simon J Cockell, Andrew Gribben, Lynne Ramsay, Peter G Blain, Urs P Mosimann, Deborah J Lett, Matthias Elstner, Douglass M Turnbull, Charles C Xiang, Michael J Brownstein, John T O'Brien, John-Paul Taylor, Johannes Attems, Alan J Thomas, Ian G McKeith, Christopher M Morris","journal":"Acta neuropathologica communications","volume":"4","number":"1","pages":"","month":"Jun","doi":"10.1186\/s40478-016-0334-3","pubmed":"27357212","pdflink":"","urllink":"","abstract":"Dementia with Lewy bodies (DLB) patients frequently experience well formed recurrent complex visual hallucinations (RCVH). This is associated with reduced blood flow or hypometabolism on imaging of the primary visual cortex. To understand these associations in DLB we used pathological and biochemical analysis of the primary visual cortex to identify changes that could underpin RCVH. Alpha-synuclein or neurofibrillary tangle pathology in primary visual cortex was essentially absent. Neurone density or volume within the primary visual cortex in DLB was also unchanged using unbiased stereology. Microarray analysis, however, demonstrated changes in neuropeptide gene expression and other markers, indicating altered GABAergic neuronal function. Calcium binding protein and GAD65\/67 immunohistochemistry showed preserved interneurone populations indicating possible interneurone dysfunction. This was demonstrated by loss of post synaptic GABA receptor markers including gephyrin, GABARAP, and Kif5A, indicating reduced GABAergic synaptic activity. Glutamatergic neuronal signalling was also altered with vesicular glutamate transporter protein and PSD-95 expression being reduced. Changes to the primary visual cortex in DLB indicate that reduced GABAergic transmission may contribute to RCVH in DLB and treatment using targeted GABAergic modulation or similar approaches using glutamatergic modification may be beneficial.","note":"","tags":"Alzheimer Disease,Amyloid beta-Peptides,Enzyme-Linked Immunosorbent Assay,Hallucinations,Humans,Image Processing, Computer-Assisted,Immunohistochemistry,Lewy Body Disease,Microarray Analysis,Neurons,RNA, Messenger,Real-Time Polymerase Chain Reaction,Visual Cortex,alpha-Synuclein,gamma-Aminobutyric Acid,tau Proteins","weight":413,"publisher":"","booktitle":"","editor":"","address":"","school":"","issn":"2051-5960","isi":"","key":"Khundakar2016","howpublished":""}
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{userid:"n.fox", "articletype":"article","pages":"686-699","author":"Raffaele Ferrari, Dena G Hernandez, Michael A Nalls, Jonathan D Rohrer, Adaikalavan Ramasamy, John B J Kwok, Carol Dobson-Stone, William S Brooks, Peter R Schofield, Glenda M Halliday, John R Hodges, Olivier Piguet, Lauren Bartley, Elizabeth Thompson, Eric Haan, Isabel Hern\u00e1ndez, Agust\u00edn Ruiz, Merc\u00e8 Boada, Barbara Borroni, Alessandro Padovani, Carlos Cruchaga, Nigel J Cairns, Luisa Benussi, Giuliano Binetti, Roberta Ghidoni, Gianluigi Forloni, Daniela Galimberti, Chiara Fenoglio, Maria Serpente, Elio Scarpini, Jordi Clarim\u00f3n, Alberto Lle\u00f3, Rafael Blesa, Maria Landqvist Wald\u00f6, Karin Nilsson, Christer Nilsson, Ian R A Mackenzie, Ging-Yuek R Hsiung, David M A Mann, Jordan Grafman, Christopher M Morris, Johannes Attems, Timothy D Griffiths, Ian G McKeith, Alan J Thomas, P Pietrini, Edward D Huey, Eric M Wassermann, Atik Baborie, Evelyn Jaros, Michael C Tierney, Pau Pastor, Cristina Razquin, Sara Ortega-Cubero, Elena Alonso, Robert Perneczky, Janine Diehl-Schmid, Panagiotis Alexopoulos, Alexander Kurz, Innocenzo Rainero, Elisa Rubino, Lorenzo Pinessi, Ekaterina Rogaeva, Peter St George-Hyslop, Giacomina Rossi, Fabrizio Tagliavini, Giorgio Giaccone, James B Rowe, Johannes C M Schlachetzki, James Uphill, John Collinge, Simon Mead, Adrian Danek, Vivianna M Van Deerlin, Murray Grossman, John Q Trojanowski, Julie van der Zee, William Deschamps, Tim Van Langenhove, Marc Cruts, Christine Van Broeckhoven, Stefano F Cappa, Isabelle Le Ber, Didier Hannequin, V\u00e9ronique Golfier, Martine Vercelletto, Alexis Brice, Benedetta Nacmias, Sandro Sorbi, Silvia Bagnoli, Irene Piaceri, J\u00f8rgen E Nielsen, Lena E Hjermind, Matthias Riemenschneider, Manuel Mayhaus, Bernd Ibach, Gilles Gasparoni, Sabrina Pichler, Wei Gu, Martin N Rossor, Nick C Fox, Jason D Warren, Maria Grazia Spillantini, Huw R Morris, Patrizia Rizzu, Peter Heutink, Julie S Snowden, Sara Rollinson, Anna Richardson, Alexander Gerhard, Amalia C Bruni, Raffaele Maletta, Francesca Frangipane, Chiara Cupidi, Livia Bernardi, Maria Anfossi, Maura Gallo, Maria Elena Conidi, Nicoletta Smirne, Rosa Rademakers, Matt Baker, Dennis W Dickson, Neill R Graff-Radford, Ronald C Petersen, David Knopman, Keith A Josephs, Bradley F Boeve, Joseph E Parisi, William W Seeley, Bruce L Miller, Anna M Karydas, Howard Rosen, John C van Swieten, Elise G P Dopper, Harro Seelaar, Yolande A L Pijnenburg, Philip Scheltens, Giancarlo Logroscino, Rosa Capozzo, Valeria Novelli, Annibale A Puca, Massimo Franceschi, Alfredo Postiglione, Graziella Milan, Paolo Sorrentino, Mark Kristiansen, Huei-Hsin Chiang, Caroline Graff, Florence Pasquier, Adeline Rollin, Vincent Deramecourt, Florence Lebert, Dimitrios Kapogiannis, Luigi Ferrucci, Stuart Pickering-Brown, Andrew B Singleton, John Hardy, Parastoo Momeni","year":"2014","title":"Frontotemporal dementia and its subtypes: a genome-wide association study.","month":"Jul","journal":"The Lancet. Neurology","publisher":"","volume":"13","number":"7","note":"","tags":"Adult,Aged,Aged, 80 and over,Female,Frontotemporal Dementia,Genome-Wide Association Study,Genotype,Humans,Male,Middle Aged","booktitle":"","editor":"","abstract":"Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. Mutations in three genes-MAPT, GRN, and C9orf72--have been associated with FTD. We sought to identify novel genetic risk loci associated with the disorder.","address":"","school":"","issn":"1474-4465","doi":"10.1016\/S1474-4422(14)70065-1","isi":"","pubmed":"24943344","key":"Ferrari2014","howpublished":"","urllink":"","refid":304,"weight":304}
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