White matter hyperintensities in progranulin-associated frontotemporal dementia: A longitudinal GENFI study
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Nick C Fox | Jennifer M. Nicholas | M. Freedman | S. Ourselin | R. Keren | G. Frisoni | J. Rowe | M. Rossor | M. Castelo‐Branco | N. Bargalló | A. Danek | R. Vandenberghe | S. Mead | R. Guerreiro | D. Thomas | C. Sudre | M. Cardoso | T. Rittman | S. Sorbi | B. Nacmias | D. Galimberti | M. Pievani | M. Bocchetta | J. Rohrer | C. Fenoglio | E. Scarpini | P. Tiraboschi | D. Cash | J. Warren | E. Rogaeva | C. Graff | H. Zetterberg | R. Bruffaerts | V. Jelic | G. Binetti | R. Laforce | M. Tartaglia | J. V. van Swieten | B. Borroni | M. Masellis | F. Tagliavini | E. Finger | A. de Mendonça | J. Bras | P. Rosa-Neto | I. Santana | R. Sánchez-Valle | A. Padovani | C. Butler | M. Synofzik | M. Vandenbulcke | V. Redaelli | A. Heslegrave | A. Lladó | A. Antonell | J. Olives | L. Benussi | R. Ghidoni | J. Nicholas | S. Ducharme | T. Cope | Linn Öijerstedt | G. Rossi | A. Gorostidi | M. Otto | R. Rademakers | C. Shoesmith | S. Prioni | A. Gerhard | J. Papma | D. Tang‐Wai | A. Verdelho | C. Maruta | S. Gauthier | M. Veldsman | R. Gasparotti | G. Miltenberger | L. Jiskoot | S. Archetti | S. Loosli | M. Balasa | J. Villanúa | H. Thonberg | J. Levin | C. Prix | V. Bessi | E. Premi | S. Gazzina | J. Panman | C. Heller | K. Moore | R. Convery | F. Moreno | G. Fumagalli | Sónia Afonso | S. Mitchell | P. Caroppo | M. Tainta | M. Cosseddu | M. R. Almeida | Catarina B. Ferreira | G. Giaccone | L. Meeter | C. Ferrari | C. Wilke | B. Santiago | C. Andersson | A. Arighi | G. Lombardi | R. van Minkelen | E. Wlasich | S. Anderl-Straub | I. Woollacott | M. Zulaica | C. Greaves | R. Taipa | S. Borrego-Écija | G. Di Fede | Benjamin Bender | M. Foiani | M. Arriba | M. Barandiarán | A. Gabilondo | R. Shafei | B. Indakoetxea | Zigor Díaz | S. Black | C. Timberlake | R. Bartha | P. Vandamme | D. Duro | M. J. Leitão | M. Tábuas-Pereira | Sonja Schonecker | Elisa Semler | T. Hoegen | Mollie Neason | Carolin Heller | Y. Pijnenburg | Hans-Otto Karnarth | T. Flanagan | R. Rademakers | Tobias Hoegen | Christin Andersson | Jaume Olives | Catharina Prix | Pietro Tiraboschi | Gabriel Miltenberger
[1] Kevin F. Bieniek,et al. Microglia in frontotemporal lobar degeneration with progranulin or C9ORF72 mutations , 2019, Annals of clinical and translational neurology.
[2] C. Haass,et al. Early lysosomal maturation deficits in microglia triggers enhanced lysosomal activity in other brain cells of progranulin knockout mice , 2018, Molecular Neurodegeneration.
[3] Konstantinos Arfanakis,et al. Evaluation of standardized and study-specific diffusion tensor imaging templates of the adult human brain: Template characteristics, spatial normalization accuracy, and detection of small inter-group FA differences , 2018, NeuroImage.
[4] Nick C Fox,et al. Pathological correlates of white matter hyperintensities in a case of progranulin mutation associated frontotemporal dementia , 2018, Neurocase.
[5] F. Barkhof,et al. Bullseye's representation of cerebral white matter hyperintensities , 2017, Journal of neuroradiology. Journal de neuroradiologie.
[6] S. Strittmatter,et al. Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice , 2017, Neuron.
[7] Alan J. Thomas,et al. PARIETAL WHITE MATTER LESIONS IN ALZHEIMER’S DISEASE ARE ASSOCIATED WITH CORTICAL NEURODEGENERATIVE PATHOLOGY AND NOT WITH SMALL-VESSEL DISEASE , 2017, Alzheimer's & Dementia.
[8] Alan J. Thomas,et al. Parietal white matter lesions in Alzheimer’s disease are associated with cortical neurodegenerative pathology, but not with small vessel disease , 2017, Acta Neuropathologica.
[9] Sébastien Ourselin,et al. Longitudinal segmentation of age‐related white matter hyperintensities , 2017, Medical Image Anal..
[10] M. Jorge Cardoso,et al. Cognitive reserve and TMEM106B genotype modulate brain damage in presymptomatic frontotemporal dementia: a GENFI study , 2017, Brain : a journal of neurology.
[11] M. Jorge Cardoso,et al. The TMEM106B risk allele is associated with lower cortical volumes in a clinically diagnosed frontotemporal dementia cohort , 2017, Journal of Neurology, Neurosurgery, and Psychiatry.
[12] M. Jorge Cardoso,et al. White matter hyperintensities are seen only in GRN mutation carriers in the GENFI cohort , 2017, NeuroImage: Clinical.
[13] Sébastien Ourselin,et al. A multi-time-point modality-agnostic patch-based method for lesion filling in multiple sclerosis , 2016, NeuroImage.
[14] M. Jorge Cardoso,et al. Serum neurofilament light chain protein is a measure of disease intensity in frontotemporal dementia , 2016, Neurology.
[15] Alexandra M. Nicholson,et al. What we know about TMEM106B in neurodegeneration , 2016, Acta Neuropathologica.
[16] B. Dubois,et al. White matter lesions in FTLD: distinct phenotypes characterize GRN and C9ORF72 mutations , 2016, Neurology: Genetics.
[17] John T. O’Brien,et al. This Work Is Licensed under a Creative Commons Attribution 4.0 International License Cortical Tau Load Is Associated with White Matter Hyperintensities , 2022 .
[18] Charles DeCarli,et al. Cognitive correlates of white matter lesion load and brain atrophy , 2015, Neurology.
[19] Daniel Rueckert,et al. Geodesic Information Flows: Spatially-Variant Graphs and Their Application to Segmentation and Fusion , 2015, IEEE Transactions on Medical Imaging.
[20] Veronica Redaelli,et al. Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: a cross-sectional analysis , 2015, The Lancet Neurology.
[21] Frederik Barkhof,et al. More atrophy of deep gray matter structures in frontotemporal dementia compared to Alzheimer's disease. , 2015, Journal of Alzheimer's disease : JAD.
[22] L. Naccache,et al. Extensive white matter involvement in patients with frontotemporal lobar degeneration: think progranulin. , 2014, JAMA neurology.
[23] A. Oliver,et al. A white matter lesion-filling approach to improve brain tissue volume measurements , 2014, NeuroImage: Clinical.
[24] Sébastien Ourselin,et al. Global image registration using a symmetric block-matching approach , 2014, Journal of medical imaging.
[25] Roberto Gasparotti,et al. Effect of TMEM106B polymorphism on functional network connectivity in asymptomatic GRN mutation carriers. , 2014, JAMA neurology.
[26] Robert V Farese,et al. Progranulin: at the interface of neurodegenerative and metabolic diseases , 2013, Trends in Endocrinology & Metabolism.
[27] L. Wahlund,et al. Frontotemporal dementia as a frontostriatal disorder: Neostriatal morphology as a biomarker and structural basis for an endophenotype , 2012, The Australian and New Zealand journal of psychiatry.
[28] J. Morris,et al. Association of TMEM106B gene polymorphism with age at onset in granulin mutation carriers and plasma granulin protein levels. , 2011, Archives of neurology.
[29] D. Geschwind,et al. TMEM106B regulates progranulin levels and the penetrance of FTLD in GRN mutation carriers , 2010, Neurology.
[30] Clifford R. Jack,et al. Patterns of brain atrophy in frontotemporal dementia with mutations in MAPT or PGRN , 2009, Alzheimer's & Dementia.
[31] C. Jack,et al. Prominent phenotypic variability associated with mutations in Progranulin , 2009, Neurobiology of Aging.
[32] N. Raz,et al. Aging white matter and cognition: Differential effects of regional variations in diffusion properties on memory, executive functions, and speed , 2009, Neuropsychologia.
[33] Peter Heutink,et al. Mutations in progranulin (GRN) within the spectrum of clinical and pathological phenotypes of frontotemporal dementia , 2008, The Lancet Neurology.
[34] Niels D Prins,et al. Cerebral small-vessel disease and decline in information processing speed, executive function and memory. , 2005, Brain : a journal of neurology.
[35] B L Miller,et al. Patterns of brain atrophy in frontotemporal dementia and semantic dementia , 2002, Neurology.
[36] K J Rothman,et al. No Adjustments Are Needed for Multiple Comparisons , 1990, Epidemiology.