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176 results on '"Rossor, M.N."'

1. Preclinical trials in autosomal dominant AD: Implementation of the DIAN-TU trial

Author

Mills, S.M., Mallmann, J., Santacruz, A.M., Fuqua, A., Carril, M., Aisen, P.S., Althage, M.C., Belyew, S., Benzinger, T.L., Brooks, W.S., Buckles, V.D., Cairns, N.J., Clifford, D., Danek, A., Fagan, A.M., Farlow, M., Fox, N., Ghetti, B., Goate, A.M., Heinrichs, D., Hornbeck, R., Jack, C., Jucker, M., Klunk, W.E., Marcus, D.S., Martins, R.N., Masters, C.M., Mayeux, R., McDade, E., Morris, J.C., Oliver, A., Ringman, J.M., Rossor, M.N., Salloway, S., Schofield, P.R., Snider, J., Snyder, P., Sperling, R.A., Stewart, C., Thomas, R.G., Xiong, C., and Bateman, R.J.

Published
2013
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4. Reply: Functional cognitive disorder: dementia's blind spot

Author

Ball, H.A., McWhirter, L., Ballard, C., Bhome, R., Blackburn, D.J., Edwards, M.J., Fox, N.C., Howard, R., Huntley, J., Isaacs, J.D., Larner, A.J., Nicholson, T.R., Pennington, C.M., Poole, N., Price, G., Price, J.P., Reuber, M., Ritchie, C., Rossor, M.N., Schott, J.M., Venneri, A., Stone, J., and Carson, A.J.

Published
2021

6. Disease-related cortical thinning in presymptomatic granulin mutation carriers

Author

Borrego-Écija, S. (Sergi), Sala-Llonch, R. (Roser), Swieten, J.C. (John) van, Borroni, B. (Barbara), Moreno, F. (Fermin), Masellis, M. (Mario), Tartaglia, C. (Carmela), Graff, C. (Caroline), Galimberti, D. (Daniela), Laforce, R. (Robert), Rowe, J.B. (James), Finger, E. (Elizabeth), Vandenberghe, R. (Rik), Tagliavini, F. (Fabrizio), De Mendonça, A. (Alexandre), Santana, I. (Isabel), Synofzik, M. (Matthis), Ducharme, S. (Simon), Levin, J. (Johannes), Danek, A. (Adrian), Gerhard, A. (Alex), Otto, M. (Markus), Butler, C. (Chris), Frisoni, G.B. (Giovanni B.), Sorbi, S. (Sandro), Heller, C. (Carolin), Bocchetta, M. (Martina), Cash, D.M. (David M), Convery, R.S. (Rhian S), Moore, K.M. (Katrina M), Rohrer, J.D. (Jonathan), Sánchez-Valle, R. (Raquel), Rossor, M.N. (Martin N.), Fox, N.C. (Nick), Woollacott, I.O.C. (Ione O.C.), Shafei, R. (Rachelle), Greaves, C. (Caroline), Neason, M. (Mollie), Guerreiro, R. (Rita), Bras, J. (Jose), Thomas, D.L. (David L), Nicholas, J. (Jennifer), Mead, S. (Simon), Meeter, L.H.H. (Lieke), Panman, J.L. (Jessica), Papma, J.M. (Janne), Thornton, A.S. (Andrew), Pijnenburg, Y.A.L. (Yolande), Indakoetxea, B. (Begoña), Gabilondo, A. (Alazne), TaintaMD, M. (Mikel), de Arriba, M. (Maria), Gorostidi, A. (Ana), Zulaica, M. (Miren), Villanua, J. (Jorge), Diaz, Z. (Zigor), Olives, J. (Jaume), Lladó, A. (Albert), Balasa, M. (Mircea), Antonell, A. (Anna), Bargallo, N. (Nuria), Premi, E. (Enrico), Cosseddu, M. (Maura), Gazzina, S. (Stefano), Padovani, A. (Alessandro), Gasparotti, R. (Roberto), Archetti, S. (Silvana), Black, S. (Sandra), Mitchell, S. (Sara), Rogaeva, E. (Ekaterina), Freedman, M. (Morris), Keren, R. (Ron), Tang-Wai, D. (David), Öijerstedt, L. (Linn), Andersson, C. (Christin), Jelic, S. (Svetislav Svetislav), Thonberg, H. (Håkan), Arighi, A. (Andrea), Fenoglio, C. (Chiara), Scarpini MD, E. (Elio), Fumagalli, G. (Giorgio), Cope, T. (Thomas), Timberlake, C. (Carolyn), Rittman, T. (Timothy), Shoesmith, C. (Christen), Bartha, R. (Robart), Rademakers, S. (Suzanne), Wilke, C. (Carlo), Bender, B. (Benjamin), Bruffaerts, R. (Rose), Vandamme, P. (Philip), Vandenbulcke, M. (Mathieu), Maruta, C. (Carolina), Ferreira, C.B. (Catarina B.), Miltenberger, G. (Gabriel), Verdelho, A. (Ana), Afonso, S. (Sónia), Taipa, R. (Ricardo), Caroppo, P. (Paola), Di Fede, G. (Giuseppe), Giaccone, G. (Giorgio), Prioni, S. (Sara), Redaelli, V. (Veronica), Rossi, G. (Giacomina), Tiraboschi, P. (Pietro), Duro, D. (Diana), Rosario Almeida, M. (Maria), Castelo-Branco, M. (Miguel), João Leitão, M. (Maria), Tabuas-Pereira, M. (Miguel), Santiago, B. (Beatriz), Gauthier, S. (Serge), Rosa-Neto, P. (Pedro), Veldsman, M. (Michele), Flanagan, T. (Toby), Prix, C. (Catharina), Hoegen, T. (Tobias), Wlasich, E. (Elisabeth), Loosli, S. (Sandra), Schonecker, S. (Sonja), Semler, E. (Elisa), Anderl-Straub, S. (Sarah), Borrego-Écija, S. (Sergi), Sala-Llonch, R. (Roser), Swieten, J.C. (John) van, Borroni, B. (Barbara), Moreno, F. (Fermin), Masellis, M. (Mario), Tartaglia, C. (Carmela), Graff, C. (Caroline), Galimberti, D. (Daniela), Laforce, R. (Robert), Rowe, J.B. (James), Finger, E. (Elizabeth), Vandenberghe, R. (Rik), Tagliavini, F. (Fabrizio), De Mendonça, A. (Alexandre), Santana, I. (Isabel), Synofzik, M. (Matthis), Ducharme, S. (Simon), Levin, J. (Johannes), Danek, A. (Adrian), Gerhard, A. (Alex), Otto, M. (Markus), Butler, C. (Chris), Frisoni, G.B. (Giovanni B.), Sorbi, S. (Sandro), Heller, C. (Carolin), Bocchetta, M. (Martina), Cash, D.M. (David M), Convery, R.S. (Rhian S), Moore, K.M. (Katrina M), Rohrer, J.D. (Jonathan), Sánchez-Valle, R. (Raquel), Rossor, M.N. (Martin N.), Fox, N.C. (Nick), Woollacott, I.O.C. (Ione O.C.), Shafei, R. (Rachelle), Greaves, C. (Caroline), Neason, M. (Mollie), Guerreiro, R. (Rita), Bras, J. (Jose), Thomas, D.L. (David L), Nicholas, J. (Jennifer), Mead, S. (Simon), Meeter, L.H.H. (Lieke), Panman, J.L. (Jessica), Papma, J.M. (Janne), Thornton, A.S. (Andrew), Pijnenburg, Y.A.L. (Yolande), Indakoetxea, B. (Begoña), Gabilondo, A. (Alazne), TaintaMD, M. (Mikel), de Arriba, M. (Maria), Gorostidi, A. (Ana), Zulaica, M. (Miren), Villanua, J. (Jorge), Diaz, Z. (Zigor), Olives, J. (Jaume), Lladó, A. (Albert), Balasa, M. (Mircea), Antonell, A. (Anna), Bargallo, N. (Nuria), Premi, E. (Enrico), Cosseddu, M. (Maura), Gazzina, S. (Stefano), Padovani, A. (Alessandro), Gasparotti, R. (Roberto), Archetti, S. (Silvana), Black, S. (Sandra), Mitchell, S. (Sara), Rogaeva, E. (Ekaterina), Freedman, M. (Morris), Keren, R. (Ron), Tang-Wai, D. (David), Öijerstedt, L. (Linn), Andersson, C. (Christin), Jelic, S. (Svetislav Svetislav), Thonberg, H. (Håkan), Arighi, A. (Andrea), Fenoglio, C. (Chiara), Scarpini MD, E. (Elio), Fumagalli, G. (Giorgio), Cope, T. (Thomas), Timberlake, C. (Carolyn), Rittman, T. (Timothy), Shoesmith, C. (Christen), Bartha, R. (Robart), Rademakers, S. (Suzanne), Wilke, C. (Carlo), Bender, B. (Benjamin), Bruffaerts, R. (Rose), Vandamme, P. (Philip), Vandenbulcke, M. (Mathieu), Maruta, C. (Carolina), Ferreira, C.B. (Catarina B.), Miltenberger, G. (Gabriel), Verdelho, A. (Ana), Afonso, S. (Sónia), Taipa, R. (Ricardo), Caroppo, P. (Paola), Di Fede, G. (Giuseppe), Giaccone, G. (Giorgio), Prioni, S. (Sara), Redaelli, V. (Veronica), Rossi, G. (Giacomina), Tiraboschi, P. (Pietro), Duro, D. (Diana), Rosario Almeida, M. (Maria), Castelo-Branco, M. (Miguel), João Leitão, M. (Maria), Tabuas-Pereira, M. (Miguel), Santiago, B. (Beatriz), Gauthier, S. (Serge), Rosa-Neto, P. (Pedro), Veldsman, M. (Michele), Flanagan, T. (Toby), Prix, C. (Catharina), Hoegen, T. (Tobias), Wlasich, E. (Elisabeth), Loosli, S. (Sandra), Schonecker, S. (Sonja), Semler, E. (Elisa), and Anderl-Straub, S. (Sarah)

Abstract

Mutations in the granulin gene (GRN) cause familial frontotemporal dementia. Understanding the structural brain changes in presymptomatic GRN carriers would enforce the use of neuroimaging biomarkers for early diagnosis and monitoring. We studied 100 presymptomatic GRN mutation carriers and 94 noncarriers from the Genetic Frontotemporal dementia initiative (GENFI), with MRI structural images. We analyzed 3T MRI structural images using the FreeSurfer pipeline to calculate the whole brain cortical thickness (CTh) for each subject. We also perform a vertex-wise general linear model to assess differences between groups in the relationship between CTh and diverse covariables as gender, age, the estimated years to onset and education. We also explored differences according to TMEM106B genotype, a possible disease modifier. Whole brain CTh did not differ between carriers and noncarriers. Both groups showed age-related cortical thinning. The group-by-age interaction analysis showed that this age-related cortical thinning was significantly greater in GRN carriers in the left superior frontal cortex. TMEM106B did not significantly influence the age-related cortical thinning. Our results validate and expand previous findings suggesting an

Published
2021
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9. Age at symptom onset and death and disease duration in genetic frontotemporal dementia: an international retrospective cohort study

Author

Moore, K.M. Nicholas, J. Grossman, M. McMillan, C.T. Irwin, D.J. Massimo, L. Van Deerlin, V.M. Warren, J.D. Fox, N.C. Rossor, M.N. Mead, S. Bocchetta, M. Boeve, B.F. Knopman, D.S. Graff-Radford, N.R. Forsberg, L.K. Rademakers, R. Wszolek, Z.K. van Swieten, J.C. Jiskoot, L.C. Meeter, L.H. Dopper, E.G. Papma, J.M. Snowden, J.S. Saxon, J. Jones, M. Pickering-Brown, S. Le Ber, I. Camuzat, A. Brice, A. Caroppo, P. Ghidoni, R. Pievani, M. Benussi, L. Binetti, G. Dickerson, B.C. Lucente, D. Krivensky, S. Graff, C. Öijerstedt, L. Fallström, M. Thonberg, H. Ghoshal, N. Morris, J.C. Borroni, B. Benussi, A. Padovani, A. Galimberti, D. Scarpini, E. Fumagalli, G.G. Mackenzie, I.R. Hsiung, G.-Y.R. Sengdy, P. Boxer, A.L. Rosen, H. Taylor, J.B. Synofzik, M. Wilke, C. Sulzer, P. Hodges, J.R. Halliday, G. Kwok, J. Sanchez-Valle, R. Lladó, A. Borrego-Ecija, S. Santana, I. Almeida, M.R. Tábuas-Pereira, M. Moreno, F. Barandiaran, M. Indakoetxea, B. Levin, J. Danek, A. Rowe, J.B. Cope, T.E. Otto, M. Anderl-Straub, S. de Mendonça, A. Maruta, C. Masellis, M. Black, S.E. Couratier, P. Lautrette, G. Huey, E.D. Sorbi, S. Nacmias, B. Laforce, R., Jr Tremblay, M.-P.L. Vandenberghe, R. Damme, P.V. Rogalski, E.J. Weintraub, S. Gerhard, A. Onyike, C.U. Ducharme, S. Papageorgiou, S.G. Ng, A.S.L. Brodtmann, A. Finger, E. Guerreiro, R. Bras, J. Rohrer, J.D. Heller, C. Convery, R.S. Woollacott, I.O. Shafei, R.M. Graff-Radford, J. Jones, D.T. Dheel, C.M. Savica, R. Lapid, M.I. Baker, M. Fields, J.A. Gavrilova, R. Domoto-Reilly, K. Poos, J.M. Van der Ende, E.L. Panman, J.L. Donker Kaat, L. Seelaar, H. Richardson, A. Frisoni, G. Mega, A. Fostinelli, S. Chiang, H.-H. Alberici, A. Arighi, A. Fenoglio, C. Heuer, H. Miller, B. Karydas, A. Fong, J. João Leitão, M. Santiago, B. Duro, D. Ferreira, C. Gabilondo, A. De Arriba, M. Tainta, M. Zulaica, M. Ferreira, C. Semler, E. Ludolph, A. Landwehrmeyer, B. Volk, A.E. Miltenberger, G. Verdelho, A. Afonso, S. Tartaglia, M.C. Freedman, M. Rogaeva, E. Ferrari, C. Piaceri, I. Bessi, V. Lombardi, G. St-Onge, F. Doré, M.-C. Bruffaerts, R. Vandenbulcke, M. Van den Stock, J. Mesulam, M.M. Bigio, E. Koros, C. Papatriantafyllou, J. Kroupis, C. Stefanis, L. Shoesmith, C. Robertson, E. Coppola, G. Da Silva Ramos, E.M. Geschwind, D.

Abstract

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49·5 years (SD 10·0; onset) and 58·5 years (11·3; death) in the MAPT group, 58·2 years (9·8; onset) and 65·3 years (10·9; death) in the C9orf72 group, and 61·3 years (8·8; onset) and 68·8 years (9·7; death) in the GRN group. Mean disease duration was 6·4 years (SD 4·9) in the C9orf72 group, 7·1 years (3·9) in the GRN group, and 9·3 years (6·4) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0·45 between individual and parental age at onset, r=0·63 between individual and mean family age at onset, r=0·58 between individual and parental age at death, and r=0·69 between individual and mean family age at death) than in either the C9orf72 group (r=0·32 individual and parental age at onset, r=0·36 individual and mean family age at onset, r=0·38 individual and parental age at death, and r=0·40 individual and mean family age at death) or the GRN group (r=0·22 individual and parental age at onset, r=0·18 individual and mean family age at onset, r=0·22 individual and parental age at death, and r=0·32 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35–62, for age at onset; 61%, 47–73, for age at death), and even more by family membership (66%, 56–75, for age at onset; 74%, 65–82, for age at death). In the GRN group, only 2% (0–10) of the variability of age at onset and 9% (3–21) of that of age of death was explained by the specific mutation, whereas 14% (9–22) of the variability of age at onset and 20% (12–30) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11–26) of the variability of age at onset and 19% (12–29) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society. © 2020 Elsevier Ltd

Published
2020

12. Mapping the onset and progression of atrophy in familial frontotemporal lobar degeneration

Author

Janssen, J.C., Schott, J.M., Cipolotti, L., Fox, N.C., Scahill, R.I., Josephs, K.A., Stevens, J.M., and Rossor, M.N.

Subjects
Temporal lobes -- Diseases, Temporal lobes -- Genetic aspects, Familial diseases -- Research, Degeneration (Pathology) -- Patient outcomes, Atrophy -- Diagnosis, Atrophy -- Development and progression, Magnetic resonance imaging, Brain mapping, Health, Psychology and mental health
Published
2005

13. Early cognitive decline in Creutzfeldt-Jakob disease associated with human growth hormone treatment

Author

Cordery, R.J., Hall, M., Cipolotti, L., Sarraj, S. Al-, O'Donovan, D.G., Davidson, L., Adlard, P., and Rossor, M.N.

Subjects
Cognition -- Evaluation -- Physiological aspects, Somatotropin -- Influence -- Physiological aspects -- Evaluation, Statistics -- Physiological aspects, Creutzfeldt-Jakob disease -- Evaluation -- Care and treatment, Health, Psychology and mental health, Influence, Evaluation, Care and treatment, Physiological aspects
Abstract

J Neurol Neurosurg Psychiatry 2003;74:1412-1416 Background: Most cases of Creutzfeldt-Jakob disease (CJD) in recipients of human cadaveric growth hormone present with a cerebellar syndrome. Dementia is thought to occur late [...]

Published
2003

14. Transient ischaemic attacks are associated with increased rates of global cerebral atrophy. (Paper)

Author

Walters, R.J.L., Fox, N.C., Schott, J.M., Crum, W.R., Stevens, J.M., Rossor, M.N., and Thomas, D.J.

Subjects
Dementia -- Risk factors -- Physiological aspects -- Psychological aspects, Cerebral ischemia -- Risk factors -- Physiological aspects -- Psychological aspects, Vascular dementia -- Risk factors -- Psychological aspects -- Physiological aspects, Cerebrovascular disease -- Psychological aspects -- Risk factors -- Physiological aspects, Binswanger's disease -- Risk factors -- Psychological aspects -- Physiological aspects, Health, Psychology and mental health, Psychological aspects, Physiological aspects, Risk factors
Abstract

Objectives: To determine whether patients presenting with a first transient ischaemic attack (TIA) subsequently show increased rates of brain atrophy compared with age matched controls; and to assess potential risk [...]

Published
2003

16. Genetics of the dementias

Author

Schott, J.M., Fox, N.C., and Rossor, M.N.

Subjects
Dementia -- Genetic aspects, Prion diseases -- Genetic aspects, Alzheimer's disease -- Genetic aspects, Creutzfeldt-Jakob disease -- Genetic aspects, Health, Psychology and mental health, Genetic aspects
Abstract

While the majority of dementias are sporadic, many diseases causing dementia can also occur on a familial basis. Some of these show an autosomal or sex linked inheritance, In others, [...]

Published
2002

17. Genetic variation across RNA metabolism and cell death gene networks is implicated in the semantic variant of primary progressive aphasia

Author

Bonham, L.W., Steele, N.Z.R., Karch, C.M., Broce, I., Geier, E.G., Wen, N.L., Momeni, P., Hardy, J., Miller, Z.A., Gorno-Tempini, M.L., Hess, C.P., Lewis, P., Miller, B.L., Seeley, W.W., Manzoni, C., Desikan, R.S., Baranzini, S.E., Ferrari, R., Yokoyama, J.S., Hernandez, D.G., Nalls, M.A., Rohrer, J.D., Ramasamy, A., Kwok, J.B.J., Dobson-Stone, C., Schofield, P.R., Halliday, G.M., Hodges, J.R., Piguet, O., Bartley, L., Thompson, E., Haan, E., Hernández, Isabel, Ruiz, A., Boada, M., Borroni, B., Padovani, A., Cruchaga, C., Cairns, N.J., Benussi, L., Binetti, G., Ghidoni, R., Forloni, G., Albani, Diego, Galimberti, D., Fenoglio, C., Serpente, M., Scarpini, E., Clarimón, J., Lleó, Alberto, Blesa, R., Landqvist Waldö, M., Nilsson, K., Nilsson, C., Mackenzie, I.R.A., Hsiung, G.Y.R., Mann, D.M.A., Grafman, J., Morris, C.M., Attems, J., Griffiths, T.D., McKeith, I.G., Thomas, A.J., Pietrini, P., Huey, E.D., Wassermann, E.M., Baborie, A., Jaros, E., Tierney, M.C., Pastor, Pau, Razquin, C., Ortega-Cubero, S., Alonso, E., Perneczky, R., Diehl-Schmid, J., Alexopoulos, P., Kurz, A., Rainero, I., Rubino, E., Pinessi, L., Rogaeva, E., St George-Hyslop, P., Rossi, G., Tagliavini, F., Giaccone, G., Rowe, J.B., Schlachetzki, J.C.M., Uphill, J., Collinge, J., Mead, S., Danek, A., Van Deerlin, V.M., Grossman, M., Trojanowski, J.Q., van der Zee, J., Cruts, M., Van Broeckhoven, C., Cappa, S.F., Leber, I., Hannequin, D., Golfier, V., Vercelletto, M., Brice, A., Nacmias, B., Sorbi, Sandro, Bagnoli, S., Piaceri, I., Nielsen, J.E., Hjermind, L.E., Riemenschneider, M., Mayhaus, M., Ibach, B., Gasparoni, G., Pichler, S., Gu, W., Rossor, M.N., Fox, N.C., Warren, J.D., Spillantini, M.G., Morris, H.R., Rizzu, P., Heutink, P., Snowden, J.S., Rollinson, S., Richardson, A., Gerhard, A., Bruni, A.C., Maletta, R., Frangipane, F., Cupidi, C., Bernardi, L., Anfossi, M., Gallo, M., Conidi, M.E., Smirne, N., Rademakers, R., Baker, M., Dickson, Dennis W., Graff-Radford, N.R., Petersen, R.C., Knopman, D., Josephs, K.A., Boeve, B.F., Parisi, J.E., Karydas, A.M., Rosen, H., van Swieten, J.C., Dopper, E.G.P., Seelaar, H., Pijnenburg, Y.A.L., Scheltens, Philip, Logroscino, G., Capozzo, R., Novelli, V., Puca, A.A., Franceschi, M., Postiglione, A., Milan, G., Sorrentino, P., Kristiansen, M., Chiang, H.H., Graff, C., Pasquier, F., Rollin, A., Deramecourt, V., Lebouvier, T., Kapogiannis, D., Ferrucci, L., Pickering-Brown, S., Singleton, A.B., Universitat Autònoma de Barcelona, Broce, Iris [0000-0003-4932-1430], Miller, Zachary A. [0000-0002-5991-3053], Lewis, Patrick [0000-0003-4537-0489], Baranzini, Sergio E. [0000-0003-0067-194X], Apollo - University of Cambridge Repository, Int FTD-Genomics Consortium, Neurology, Amsterdam Neuroscience - Neurodegeneration, Divisions, and CCA - Imaging and biomarkers

Subjects
0301 basic medicine, Aging, Transcription, Genetic, Gene regulatory network, lcsh:Medicine, Genome-wide association study, Apoptosis, Neurodegenerative, Primary progressive aphasia, Cohort Studies, 0302 clinical medicine, 692/617/375/132, Risk Factors, Databases, Genetic, 2.1 Biological and endogenous factors, Gene Regulatory Networks, Protein Interaction Maps, Aetiology, lcsh:Science, Multidisciplinary, Neurodegeneration, Neurodegenerative diseases, article, Frontotemporal lobar degeneration, 631/208/205, Single Nucleotide, Phenotype, ddc, 3. Good health, DNA-Binding Proteins, Frontotemporal Dementia (FTD), 692/617/375/365, Neurological, Medical genetics, 38/39, Engineering sciences. Technology, Transcription, Biotechnology, medicine.medical_specialty, Computational biology, Biology, Polymorphism, Single Nucleotide, 03 medical and health sciences, Databases, Rare Diseases, Genetic, medicine, Aphasia, Acquired Cognitive Impairment, Genetics, Humans, Primary Progressive Nonfluent Aphasia, Polymorphism, Gene, Genetic association study, International FTD-Genomics Consortium, lcsh:R, Human Genome, Neurosciences, medicine.disease, Brain Disorders, 631/208/199, 030104 developmental biology, Gene Expression Regulation, RNA, lcsh:Q, Dementia, Gene expression, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

The semantic variant of primary progressive aphasia (svPPA) is a clinical syndrome characterized by neurodegeneration and progressive loss of semantic knowledge. Unlike many other forms of frontotemporal lobar degeneration (FTLD), svPPA has a highly consistent underlying pathology composed of TDP-43 (a regulator of RNA and DNA transcription metabolism). Previous genetic studies of svPPA are limited by small sample sizes and a paucity of common risk variants. Despite this, svPPA’s relatively homogenous clinicopathologic phenotype makes it an ideal investigative model to examine genetic processes that may drive neurodegenerative disease. In this study, we used GWAS metadata, tissue samples from pathologically confirmed frontotemporal lobar degeneration, and in silico techniques to identify and characterize protein interaction networks associated with svPPA risk. We identified 64 svPPA risk genes that interact at the protein level. The protein pathways represented in this svPPA gene network are critical regulators of RNA metabolism and cell death, such as SMAD proteins and NOTCH1. Many of the genes in this network are involved in TDP-43 metabolism. Contrary to the conventional notion that svPPA is a clinical syndrome with few genetic risk factors, our analyses show that svPPA risk is complex and polygenic in nature. Risk for svPPA is likely driven by multiple common variants in genes interacting with TDP-43, along with cell death,x` working in combination to promote neurodegeneration.

Published
2019

20. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease

Author

Preische, O., Schultz, S.A., Apel, A., Kuhle, J., Kaeser, S.A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C.L., Martins, R., Schofield, P.R., Rossor, M.N., Graff-Radford, N.R., Salloway, S., Ghetti, B., Ringman, J.M., Noble, J.M., Chhatwal, J., Goate, A.M., Benzinger, T.L.S., Morris, J.C., Bateman, R.J., Wang, G., Fagan, A.M., McDade, E.M., Gordon, B.A., Jucker, M., Allegri, R., Amtashar, F., Bateman, R., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D’Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Lee, J-H, Marcus, D., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Morris, J., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Preische, O., Schultz, S.A., Apel, A., Kuhle, J., Kaeser, S.A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C.L., Martins, R., Schofield, P.R., Rossor, M.N., Graff-Radford, N.R., Salloway, S., Ghetti, B., Ringman, J.M., Noble, J.M., Chhatwal, J., Goate, A.M., Benzinger, T.L.S., Morris, J.C., Bateman, R.J., Wang, G., Fagan, A.M., McDade, E.M., Gordon, B.A., Jucker, M., Allegri, R., Amtashar, F., Bateman, R., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D’Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Lee, J-H, Marcus, D., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Morris, J., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., and Xu, X.

Abstract

Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. Here we leverage the unique characteristics of the Dominantly Inherited Alzheimer Network and ultrasensitive immunoassay technology to demonstrate that NfL levels in the cerebrospinal fluid (n = 187) and serum (n = 405) are correlated with one another and are elevated at the presymptomatic stages of familial Alzheimer’s disease. Longitudinal, within-person analysis of serum NfL dynamics (n = 196) confirmed this elevation and further revealed that the rate of change of serum NfL could discriminate mutation carriers from non-mutation carriers almost a decade earlier than cross-sectional absolute NfL levels (that is, 16.2 versus 6.8 years before the estimated symptom onset). Serum NfL rate of change peaked in participants converting from the presymptomatic to the symptomatic stage and was associated with cortical thinning assessed by magnetic resonance imaging, but less so with amyloid-β deposition or glucose metabolism (assessed by positron emission tomography). Serum NfL was predictive for both the rate of cortical thinning and cognitive changes assessed by the Mini–Mental State Examination and Logical Memory test. Thus, NfL dynamics in serum predict disease progression and brain neurodegeneration at the early presymptomatic stages of familial Alzheimer’s disease, which supports its potential utility as a clinically useful biomarker.

Published
2019

21. Young onset dementia

Author

Sampson, E.L., Warren, J.D., and Rossor, M.N.

Subjects
Dementia -- Care and treatment -- Diagnosis, Health, Diagnosis, Care and treatment
Abstract

Postgrad Med J 2004;80:125-139. doi: 10.1136/pgmj.2003.011171 Young onset dementia is a challenging clinical problem with potentially devastating medical and social consequences. The differential diagnosis is wide, and includes a number [...]

Published
2004

22. Transmission and age-at-onset patterns in familial Alzheimer's disease: evidence for heterogeneity

Author

Farrer, L.A., Myers, R.H., Cupples, L.A., St. George-Hyslop, P.H., Bird, T.D., Rossor, M.N., Mullan, M.J., Polinsky, R., Nee, L., Heston, L., Van Broeckhoven, C., Martin, J-J., Crapper-McLachlan, D., and Growdon, J.H.

Subjects
Alzheimer's disease -- Genetic aspects, Health, Psychology and mental health
Abstract

The majority of cases of Alzheimer's disease (AD) occur sporadically. However, there are some families in which Alzheimer's disease seems to be passed from generation to generation as an inherited trait. Although these cases of familial Alzheimer's disease (FAD) constitute only a small minority, they may provide important clues to the development of the disease in general. Furthermore, there has been some suggestion that even in the sporadic cases which are not, strictly speaking, inherited, there may still be a strong contribution of an individual's genetic makeup to the ultimate development of AD. A study was undertaken to explore in greater detail the mode of inheritance of FAD. Seventy affected family groups were studied, consisting of 541 affected and 1,066 unaffected offspring of parents with AD. Such studies are complicated by the fact that unaffected offspring may simply not be old enough to develop the symptoms of AD, and any investigation of the inheritance of the disorder must use statistical methods to take this possibility into account. Overall, a rate of Alzheimer's disease of 64 percent (by age 87) was observed for the children of parents with FAD. This figure is slightly higher than the 50 percent which would be expected if the disorder were randomly passed from generation to generation as a dominant trait. However, when the families were grouped by average age of onset, a different pattern emerged. By defining 'early-onset' AD as disease symptoms beginning before the age of 58, it was found that the statistics of FAD differed for early- and late-onset disease. In families with early-onset FAD, the rate among offspring of affected parents was 53 percent, very close to the theoretically expected 50 percent. In contrast, among the late-onset families, in which disease symptoms first appeared after the age of 58, the rate of disease among offspring of affected parents was 86 percent, significantly higher. These observations suggest that the early-onset disease may be inherited as a simple dominant trait, while the late-onset disease may have a more complicated mode of inheritance which is not yet understood. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

23. The grasp and other primitive reflexes. (Review: Physical Signs)

Author

Schott, J.M. and Rossor, M.N.

Subjects
Reflexes -- Research, Central nervous system -- Research, Health, Psychology and mental health, Research
Abstract

Primitive reflexes are typically present in childhood, suppressed during normal development, and may reappear with diseases of the brain, particularly those affecting the frontal lobes. In this review we discuss [...]

Published
2003

25. Sequence analysis of tau in familial and sporadic progressive supranuclear palsy. (Short Report)

Author

Morris, H.R., Katzenschlager, R., Janssen, J.C., Brown, J.M., Ozansoy, M., Quinn, N., Revesz, T., Rossor, M.N., Daniel, S.E., Wood, N.W., and Lees, A.J.

Subjects
Familial diseases -- Research -- Genetic aspects, Neurofibrils -- Physiological aspects -- Research, Parkinson's disease -- Genetic aspects -- Research, Progressive supranuclear palsy -- Genetic aspects -- Research, Health, Psychology and mental health, Physiological aspects, Research, Genetic aspects
Abstract

Progressive supranuclear palsy (PSP) is a tau deposition neurodegenerative disorder which usually occurs in sporadic form and is associated with a common variant of the tau gene. Rare familial forms [...]

Published
2002

26. [Accepted Manuscript] Presymptomatic atrophy in autosomal dominant Alzheimer's disease: A serial MRI study

Author

Kinnunen, K.M., Cash, D.M., Poole, T., Frost, C., Benzinger, T.L.S., Ahsan, R.L., Leung, K.K., Cardoso, M.J., Modat, M., Malone, I.B., Morris, J.C., Bateman, R.J., Marcus, D.S., Goate, A., Salloway, S., Correia, S., Sperling, R.A., Chhatwal, J.P., Mayeux, R., Brickman, A.M., Martins, R.N., Farlow, M.R., Ghetti, B., Saykin, A.J., Jack, C.R. Jr, Schofield, P.R., McDade, E., Weiner, M.W., Ringman, J.M., Thompson, P.M., Masters, C.L., Rowe, C.C., Rossor, M.N., Ourselin, S., Fox, N.C., and Dominantly Inherited Alzheimer Network (DIAN), .

Subjects
sense organs, skin and connective tissue diseases
Abstract

Identifying at what point atrophy rates first change in Alzheimer's disease is important for informing design of presymptomatic trials. Serial T1-weighed magnetic resonance imaging scans of 94 participants (28 noncarriers, 66 carriers) from the Dominantly Inherited Alzheimer Network were used to measure brain, ventricular, and hippocampal atrophy rates. For each structure, nonlinear mixed-effects models estimated the change-points when atrophy rates deviate from normal and the rates of change before and after this point. Atrophy increased after the change-point, which occurred 1-1.5 years (assuming a single step change in atrophy rate) or 3-8 years (assuming gradual acceleration of atrophy) before expected symptom onset. At expected symptom onset, estimated atrophy rates were at least 3.6 times than those before the change-point. Atrophy rates are pathologically increased up to seven years before "expected onset". During this period, atrophy rates may be useful for inclusion and tracking of disease progression.

Published
2017

27. The cultural context of visual hallucinations

Author

Knight, W.D., Fox, N.C., Rossor, M.N., and Warren, J.D.

Subjects
Hallucinations and illusions -- Care and treatment, Social values -- Influence, Health
Published
2008

28. Prion dementia without characteristic pathology

Author

Collinge, J., Owen, F., Poulter, M., Leach, M., Crow, T.J., Rossor, M.N., Hardy, J., Mullan, M.J., Janota, I., and Lantos, P.L.

Subjects
Nervous system diseases -- Diagnosis, Spongiform encephalopathy -- Genetic aspects, Dementia -- Genetic aspects
Published
1990

29. RATIONAL IMAGING Suspected early dementia

Author

Schott, J.M., Warren, J.D., Barkhof, F., Rossor, M.N., Fox, N.C., Radiology and nuclear medicine, Neurology, and NCA - Neurodegeneration

Published
2011

33. Preface

Author

Emson, P.C., primary, Rossor, M.N., additional, and Tohyama, M., additional

Published
1986
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35. Seeing what Alzheimer saw--with magnetic resonance microscopy

Author

Fox, N.C. and Rossor, M.N.

Abstract

The search for methods to detect in vivo the histopathology of Alzheimer disease moves a step closer with a recent demonstration that amyloid plaques in autopsy specimens can be visualized with magnetic resonance microscopy., Author(s): N.C. Fox [1]; M.N. Rossor [1] Alzheimer disease is the most common cause of dementia, particularly in the elderly. As such, it represents a major medical challenge; some 15 [...]

Published
2000
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36. Neurofilament inclusion body disease: a new proteinopathy?

Author

Josephs, K.A., Holton, J.L., Rossor, M.N., Braendgaard, H., Ozawa, T., Fox, N.C., Petersen, R.C., Pearl, G.S., Ganguly, M., Rosa, P., Laursen, H., Parisi, J.E., Waldemar, G., Quinn, N.P., Dickson, D.W., and Revesz, T.

Published
2003

37. Erratum to “Preclinical trials in autosomal dominant AD: Implementation of the DIAN-TU trial” [Rev. Neurol. 169 (10) (2013) 737–743]

Author

Mills, S.M., primary, Mallmann, J., additional, Santacruz, A.M., additional, Fuqua, A., additional, Carril, M., additional, Aisen, P.S., additional, Althage, M.C., additional, Belyew, S., additional, Benzinger, T.L., additional, Brooks, W.S., additional, Buckles, V.D., additional, Cairns, N.J., additional, Clifford, D., additional, Danek, A., additional, Fagan, A.M., additional, Farlow, M., additional, Fox, N., additional, Ghetti, B., additional, Goate, A.M., additional, Heinrichs, D., additional, Hornbeck, R., additional, Jack, C., additional, Jucker, M., additional, Klunk, W.E., additional, Marcus, D.S., additional, Martins, R.N., additional, Masters, C.M., additional, Mayeux, R., additional, McDade, E., additional, Morris, J.C., additional, Oliver, A., additional, Ringman, J.M., additional, Rossor, M.N., additional, Salloway, S., additional, Schofield, P.R., additional, Snider, J., additional, Snyder, P., additional, Sperling, R.A., additional, Stewart, C., additional, Thomas, R.G., additional, Xiong, C., additional, and Bateman, R.J., additional

Published
2013
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39. FUS pathology defines the majority of tau-and TDP-43-negative frontotemporal lobar degeneration

Author

Urwin, H. (Hazel), Josephs, K.A. (Keith), Rohrer, J.D. (Jonathan), Mackenzie, I.R.A. (Ian), Neumann, H.A.M. (Martino), Authier, A. (Astrid), Seelaar, H. (Harro), Swieten, J.C. (John) van, Brown, J.M. (Jeremy), Johannsen, P. (Peter), Nielsen, J.E. (Jorgen), Holm, I.E. (Ida), Dickson, D. (Dennis), Rademakers, R. (Rosa), Graff-Radford, N.R. (Neill), Parisi, J.E. (Joseph), Petersen, R.C. (Ronald), Hatanpaa, K.J. (Kimmo), White III, C.L. (Charles), Geser, F. (Felix), Deerlin, V.M. (Vivianna), Weiner, M.F. (Myron), Trojanowski, J.Q. (John), Miller, B.L. (Bruce Lars), Seeley, W. (William), Zee, J. (Jill) van der, Kumar-Singh, S. (Samir), Engelborghs, S. (Sebastiaan), Deyn, P.P. (Peter) de, Broeckhoven, C. (Christine) van, Bigio, E.H. (Eileen), Deng, H-X. (Han-Xiang), Halliday, G.M. (Glenda Margaret), Kril, J.J. (Jillian), Munoz, D.G. (David), Mann, D. (David), Pickering-Brown, S. (Stuart), Doodeman, V. (Valerie), Adamson, G. (Gary), Ghazi-Noori, S. (Shabnam), Fisher, E.M.C. (Elizabeth), Holton, J.L. (Janice), Revesz, T. (Tamas), Rossor, M.N. (Martin), Collinge, J. (John), Mead, S. (Simon), Isaacs, A.M. (Adrian), Urwin, H. (Hazel), Josephs, K.A. (Keith), Rohrer, J.D. (Jonathan), Mackenzie, I.R.A. (Ian), Neumann, H.A.M. (Martino), Authier, A. (Astrid), Seelaar, H. (Harro), Swieten, J.C. (John) van, Brown, J.M. (Jeremy), Johannsen, P. (Peter), Nielsen, J.E. (Jorgen), Holm, I.E. (Ida), Dickson, D. (Dennis), Rademakers, R. (Rosa), Graff-Radford, N.R. (Neill), Parisi, J.E. (Joseph), Petersen, R.C. (Ronald), Hatanpaa, K.J. (Kimmo), White III, C.L. (Charles), Geser, F. (Felix), Deerlin, V.M. (Vivianna), Weiner, M.F. (Myron), Trojanowski, J.Q. (John), Miller, B.L. (Bruce Lars), Seeley, W. (William), Zee, J. (Jill) van der, Kumar-Singh, S. (Samir), Engelborghs, S. (Sebastiaan), Deyn, P.P. (Peter) de, Broeckhoven, C. (Christine) van, Bigio, E.H. (Eileen), Deng, H-X. (Han-Xiang), Halliday, G.M. (Glenda Margaret), Kril, J.J. (Jillian), Munoz, D.G. (David), Mann, D. (David), Pickering-Brown, S. (Stuart), Doodeman, V. (Valerie), Adamson, G. (Gary), Ghazi-Noori, S. (Shabnam), Fisher, E.M.C. (Elizabeth), Holton, J.L. (Janice), Revesz, T. (Tamas), Rossor, M.N. (Martin), Collinge, J. (John), Mead, S. (Simon), and Isaacs, A.M. (Adrian)

Abstract

Through an international consortium, we have collected 37 tau-and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. This FTLD-FUS

Published
2010
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41. The genetic causes of basal ganglia calcification, dementia, and bone cysts: DAP12 and TREM2

Author

Bianchin, M. M., primary, Lima, J. E., additional, Natel, J., additional, Sakamoto, A. C., additional, Klunemann, H., additional, Ridha, B.H., additional, Magy, L., additional, Wherrett, J.R., additional, Hemelsoet, D.M., additional, Keen, R.W., additional, DeBleecker, J.L., additional, Rossor, M.N., additional, Marienhagen, J., additional, Klein, H.E., additional, Peltonen, L., additional, and Paloneva, J., additional

Published
2006
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42. Potassium channel antibody associated encephalitis: a potentially treatable non-paraneoplastic limbic encephalitis

Author

Schott, J.M., Vincent, A., Clover, L., Buckley, C., Gabel, A., Lang, B., Omer, S., Bien, C.G., Palace, J., and Rossor, M.N.

Subjects
Encephalitis -- Research -- Care and treatment, Health, Psychology and mental health, Care and treatment, Research
Abstract

Background: Three cases of non-paraneoplastic reversible limbic encephalitis (LE) associated with voltage-gated potassium channel antibodies (VGKC-Ab) have previously been reported. We aimed to define the phenotypic features of this syndrome [...]

Published
2004

44. New year, new editorial team

Author

Rossor, M.N. and Hanna, M.G.

Subjects
Health, Psychology and mental health
Abstract

The New Year brings a change of editorship; after seven years of exceptional custodianship the journal says goodbye to Professor Chris Kennard. During his tenure he has maintained the key [...]

Published
2004

45. Cerebral and cerebellar atrophy on serial magnetic resonance imaging in an initially symptom free subject at risk of familial prion disease

Author

Fox, N.C., Freeborough, P.A>, Mekkaoui, K.F., Stevens, J.M., and Rossor, M.N.

Subjects
Magnetic resonance imaging -- Case studies, Creutzfeldt-Jakob disease -- Case studies, Health, Case studies
Abstract

Prion diseases are transmissible neurodegenerative conditions which occur in sporadic, acquired, or inherited forms. Sporadic Creutzfeldt-Jakob disease presents as a rapidly progressive dementia with myoclonus, most patients showing characteristic pseudoperiodic [...]

Published
1997

49. Early onset familial Alzheimer's disease: mutation frequency in 31 families. (ABN Abstracts)

Author

Janssen, J.C., Beck, J.A., Campbell, T.A., Dickinson, A., Fox, N.C., Harvey, R.J., Houlden, H., Rossor, M.N., and Collinge, J.

Subjects
Neurology -- Research, Health, Psychology and mental health, Research
Abstract

Background: Three causative genes have been identified for autosomal dominant Alzheimer's disease (AD): the amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) genes. In addition a risk [...]

Published
2002

50. Mapping the evolution of regional atrophy in Alzheimer's disease using fluid registered MRI. (ABN Abstracts)

Author

Schott, J.M., Scahill, R.I., Stevens, J.M., Rossor, M.N., and Fox, N.C.

Subjects
Atrophy -- Development and progression, Magnetic resonance imaging, Alzheimer's disease -- Development and progression, Health, Psychology and mental health, Development and progression
Abstract

Objective: To assess altering patterns of significant regional atrophy during the progression of Alzheimer's disease (AD). Methods: Patients with presymptomatic AD (n=4), mild AD (n=10) and moderate AD (n=12) were [...]

Published
2002

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