M
Matthew Nolan
Researcher at King's College London
Publications - 12
Citations - 476
Matthew Nolan is an academic researcher from King's College London. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Neuropathology. The author has an hindex of 7, co-authored 10 publications receiving 372 citations. Previous affiliations of Matthew Nolan include University of Oxford.
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Journal ArticleDOI
Mutations in the vesicular trafficking protein annexin A11 are associated with amyotrophic lateral sclerosis.
Bradley N. Smith,Simon Topp,Claudia Fallini,Hideki Shibata,Han-Jou Chen,Claire Troakes,Andrew P. King,Nicola Ticozzi,Kevin P. Kenna,Athina Soragia-Gkazi,Jack W. Miller,Akane Sato,Diana Marques Dias,Maryangel Jeon,Caroline Vance,Chun Hao Wong,Martina de Majo,Wejdan Kattuah,Jacqueline C. Mitchell,Emma L. Scotter,Nicholas W Parkin,Peter C. Sapp,Matthew Nolan,Peter J. Nestor,Michael A. Simpson,Michael E. Weale,Monkel Lek,Monkel Lek,Frank Baas,J M Vianney de Jong,Anneloor L.M.A. ten Asbroek,Alberto Garcia Redondo,Jesús Esteban-Pérez,Cinzia Tiloca,Federico Verde,Stefano Duga,Nigel Leigh,Hardev Pall,Karen E. Morrison,Ammar Al-Chalabi,Pamela J. Shaw,Janine Kirby,Martin R Turner,Kevin Talbot,Orla Hardiman,Jonathan D. Glass,Jacqueline de Belleroche,Masatoshi Maki,Stephen E. Moss,Christopher C.J. Miller,Cinzia Gellera,Antonia Ratti,Safa Al-Sarraj,Robert H. Brown,Vincenzo Silani,John Landers,Christopher Shaw +56 more
TL;DR: It is concluded that mutations in ANXA11 are associated with ALS and implicate defective intracellular protein trafficking in disease pathogenesis.
Journal ArticleDOI
Pathogenesis of FUS-associated ALS and FTD: insights from rodent models.
TL;DR: The evidence for FUS pathogenicity in ALS/FTD is discussed, the experimental approaches used and phenotypic features of FUS rodent models reported to date are reviewed, and their contribution to the understanding of pathogenic mechanisms are outlined.
Journal ArticleDOI
Dipeptide repeat protein inclusions are rare in the spinal cord and almost absent from motor neurons in C9ORF72 mutant amyotrophic lateral sclerosis and are unlikely to cause their degeneration
Jorge Gomez-Deza,Youn-Bok Lee,Claire Troakes,Matthew Nolan,Safa Al-Sarraj,Jean-Marc Gallo,Christopher Shaw +6 more
TL;DR: TDP-43 cytoplasmic aggregation is the dominant feature of ALS spinal cord pathology irrespective of C9ORF72 mutation status, and the near absence of DPR inclusions in spinal cord motor neurons challenges their contribution to lower motor neuron degeneration in ALS-C9+ve cases.
Journal ArticleDOI
Genome‐wide significant schizophrenia risk variation on chromosome 10q24 is associated with altered cis‐regulation of BORCS7, AS3MT, and NT5C2 in the human brain
Rodrigo R.R. Duarte,Claire Troakes,Matthew Nolan,Deepak Srivastava,Robin M. Murray,Nicholas John Bray,Nicholas John Bray +6 more
TL;DR: This study implicates altered neural expression of BORCS7, AS3MT, and NT5C2 in susceptibility to schizophrenia arising from genetic variation at the chromosome 10q24 locus.
Journal ArticleDOI
ALS-FUS pathology revisited: singleton FUS mutations and an unusual case with both a FUS and TARDBP mutation
Andy King,Andy King,Claire Troakes,Bradley N. Smith,Matthew Nolan,Olimpia Curran,Olimpia Curran,Caroline Vance,Christopher Shaw,Safa Al-Sarraj,Safa Al-Sarraj +10 more
TL;DR: Cases of ALS-FUS are confirmed to be mainly a lower motor neuron disease and to have pathology that does not appear to neatly correlate with clinical features or genetics, and the case with both a FUS and TARDBP mutation reveals an intriguing pathological profile.