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Christopher C.J. Miller
Researcher at King's College London
Publications - 128
Citations - 16180
Christopher C.J. Miller is an academic researcher from King's College London. The author has contributed to research in topics: Phosphorylation & Amyloid precursor protein. The author has an hindex of 58, co-authored 124 publications receiving 14501 citations. Previous affiliations of Christopher C.J. Miller include Medical Research Council & University of Cambridge.
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Journal ArticleDOI
TDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis
Jemeen Sreedharan,Ian P. Blair,Vineeta B. Tripathi,Xun Hu,Caroline Vance,Boris Rogelj,Steven Ackerley,Steven Ackerley,Jennifer C Durnall,Kelly L. Williams,Emanuele Buratti,Francisco E. Baralle,Jacqueline de Belleroche,J. Douglas Mitchell,P. Nigel Leigh,Ammar Al-Chalabi,Christopher C.J. Miller,Christopher C.J. Miller,Garth A. Nicholson,Garth A. Nicholson,Christopher Shaw +20 more
TL;DR: The evidence suggests a pathophysiological link between TDP-43 and ALS, and neighboring mutations in a highly conserved region of TARDBP in sporadic and familial ALS cases.
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Mutations in FUS, an RNA Processing Protein, Cause Familial Amyotrophic Lateral Sclerosis Type 6
Caroline Vance,Boris Rogelj,Tibor Hortobágyi,Kurt J. De Vos,Agnes L. Nishimura,Jemeen Sreedharan,Xun Hu,Bradley N. Smith,Deborah Ruddy,Paul Wright,Jeban Ganesalingam,Kelly L. Williams,Vineeta B. Tripathi,Safa Al-Saraj,Ammar Al-Chalabi,P. Nigel Leigh,Ian P. Blair,Garth A. Nicholson,Garth A. Nicholson,Jackie de Belleroche,Jean-Marc Gallo,Christopher C.J. Miller,Christopher C.J. Miller,Christopher Shaw +23 more
TL;DR: A missense mutation in the gene encoding fused in sarcoma (FUS) in a British kindred, linked to ALS6, is identified, which suggests that a common mechanism may underlie motor neuron degeneration.
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Role of Axonal Transport in Neurodegenerative Diseases
TL;DR: The role of axonal transport in neurodegenerative disease is reviewed and disruption of axon transport is an early and perhaps causative event in many of these diseases.
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Evidence of widespread cerebral microglial activation in amyotrophic lateral sclerosis: an [11C](R)-PK11195 positron emission tomography study
Martin R Turner,Annachiara Cagnin,Federico Turkheimer,Federico Turkheimer,Christopher C.J. Miller,Christopher Shaw,David J. Brooks,Peter Leigh,Richard B. Banati,Richard B. Banati +9 more
TL;DR: The findings indicate that cerebral microglial activation can be detected in vivo during the evolution of ALS, and support the previous observations that cerebral pathology is widespread, and argue for the development of therapeutic strategies aimed at inflammatory pathways.
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ER–mitochondria associations are regulated by the VAPB–PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43
Radu Stoica,Kurt J. De Vos,Kurt J. De Vos,Sebastien Paillusson,Sarah M. Mueller,Rosa M. Sancho,Kwok-Fai Lau,Kwok-Fai Lau,Gema Vizcay-Barrena,Wen Lang Lin,Ya Fei Xu,Jada Lewis,Dennis W. Dickson,Leonard Petrucelli,Jacqueline C. Mitchell,Christopher Shaw,Christopher C.J. Miller +16 more
TL;DR: It is demonstrated that the ER-resident protein VAPB interacts with the mitochondrial protein tyrosine phosphatase-interacting protein-51 (PTPIP51) to regulate ER–mitochondria associations and that TDP-43, a protein pathologically linked to amyotrophic lateral sclerosis and fronto-temporal dementia perturbs ER–Mitochondria interactions.