J
Joanne Betts
Researcher at Newcastle University
Publications - 8
Citations - 1773
Joanne Betts is an academic researcher from Newcastle University. The author has contributed to research in topics: Mitochondrial DNA & Neural stem cell. The author has an hindex of 7, co-authored 8 publications receiving 1647 citations. Previous affiliations of Joanne Betts include University College London & University of Newcastle.
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Journal ArticleDOI
High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease.
Andreas Bender,Kim J. Krishnan,Christopher Morris,Geoffrey A. Taylor,Amy K. Reeve,Robert H. Perry,Evelyn Jaros,Joshua S Hersheson,Joanne Betts,Thomas Klopstock,Robert W. Taylor,Douglass M. Turnbull +11 more
TL;DR: It is shown that in substantia nigra neurons from both aged controls and individuals with Parkinson disease, there is a high level of deleted mitochondrial DNA, suggesting that somatic mtDNA deletions are important in the selective neuronal loss observed in brain aging and in Parkinson disease.
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Molecular neuropathology of MELAS: level of heteroplasmy in individual neurones and evidence of extensive vascular involvement
Joanne Betts,Evelyn Jaros,Robert H. Perry,Andrew M. Schaefer,Robert W. Taylor,Zeinab Abdel-All,Robert N. Lightowlers,D.M. Turnbull +7 more
TL;DR: It is proposed that coupling of the vascular mitochondrial dysfunction with cortical spreading depression (CSD) might underlie the selective distribution of ischaemic lesions in the posterior cortex in MELAS patients.
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Mitochondrial DNA damage in non-melanoma skin cancer
TL;DR: This work provides the first quantitative data for the incidence of the common deletion as well as the first report of specific tandem duplications in tumours from any tissue, and shows that there are clear differences in the distribution of deletions between the tumour and the histologically normal perilesional skin.
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Inhibition of oxidative metabolism leads to p53 genetic inactivation and transformation in neural stem cells
Stefano Bartesaghi,Vincenzo Graziano,Sara Galavotti,Nick V. Henriquez,Joanne Betts,Jayeta Saxena,Valentina Minieri,A Deli,Anna Karlsson,L. Miguel Martins,Melania Capasso,Pierluigi Nicotera,Sebastian Brandner,Vincenzo De Laurenzi,Paolo Salomoni +14 more
TL;DR: In this paper, the p53 tumor suppressor is genetically inactivated in a large proportion of high grade glioma (HGG) cases, which is caused by increased reactive oxygen species and associated oxidative DNA damage.
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Neuropathological aspects of mitochondrial DNA disease.
TL;DR: Important features from neuropathological studies available are detailed and deficiencies that are currently limiting the understanding of mitochondrial DNA disease are highlighted.