Edward Wild (neuroscientist)

Last updated
Prof Edward John Wild
Prof Edward Wild in Toronto, May 2023.jpg
Edward Wild in May 2023
Born
UK
NationalityBritish
Alma mater Christ's College, Cambridge (1996–2001)
University College London (2005–2008)
Known forHuntington's disease research and outreach
Awards Huntington's Disease Society of America Researcher of the Year, 2014;
Huntington Society of Canada Community Leadership Award, 2013;
Huntington Study Group Insight of the Year, 2015.
Scientific career
Fields Neuroscience
Institutions UCL Institute of Neurology;
National Hospital for Neurology and Neurosurgery
Thesis Identification and evaluation of biomarkers for Huntington's disease  (2009)
Doctoral advisor Sarah Tabrizi
Website edwild.com

Edward Wild, also known as Ed Wild, is a British neurologist and neuroscientist in the field of Huntington's disease and an advocate for scientific outreach to the public. [1] He co-founded the Huntington's research news platform HDBuzz in 2010. [2] He is a professor of neurology at UCL Institute of Neurology and is an associate director of the UCL Huntington's Disease Centre. [3] He is also a consultant neurologist at the National Hospital for Neurology and Neurosurgery in London. [4]

Contents

Career

Wild studied medicine at Christ's College, Cambridge. [5] In his early career, he studied and published on the neurological phenomenon of déjà vu. [6] He undertook a PhD, supervised by professor Sarah Tabrizi, at the UCL Institute of Neurology, Queen Square, London, [7] during which he published research on biomarkers for Huntington's disease using magnetic resonance imaging measures of brain atrophy [8] [9] [10] [11] and biochemical analysis of blood. [12] [13] Wild and Tabrizi continue to work together at the UCL Huntington's Disease Centre. [14]

Wild and colleagues described a novel pathogenic pathway of immune activation in Huntington's [15] [16] which later became the basis of clinical trials of immune-targeted therapies. [17] In 2015, he published the first successful detection and quantification of mutant huntingtin protein (the known cause of Huntington's) in human cerebrospinal fluid, using a novel 'single-molecule counting' immunoassay. This finding was noted as a 'research highlight' by Nature Reviews Neurology and won Wild the Huntington Study group 'Insight of the Year' award in 2015. [18] [19] [20] He has also published novel genetic causes of 'phenocopy' syndromes that mimic Huntington's disease. [21] [22]

Wild's research since 2017 has focused on the potential of neurofilament light and mutant huntingtin protein [23] [24] as biomarkers for Huntington's disease onset and progression. His work has shown that NFL has better prognostic value in Huntington's disease, but that mutant huntingtin might be a valuable marker for early and sensitive detection of change in clinical huntingtin-lowering trials. [25] [24] He was a senior investigator in the clinical programme studying the antisense oligonucleotide tominersen to lower mutant huntingtin production in HD, [26] and gave the first dose of the drug to a patient in 2015. [27] [28] [29]

He serves on the Medical Advisory Panel of the UK Huntington's Disease Association, [2] the Editorial Board of the Journal of Huntington's Disease, [30] the Association of British Neurologists Neurogenetics Advisory Panel, [31] and the Translational Neurology Panel of the European Academy of Neurology. [32] He is a member of the Executive Committee of the European Huntington's Disease Network [33] and Co-lead facilitator of the Network’s Biomarkers Working Group. [34] He is a founder member of the advisory panel to the UK All-Party Parliamentary Group on Huntington's disease. [35] [36]

He was promoted to professor of neurology in October 2020, in the UCL Faculty of Brain Sciences. [37] As of September 2022, Wild has authored 7 book chapters [3] and 150 peer-reviewed publications with over 12,000 citations. [38]

Public engagement work

In 2010, with Jeff Carroll, Wild founded HDBuzz, an online source of accessible news about Huntington's disease research, [39] [40] that has received awards from patient advocacy groups. [41] He said he helped establish HDBuzz to provide tempered research news to counter the hype of medical press releases about HD. [42] He has commented that common online opinions that people with Huntington's disease should not be allowed to have children "borders on historical eugenics-type thinking". [43] He has described Huntington's as "the most curable incurable brain disorder" because of the possibility of targeting treatments to its known genetic cause. [44] [45]

Wild appeared in the documentary feature film The Inheritance [46] [47] and was a judge for the 2015 British Library / Europe PubMed Central 'Access to Understanding' contest for science writers. [48] He has appeared on the BBC Radio Naked Scientists programme. [49] In July 2016, he appeared on BBC Radio 4's Woman's Hour programme talking about Huntington's disease with Jenni Murray. [50] In December 2017, he appeared on RTE Radio 1 talking about Huntington's disease treatments. [51] In 2020, he appeared in the Ken Burns PBS documentary The Gene: An Intimate History. [52] [53]

In 2021, he wrote the afterword of Patient 1, [54] a book by Charlotte Raven about her experiences with Huntington's disease, including her participation on the trial of the experimental drug tominersen. [29] Wild is Raven's doctor and injected her with the first dose of tominersen on the Gen-Peak trial. [29]

Personal life

Wild lives in East London with his partner Joel. They have a cat and a chihuahua, Riley. [29]

Awards and honours

Related Research Articles

Anita Elizabeth Harding was an Irish-British neurologist, and Professor of Clinical Neurology at the Institute of Neurology of the University of London. She is known for the discovery with Ian Holt and John Morgan-Hughes of the "first identification of a mitochondrial DNA mutation in human disease and the concept of tissue heteroplasmy of mutant mitochondrial DNA", published in Nature in 1986. In 1985 she established the first neurogenetics research group in the United Kingdom at the UCL Institute of Neurology.

<span class="mw-page-title-main">Huntington's disease</span> Inherited neurodegenerative disorder

Huntington's disease (HD), also known as Huntington's chorea, is an incurable neurodegenerative disease that is mostly inherited. The earliest symptoms are often subtle problems with mood or mental/psychiatric abilities. A general lack of coordination and an unsteady gait often follow. It is also a basal ganglia disease causing a hyperkinetic movement disorder known as chorea. As the disease advances, uncoordinated, involuntary body movements of chorea become more apparent. Physical abilities gradually worsen until coordinated movement becomes difficult and the person is unable to talk. Mental abilities generally decline into dementia, depression, apathy, and impulsivity at times. The specific symptoms vary somewhat between people. Symptoms usually begin between 30 and 50 years of age, and can start at any age but are usually seen around the age of 40. The disease may develop earlier in each successive generation. About eight percent of cases start before the age of 20 years, and are known as juvenile HD, which typically present with the slow movement symptoms of Parkinson's disease rather than those of chorea.

Chorea is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias. The term chorea is derived from the Ancient Greek: χορεία, as the quick movements of the feet or hands are comparable to dancing.

Neurofilaments (NF) are classed as type IV intermediate filaments found in the cytoplasm of neurons. They are protein polymers measuring 10 nm in diameter and many micrometers in length. Together with microtubules (~25 nm) and microfilaments (7 nm), they form the neuronal cytoskeleton. They are believed to function primarily to provide structural support for axons and to regulate axon diameter, which influences nerve conduction velocity. The proteins that form neurofilaments are members of the intermediate filament protein family, which is divided into six types based on their gene organization and protein structure. Types I and II are the keratins which are expressed in epithelia. Type III contains the proteins vimentin, desmin, peripherin and glial fibrillary acidic protein (GFAP). Type IV consists of the neurofilament proteins NF-L, NF-M, NF-H and α-internexin. Type V consists of the nuclear lamins, and type VI consists of the protein nestin. The type IV intermediate filament genes all share two unique introns not found in other intermediate filament gene sequences, suggesting a common evolutionary origin from one primitive type IV gene.

<span class="mw-page-title-main">Huntingtin</span> Gene and protein involved in Huntingtons disease

Huntingtin(Htt) is the protein coded for in humans by the HTT gene, also known as the IT15 ("interesting transcript 15") gene. Mutated HTT is the cause of Huntington's disease (HD), and has been investigated for this role and also for its involvement in long-term memory storage.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

<span class="mw-page-title-main">Neurofilament light polypeptide</span> Protein-coding gene in the species Homo sapiens

Neurofilament light polypeptide, also known as neurofilament light chain, abbreviated to NF-L or Nfl and with the HGNC name NEFL is a member of the intermediate filament protein family. This protein family consists of over 50 human proteins divided into 5 major classes, the Class I and II keratins, Class III vimentin, GFAP, desmin and the others, the Class IV neurofilaments and the Class V nuclear lamins. There are four major neurofilament subunits, NF-L, NF-M, NF-H and α-internexin. These form heteropolymers which assemble to produce 10nm neurofilaments which are only expressed in neurons where they are major structural proteins, particularly concentrated in large projection axons. Axons are particularly sensitive to mechanical and metabolic compromise and as a result axonal degeneration is a significant problem in many neurological disorders. The detection of neurofilament subunits in CSF and blood has therefore become widely used as a biomarker of ongoing axonal compromise. The NF-L protein is encoded by the NEFL gene. Neurofilament light chain is a biomarker that can be measured with immunoassays in cerebrospinal fluid and plasma and reflects axonal damage in a wide variety of neurological disorders. It is a useful marker for disease monitoring in amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease, and more recently Huntington's disease. It is also promising marker for follow-up of patients with brain tumors. Higher levels of blood or CSF NF-L have been associated with increased mortality, as would be expected as release of this protein reflects ongoing axonal loss. Recent work performed as a collaboration between EnCor Biotechnology Inc. and the University of Florida showed that the NF-L antibodies employed in the most widely used NF-L assays are specific for cleaved forms of NF-L generated by proteolysis induced by cell death. Methods used in different studies for NfL measurement are sandwich enzyme-linked immunosorbent assay (ELISA), electrochemiluminescence, and high-sensitive single molecule array (SIMOA).

Pridopidine is an orally administrated small molecule investigational drug. Pridopidine is a selective and potent Sigma-1 Receptor agonist. It is being developed by Prilenia Therapeutics and is currently in late-stage clinical development for Huntington’s disease (HD) and Amyotrophic Lateral Sclerosis (ALS).

<span class="mw-page-title-main">Charles Sabine</span>

Charles Edward Sabine, is an Emmy Award-winning television journalist who worked for the US Network NBC News for twenty-six years, before becoming a global spokesman for patients and families with degenerative brain diseases. He is active throughout advocacy and charity sectors across four continents and founder of the Hidden No More Foundation. He has 2 children, Roman and Sabrina.

The Hereditary Disease Foundation (HDF) aims to cure genetic disorders, notably Huntington's disease, by supporting basic biomedical research.

Clinical neuroscience is a branch of neuroscience that focuses on the scientific study of fundamental mechanisms that underlie diseases and disorders of the brain and central nervous system. It seeks to develop new ways of conceptualizing and diagnosing such disorders and ultimately of developing novel treatments.

<span class="mw-page-title-main">Jeff Carroll</span>

Jeffrey Bryan Carroll is an American scientific researcher in the field of Huntington's disease (HD). As a carrier of the abnormal gene that causes HD, he is also a public advocate for families affected by the disease, and co-founder of the HD research news platform HDBuzz. His life and work were the subject of a 2011 Gemini award-nominated CBC documentary feature. Carroll is an Associate Professor of neuroscience in the Department of Psychology at Western Washington University.

<span class="mw-page-title-main">Sarah Tabrizi</span> British neurologist and neuroscientist

Sarah Joanna Tabrizi FMedSci is a British neurologist and neuroscientist in the field of neurodegeneration, particularly Huntington's disease. She is a Professor and Joint Head of the Department of Neurodegenerative Diseases at the UCL Institute of Neurology; the founder and Director of the UCL Huntington's Disease Centre; a Principal Investigator at the UK Dementia Research Institute at UCL; and an Honorary Consultant Neurologist at the National Hospital for Neurology and Neurosurgery, Queen Square, London, where she established the Multidisciplinary Huntington's Disease Clinic. The UCL Huntington’s Disease Centre was officially opened on 1 March 2017 by UCL President and Provost Professor Michael Arthur.

Huntington's disease-like syndromes are a family of inherited neurodegenerative diseases that closely resemble Huntington's disease (HD) in that they typically produce a combination of chorea, cognitive decline or dementia and behavioural or psychiatric problems.

Mary M. Reilly FRCP is an Irish neurologist who works at National Hospital for Neurology and Neurosurgery. She studies peripheral neuropathy. She is the President of the Association of British Neurologists.

Michelle Gray is an American neuroscientist and assistant professor of neurology and neurobiology at the University of Alabama Birmingham. Gray is a researcher in the study of the biological basis of Huntington's disease (HD). In her postdoctoral work, she developed a transgenic mouse line, BACHD, that is now used worldwide in the study of HD. Gray's research now focuses on the role of glial cells in HD. In 2020 Gray was named one of the 100 Inspiring Black Scientists in America by Cell Press. She is also a member of the Hereditary Disease Foundation’s scientific board.

The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons. The NVU addresses the brain's unique dilemma of having high energy demands yet low energy storage capacity. In order to function properly, the brain must receive substrates for energy metabolism–mainly glucose–in specific areas, quantities, and times. Neurons do not have the same ability as, for example, muscle cells, which can use up their energy reserves and refill them later; therefore, cerebral metabolism must be driven in the moment. The neurovascular unit facilitates this ad hoc delivery and, thus, ensures that neuronal activity can continue seamlessly.

Hilal Lashuel is an American-Yemeni neuroscientist and chemist, currently an associate professor at the EPFL. His research focuses on protein misfolding and aggregation in the pathogenesis of Alzheimer's and Parkinson's diseases.

<span class="mw-page-title-main">Bernhard Landwehrmeyer</span> German neurologist and neuroscientist (born 1960)

Georg Bernhard Landwehrmeyer FRCP is a German neurologist and neuroscientist in the field of neurodegeneration primarily focusing on Huntington's disease. Landwehrmeyer is a professor of neurology at Ulm University Hospital. He was one of the founders of the European Huntington's Disease Network (EHDN) in 2004 and was chairman of its executive committee until 2014.

Dimitri Krainc, MD, PhD, is the Aaron Montgomery Ward Professor and Chairman of the Ken & Ruth Davee Department of Neurology and Director of the Simpson Querrey Center for Neurogenetics at Northwestern University Feinberg School of Medicine. After completing his medical training at the University of Zagreb, Krainc spent more than two decades at the Massachusetts General Hospital and Harvard Medical School, where he completed his research and clinical training and served on faculty until relocating to Northwestern University in 2013. He has dedicated his scientific career to studying molecular pathways in the pathogenesis of neurodegeneration. Informed by genetic causes of disease, his work has uncovered key mechanisms across different neurodegenerative disorders that have led to pioneering design and development of targeted therapies. He has received numerous awards and recognitions for his work, including the Javits Neuroscience Investigator Award and the Outstanding Investigator award from NIH, and was elected to the Association of American Physicians, the National Academy of Medicine, and the National Academy of Inventors. He is the principal founding scientist of two biotech companies and serves as Venture Partner at OrbiMed. Krainc is President-elect of the American Neurological Association.

References

  1. ↑ Yohrling GJ, Vetter LA (2017). "Stewarding Hope: The Evolving Landscape of Huntington's Disease Science Communications". J Huntingtons Dis. 6 (1): 33–35. doi:10.3233/JHD-160230. PMID   28128771.
  2. 1 2 "HD Centre - People - Team Wild". UCL Queen Square Institute of Neurology. 17 October 2019. Retrieved 2 December 2021.
  3. 1 2 3 "UCL Iris Profile – Prof. Edward Wild" . Retrieved 2 December 2021.
  4. ↑ Hayden, Erika (23 February 2016). "Should you edit your children's genes?". Nature. 530 (7591): 402–405. Bibcode:2016Natur.530..402C. doi: 10.1038/530402a . PMID   26911764.
  5. ↑ "Christ's College Pieces Magazine". 27 July 2021.
  6. ↑ Phillips, Helen (25 March 2009). "Déjà vu: Where fact meets fantasy". New Scientist. pp. 3, 5. Archived from the original on 13 April 2016. Retrieved 31 March 2016.{{cite web}}: CS1 maint: bot: original URL status unknown (link)
  7. ↑ Wild, Edward (June 2009). Identification and evaluation of biomarkers for Huntington's disease (PhD Thesis). UCL Discovery Institutional Document Repository (Doctoral). University College London.
  8. ↑ Dorsey, E. Ray; Beck, Christopher A.; Darwin, Kristin; Nichols, Paige; Brocht, Alicia F. D.; Biglan, Kevin M.; Shoulson, Ira; for the Huntington Study Group COHORT Investigators (2013-12-01). "Natural History of Huntington Disease". JAMA Neurology. 70 (12): 1520–1530. doi:10.1001/jamaneurol.2013.4408. ISSN   2168-6149. PMID   24126537.
  9. ↑ Wild, Edward J.; Henley, Susie M. D.; Hobbs, Nicola Z.; Frost, Chris; MacManus, David G.; Barker, Roger A.; Fox, Nick C.; Tabrizi, Sarah J. (2010-05-15). "Rate and acceleration of whole-brain atrophy in premanifest and early Huntington's disease". Movement Disorders. 25 (7): 888–895. doi:10.1002/mds.22969. ISSN   1531-8257. PMC   9136537 . PMID   20461806. S2CID   33524701.
  10. ↑ Henley, Susie M. D.; Wild, Edward J.; Hobbs, Nicola Z.; Frost, Chris; MacManus, David G.; Barker, Roger A.; Fox, Nick C.; Tabrizi, Sarah J. (2009-04-30). "Whole-brain atrophy as a measure of progression in premanifest and early Huntington's disease". Movement Disorders. 24 (6): 932–936. doi:10.1002/mds.22485. ISSN   1531-8257. PMID   19243073. S2CID   206239857.
  11. ↑ Wild, Edward; Hobbs, Nicola; Henley, Susie (2011). "Huntington's Disease and Dementia". Neuroimaging in Dementia. Springer-Verlag. ISBN   978-3642008177.
  12. ↑ Wild, Edward J.; Tabrizi, Sarah J. (2008-01-01). "Biomarkers for Huntington's disease". Expert Opinion on Medical Diagnostics. 2 (1): 47–62. doi:10.1517/17530059.2.1.47. ISSN   1753-0059. PMID   23485116.
  13. ↑ Weiss, Andreas; Träger, Ulrike; Wild, Edward J.; Grueninger, Stephan; Farmer, Ruth; Landles, Christian; Scahill, Rachael I.; Lahiri, Nayana; Haider, Salman (2012-10-01). "Mutant huntingtin fragmentation in immune cells tracks Huntington's disease progression". The Journal of Clinical Investigation. 122 (10): 3731–3736. doi:10.1172/JCI64565. ISSN   1558-8238. PMC   3461928 . PMID   22996692.
  14. ↑ Tabrizi, Sarah J.; Flower, Michael D.; Ross, Christopher A.; Wild, Edward J. (October 2020). "Huntington disease: new insights into molecular pathogenesis and therapeutic opportunities". Nature Reviews Neurology. 16 (10): 529–546. doi:10.1038/s41582-020-0389-4. PMID   32796930. S2CID   221129777.
  15. ↑ Björkqvist, M; Wild, EJ; Thiele, J; Silvestroni, A; Andre, R; Lahiri, N; Raibon, E; Lee, RV; Benn, CL; Soulet, D; Magnusson, A; Woodman, B; Landles, C; Pouladi, MA; Hayden, MR; Khalili-Shirazi, A; Lowdell, MW; Brundin, P; Bates, GP; Leavitt, BR; Möller, T; Tabrizi, SJ (4 August 2008). "A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington's disease". The Journal of Experimental Medicine. 205 (8): 1869–77. doi:10.1084/jem.20080178. PMC   2525598 . PMID   18625748.
  16. ↑ Dalrymple, A; Wild, EJ; Joubert, R; Sathasivam, K; Björkqvist, M; Petersén, A; Jackson, GS; Isaacs, JD; Kristiansen, M; Bates, GP; Leavitt, BR; Keir, G; Ward, M; Tabrizi, SJ (July 2007). "Proteomic profiling of plasma in Huntington's disease reveals neuroinflammatory activation and biomarker candidates". Journal of Proteome Research. 6 (7): 2833–40. doi:10.1021/pr0700753. PMID   17552550.
  17. ↑ "A Clinical Study in Subjects With Huntington's Disease to Assess the Efficacy and Safety of Three Oral Doses of Laquinimod - Full Text View". ClinicalTrials.gov. Retrieved 2016-03-31.
  18. ↑ Wild, EJ; Boggio, R; Langbehn, D; Robertson, N; Haider, S; Miller, JR; Zetterberg, H; Leavitt, BR; Kuhn, R; Tabrizi, SJ; Macdonald, D; Weiss, A (May 2015). "Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington's disease patients". The Journal of Clinical Investigation. 125 (5): 1979–86. doi:10.1172/JCI80743. PMC   4463213 . PMID   25844897.
  19. ↑ Chase, Alex (21 April 2015). "Huntington disease: Cerebrospinal fluid and MRI biomarkers for prodromal HD". Nature Reviews Neurology. 11 (5): 245. doi:10.1038/nrneurol.2015.63. PMID   25896083. S2CID   38300571.
  20. 1 2 "Announcing HSG's 2015 Award Winners". Huntington Study Group. Archived from the original on 2021-11-26. Retrieved 2016-03-31.
  21. ↑ Hensman Moss, DJ; Poulter, M; Beck, J; Hehir, J; Polke, JM; Campbell, T; Adamson, G; Mudanohwo, E; McColgan, P; Haworth, A; Wild, EJ; Sweeney, MG; Houlden, H; Mead, S; Tabrizi, SJ (28 January 2014). "C9orf72 expansions are the most common genetic cause of Huntington disease phenocopies". Neurology. 82 (4): 292–9. doi:10.1212/WNL.0000000000000061. PMC   3929197 . PMID   24363131.
  22. ↑ Wild, EJ; Mudanohwo, EE; Sweeney, MG; Schneider, SA; Beck, J; Bhatia, KP; Rossor, MN; Davis, MB; Tabrizi, SJ (15 April 2008). "Huntington's disease phenocopies are clinically and genetically heterogeneous". Movement Disorders. 23 (5): 716–20. doi:10.1002/mds.21915. PMID   18181206. S2CID   3086383.
  23. ↑ "Huntington's disease trial test is 'major advance'". BBC News. 8 June 2017.
  24. 1 2 Byrne, Lauren M.; Rodrigues, Filipe B.; Johnson, Eileanor B.; Wijeratne, Peter A.; De Vita, Enrico; Alexander, Daniel C.; Palermo, Giuseppe; Czech, Christian; Schobel, Scott; Scahill, Rachael I.; Heslegrave, Amanda; Zetterberg, Henrik; Wild, Edward J. (12 September 2018). "Evaluation of mutant huntingtin and neurofilament proteins as potential markers in Huntington's disease". Science Translational Medicine. 10 (458): eaat7108. doi:10.1126/scitranslmed.aat7108. PMID   30209243. S2CID   206695500.
  25. ↑ Rodrigues, Filipe B.; Byrne, Lauren M.; Tortelli, Rosanna; Johnson, Eileanoir B.; Wijeratne, Peter A.; Arridge, Marzena; De Vita, Enrico; Ghazaleh, Naghmeh; Houghton, Richard; Furby, Hannah; Alexander, Daniel C.; Tabrizi, Sarah J.; Schobel, Scott; Scahill, Rachael I.; Heslegrave, Amanda; Zetterberg, Henrik; Wild, Edward J. (16 December 2020). "Mutant huntingtin and neurofilament light have distinct longitudinal dynamics in Huntington's disease". Science Translational Medicine. 12 (574): eabc2888. doi:10.1126/scitranslmed.abc2888. PMC   7611886 . PMID   33328328.
  26. ↑ Tabrizi, Sarah J.; Leavitt, Blair R.; Landwehrmeyer, G. Bernhard; Wild, Edward J.; Saft, Carsten; Barker, Roger A.; Blair, Nick F.; Craufurd, David; Priller, Josef; Rickards, Hugh; Rosser, Anne; Kordasiewicz, Holly B.; Czech, Christian; Swayze, Eric E.; Norris, Daniel A.; Baumann, Tiffany; Gerlach, Irene; Schobel, Scott A.; Paz, Erika; Smith, Anne V.; Bennett, C. Frank; Lane, Roger M. (13 June 2019). "Targeting Huntingtin Expression in Patients with Huntington's Disease". New England Journal of Medicine. 380 (24): 2307–2316. doi: 10.1056/NEJMoa1900907 . hdl: 20.500.11820/7da73cfb-3c2d-4f2e-9b92-463a6c7ad4de . PMID   31059641. S2CID   146811503.
  27. ↑ Whipple, Tom. "Huntington's breakthrough offers hope to thousands". The Times. Retrieved 2 December 2021.
  28. ↑ Devlin, Hannah (11 December 2017). "Excitement as trial shows Huntington's drug could slow progress of disease". the Guardian. Retrieved 2 December 2021.
  29. 1 2 3 4 Louise, Carpenter (30 October 2021). "Charlotte Raven: Huntington's disease is 'a burden that is almost impossible to bear'". The Times. Retrieved 2 December 2021.
  30. ↑ "Journal of Huntington's Disease". IOS Press. Retrieved 2016-03-31.
  31. ↑ "Association of British Neurologists Annual Report 2020-21" (PDF). Association of British Neurologists. Retrieved 2 December 2021.
  32. ↑ "Neuroscience/Translational neurology". European Academy of Neurology.
  33. ↑ "EHDN Structure – European Huntington's Disease Network". ehdn.org. Retrieved 2022-10-19.
  34. ↑ "Biomarkers Working Group – European Huntington's Disease Network". EHDN. Retrieved 2 December 2021.
  35. ↑ Harrison, Jacqueline (December 2013). The 'hidden no more' mass lobby June 2010 - using oral histories and cultural representations to explore the concealment of Huntington's disease. (Masters Thesis). University of Huddersfield Repository (masters).
  36. ↑ "Massive Underestimation In The Prevalence Of Huntington's Disease In The UK Population". Science 2.0. 27 August 2014. Retrieved 2016-03-31.
  37. ↑ "Promotions 2019-20 - Professors". UCL Human Resources. 29 June 2020.
  38. ↑ "Dr Edward J Wild". Google Scholar Citations. Retrieved 2 November 2021.
  39. ↑ Macleod, Rhona; Tibben, Aad (20 March 2014). Huntington's Disease (4 ed.). Oxford University Press. p. 171. ISBN   978-0199370474.
  40. ↑ Kenneally, Christine (2015). The Best Australian Science Writing. NewSouth. ISBN   9781742242231.
  41. ↑ "2014 Science Communication Awards: The winning entries". AMRC - Association of Medical Research Charities. Archived from the original on 2014-05-02. Retrieved 2016-09-30.
  42. ↑ Peter, Forbes (20 March 2018). "How close are we to a cure for Huntington's?". The Independent. Retrieved 2 December 2021.
  43. ↑ Brewer, Kirstie (11 June 2021). "Huntington's disease won't stop me having a baby". BBC News.
  44. ↑ "Researcher Hopeful, Sure of Future Cure for Huntington's Disease". Huntington's Disease News. BioNews Network. 22 July 2016.
  45. ↑ Wild, Edward J. (May 2016). "Huntington's Disease: The Most Curable Incurable Brain Disorder?". eBioMedicine. 8: 3–4. doi:10.1016/j.ebiom.2016.05.023. PMC   4919568 . PMID   27428401.
  46. ↑ "Watch The Inheritance Online | Vimeo On Demand". Vimeo. Retrieved 2016-03-31.
  47. ↑ "Edward Wild". IMDb. Retrieved 4 May 2016.
  48. ↑ "Access to Understanding Science Writing Competition 2015" (PDF). Access to Understanding. Europe PubMed Central.
  49. ↑ "Huntington's And Immunity - Dr Ed Wild, University College London". The Naked Scientists. 25 October 2009. Retrieved 2016-04-01.
  50. ↑ "Listener Week. The Hayes Sisters; Huntington's Disease; Coping with the school holidays on a low income". Woman's Hour. BBC Radio 4. Retrieved 15 July 2016.
  51. ↑ "Morning Ireland - Breakthrough made in efforts to counter Huntington's disease". RTE Radio. RTE. Retrieved 2 December 2021.
  52. ↑ Burns, Ken. "The Gene - Part 1: Dawn of the Modern Age of Genetics - Episode 1". PBS. Retrieved 2 December 2021.
  53. ↑ "Part 1: Dawn of the Modern Age of Genetics". Ken Burns Presents: The Gene. 7 April 2020. Retrieved 2 December 2021.
  54. ↑ Raven, Charlotte; Wild, Edward (4 November 2021). Patient 1. Penguin.
  55. ↑ "World-Renowned International Huntington Neurologists and Researchers to be featured at the Huntington Society of Canada's National Conference" (PDF). Huntington Society of Canada.
  56. ↑ "Carroll receives HDSA Researcher of the Year award". Western Today. Retrieved 2016-03-31.
  57. ↑ "UCL HD Centre wins two prestigious 'Insight of the Year' awards". UCL Queen Square Institute of Neurology. September 12, 2017.
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