Tamas Revesz

Summary

Affiliation: University College London
Country: UK

Publications

  1. ncbi request reprint Rosai-Dorfman disease presenting with widespread intracranial and spinal cord involvement
    Desmond P Kidd
    Department of Clinical Neurosciences, Royal Free Hospital, London, UK
    Neurology 67:1551-5. 2006
  2. pmc Widespread Lewy body and tau accumulation in childhood and adult onset dystonia-parkinsonism cases with PLA2G6 mutations
    Coro Paisan-Ruiz
    Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK
    Neurobiol Aging 33:814-23. 2012
  3. ncbi request reprint Sporadic and familial cerebral amyloid angiopathies
    Tamas Revesz
    Queen Square Brain Bank, Department of Molecular Pathogenesis, University College London, UK
    Brain Pathol 12:343-57. 2002
  4. pmc Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies
    Tamas Revesz
    Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, Queen Square, London WC1N3BG, UK
    Acta Neuropathol 118:115-30. 2009
  5. ncbi request reprint Anatamopathological spectrum of tauopathies
    Tamas Revesz
    Queen Square Brain Bank, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom
    Mov Disord 18:S13-20. 2003
  6. ncbi request reprint Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view
    Tamas Revesz
    Queen Square Brain Bank, Department of Molecular Neuroscience and Division of Neuropathology, Institute of Neurology, University College London, London, United Kingdom
    J Neuropathol Exp Neurol 62:885-98. 2003
  7. ncbi request reprint Cytoskeletal pathology in familial cerebral amyloid angiopathy (British type) with non-neuritic amyloid plaque formation
    T Revesz
    Department of Neuropathology, Institute of Neurology, London, UK
    Acta Neuropathol 97:170-6. 1999
  8. pmc Parietal lobe deficits in frontotemporal lobar degeneration caused by a mutation in the progranulin gene
    Jonathan D Rohrer
    Dementia Research Centre, Institute of Neurology, University College London, London, England
    Arch Neurol 65:506-13. 2008
  9. doi request reprint Concomitant progressive supranuclear palsy and multiple system atrophy: more than a simple twist of fate?
    Laura Silveira-Moriyama
    Reta Lila Weston Institute for Neurological Studies, UCL Institute of Neurology, London, UK
    Neurosci Lett 467:208-11. 2009
  10. pmc TDP-43 pathology in a patient carrying G2019S LRRK2 mutation and a novel p.Q124E MAPT
    Helen Ling
    Reta Lila Weston Institute of Neurological Studies and Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK
    Neurobiol Aging 34:2889.e5-9. 2013

Detail Information

Publications116 found, 100 shown here

  1. ncbi request reprint Rosai-Dorfman disease presenting with widespread intracranial and spinal cord involvement
    Desmond P Kidd
    Department of Clinical Neurosciences, Royal Free Hospital, London, UK
    Neurology 67:1551-5. 2006
    ..Using data from two cases, we present the clinical manifestations, pathology, and treatment, and review the literature regarding the ocular and neurologic manifestations. Finally, we discuss the optimum management of this disorder...
  2. pmc Widespread Lewy body and tau accumulation in childhood and adult onset dystonia-parkinsonism cases with PLA2G6 mutations
    Coro Paisan-Ruiz
    Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK
    Neurobiol Aging 33:814-23. 2012
    ..Later onset cases tended to have less tau involvement but still severe alpha-synuclein pathology. The clinical and neuropathological features clearly represent a link between PLA2G6 and parkinsonian disorders...
  3. ncbi request reprint Sporadic and familial cerebral amyloid angiopathies
    Tamas Revesz
    Queen Square Brain Bank, Department of Molecular Pathogenesis, University College London, UK
    Brain Pathol 12:343-57. 2002
    ..We also discuss data relevant to the pathomechanism of the different forms of CAA with an emphasis on the most common A beta-related types...
  4. pmc Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies
    Tamas Revesz
    Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, Queen Square, London WC1N3BG, UK
    Acta Neuropathol 118:115-30. 2009
    ..In this review, the characteristic morphological features of the different CAAs is described and the implication of the biochemical, genetic and transgenic animal data for the pathogenesis of CAA is discussed...
  5. ncbi request reprint Anatamopathological spectrum of tauopathies
    Tamas Revesz
    Queen Square Brain Bank, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom
    Mov Disord 18:S13-20. 2003
    ....
  6. ncbi request reprint Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view
    Tamas Revesz
    Queen Square Brain Bank, Department of Molecular Neuroscience and Division of Neuropathology, Institute of Neurology, University College London, London, United Kingdom
    J Neuropathol Exp Neurol 62:885-98. 2003
    ..This review addresses issues related to the correlation between morphology, biochemistry, and genetics, and briefly discusses both the pathogenesis and animal models of CAAs...
  7. ncbi request reprint Cytoskeletal pathology in familial cerebral amyloid angiopathy (British type) with non-neuritic amyloid plaque formation
    T Revesz
    Department of Neuropathology, Institute of Neurology, London, UK
    Acta Neuropathol 97:170-6. 1999
    ..In FAB severe cytoskeletal pathology is present in areas most affected by amyloid plaque deposits, thus suggesting a localised neurotoxic effect of the poorly characterised amyloidogenic peptide characteristic of this condition...
  8. pmc Parietal lobe deficits in frontotemporal lobar degeneration caused by a mutation in the progranulin gene
    Jonathan D Rohrer
    Dementia Research Centre, Institute of Neurology, University College London, London, England
    Arch Neurol 65:506-13. 2008
    ..To describe the clinical, neuropsychologic, and radiologic features of a family with a C31LfsX35 mutation in the progranulin gene CCDS11483.1)...
  9. doi request reprint Concomitant progressive supranuclear palsy and multiple system atrophy: more than a simple twist of fate?
    Laura Silveira-Moriyama
    Reta Lila Weston Institute for Neurological Studies, UCL Institute of Neurology, London, UK
    Neurosci Lett 467:208-11. 2009
    ..The growing number of collective case reports, including the one reported here, might suggest an increased prevalence of concomitant PSP and MSA than what would be expected by chance...
  10. pmc TDP-43 pathology in a patient carrying G2019S LRRK2 mutation and a novel p.Q124E MAPT
    Helen Ling
    Reta Lila Weston Institute of Neurological Studies and Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK
    Neurobiol Aging 34:2889.e5-9. 2013
    ..The role of the MAPT variant in the clinical and pathological manifestation in LRRK2 cases remains to be determined. ..
  11. ncbi request reprint Pathological tau burden and distribution distinguishes progressive supranuclear palsy-parkinsonism from Richardson's syndrome
    David R Williams
    Queen Square Brain Bank for Neurological Disorders, London, UK
    Brain 130:1566-76. 2007
    ..The grading system we have developed provides an easy-to-use and sensitive tool for the morphological assessment of PSP-tau pathology and allows for consideration of the clinical diversity that is known to occur in PSP...
  12. pmc A distinct clinical, neuropsychological and radiological phenotype is associated with progranulin gene mutations in a large UK series
    Jonathan Beck
    MRC Prion Unit, Department of Neurodegenerative Disease, UCL Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
    Brain 131:706-20. 2008
    ..Finally, we confirmed a modifying effect of APOE-E4 genotype on clinical phenotype with a later onset in the GRN carriers suggesting that this gene has distinct phenotypic effects in different neurodegenerative diseases...
  13. doi request reprint Multiple system atrophy-parkinsonism with slow progression and prolonged survival: a diagnostic catch
    Igor N Petrovic
    National Hospital for Neurology and Neurosurgery, Queen Square, and the Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, London, United Kingdom
    Mov Disord 27:1186-90. 2012
    ..Multiple system atrophy (MSA) is a neurodegenerative disease leading to severe physical impairment, with a disease duration from onset to death of 6-9 years...
  14. pmc Frontotemporal dementia with the C9ORF72 hexanucleotide repeat expansion: clinical, neuroanatomical and neuropathological features
    Colin J Mahoney
    Dementia Research Centre, Department of Neurodegenerative Diseases, UCL Institute of Neurology, London WC1N 3BG, UK
    Brain 135:736-50. 2012
    ....
  15. doi request reprint Lewy- and Alzheimer-type pathologies in Parkinson's disease dementia: which is more important?
    Yaroslau Compta
    Queen Square Brain Bank for Neurological Disorders, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK
    Brain 134:1493-505. 2011
    ..Cortical amyloid-β and age at disease onset seem to determine the rate to dementia...
  16. ncbi request reprint NR4A2 genetic variation in sporadic Parkinson's disease: a genewide approach
    Daniel G Healy
    Department of Molecular Neuroscience, Institute of Neurology, London, United Kingdom
    Mov Disord 21:1960-3. 2006
    ..Here, we use a haplotype-tagging approach in 802 PD patients and 784 controls and demonstrate that common genetic variation, including NR4A2 haplotypes, does not influence the risk of PD in the Caucasian population...
  17. ncbi request reprint Disentangling the relationship between lewy bodies and nigral neuronal loss in Parkinson's disease
    Laura Parkkinen
    Queen Square Brain Bank for Neurological Disorders, London, UK
    J Parkinsons Dis 1:277-86. 2011
    ..Our data also provides no support for a primary pathogenic role of LBs as neither their distribution nor density was associated with the severity of nigral cell loss. ..
  18. doi request reprint Identification and quantification of oligodendrocyte precursor cells in multiple system atrophy, progressive supranuclear palsy and Parkinson's disease
    Zeshan Ahmed
    Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK
    Brain Pathol 23:263-73. 2013
    ..These findings raise the possibility that OPCs could be available to repair disease-associated damage in MSA, consistent with their biological function...
  19. doi request reprint Glucocerebrosidase mutations do not cause increased Lewy body pathology in Parkinson's disease
    Laura Parkkinen
    Queen Square Brain Bank for Neurological Disorders, Institute of Neurology, University College London, UK
    Mol Genet Metab 103:410-2. 2011
    ..Our results do not support GBA carriers to have a more advanced neuropathologic disease i.e. increased density of protein aggregates...
  20. doi request reprint Hyposmia in progressive supranuclear palsy
    Laura Silveira-Moriyama
    Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, London, United Kingdom
    Mov Disord 25:570-7. 2010
    ..Further prospective studies including patients with early PSP and PSP-P with postmortem confirmation might help clarify if smell tests could be useful when the differential diagnosis lies between PD and PSP...
  21. doi request reprint Parkinson's disease
    Andrew J Lees
    Department of Molecular Neuroscience and Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, University College London and the National Hospital for Neurology and Neurosurgery, London, UK
    Lancet 373:2055-66. 2009
    ..Embryonic stem cells and gene therapy are promising research therapeutic approaches...
  22. ncbi request reprint Mutations in the gene LRRK2 encoding dardarin (PARK8) cause familial Parkinson's disease: clinical, pathological, olfactory and functional imaging and genetic data
    Naheed L Khan
    Department of Molecular Neuroscience, Institute of Neurology, London, UK
    Brain 128:2786-96. 2005
    ....
  23. pmc α-Synucleinopathy associated with G51D SNCA mutation: a link between Parkinson's disease and multiple system atrophy?
    Aoife P Kiely
    Queen Square Brain Bank, UCL Institute of Neurology, London, UK
    Acta Neuropathol 125:753-69. 2013
    ..Greater understanding of the disease mechanism underlying the G51D mutation could aid in understanding of α-synuclein biology and its impact on disease phenotype...
  24. pmc The midbrain to pons ratio: a simple and specific MRI sign of progressive supranuclear palsy
    Luke A Massey
    Sara Koe PSP Research Centre, Rita Lila Weston Institute for Neurology Studies and Queen Square Brain Bank, Department of Molecular Neurosciences, UCL Institute of Neurology, London, UK
    Neurology 80:1856-61. 2013
    ..We aimed to develop in histologically proven disease a simple measure of the midbrain and pons on sagittal MRI to identify PSP...
  25. doi request reprint Parkin disease: a clinicopathologic entity?
    Karen M Doherty
    Reta Lila Weston Institute for Neurological Studies, University College London, London, England
    JAMA Neurol 70:571-9. 2013
    ..The few available detailed neuropathologic reports suggest that homozygous and compound heterozygous parkin mutations are characterized by severe substantia nigra pars compacta neuronal loss...
  26. pmc The MAPT p.A152T variant is a risk factor associated with tauopathies with atypical clinical and neuropathological features
    Eleanna Kara
    Reta Lila Weston Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK
    Neurobiol Aging 33:2231.e7-2231.e14. 2012
    ..We suggest that the A152T variant is a risk factor associated with the development of atypical neurodegenerative conditions with abnormal tau accumulation...
  27. doi request reprint Transportin1: a marker of FTLD-FUS
    Jack Brelstaff
    Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, UK
    Acta Neuropathol 122:591-600. 2011
    ..Our biochemical investigations demonstrate that urea-soluble TRN1 is present in aFTLD-U and NIFID, but not in normal control brains. These findings implicate abnormalities of FUS transport in the pathogenesis of FTLD-FUS...
  28. ncbi request reprint UCHL-1 is not a Parkinson's disease susceptibility gene
    Daniel G Healy
    Department of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom
    Ann Neurol 59:627-33. 2006
    ..The strongest evidence comes from a meta-analysis of small studies that reported the S18Y polymorphism as protective against PD, after pooling studies of white and Asian subjects. Here, we present data that challenge this association...
  29. ncbi request reprint Voxel-based morphometry in tau-positive and tau-negative frontotemporal lobar degenerations
    Jennifer L Whitwell
    Dementia Research Centre, Institute of Neurology, London, UK
    Neurodegener Dis 1:225-30. 2004
    ..Correlations between regional patterns of tissue loss and specific proteinopathies have not been established...
  30. doi request reprint Cortical alpha-synuclein load is associated with amyloid-beta plaque burden in a subset of Parkinson's disease patients
    Tammaryn Lashley
    Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK
    Acta Neuropathol 115:417-25. 2008
    ....
  31. pmc A comparative clinical, pathological, biochemical and genetic study of fused in sarcoma proteinopathies
    Tammaryn Lashley
    Queen Square Brain Bank, Institute of Neurology, Queen Square, London WC1N 3BG, UK
    Brain 134:2548-64. 2011
    ..The co-existence of fused in sarcoma-positive inclusions in both motor neurons and extramotor cerebral structures is a characteristic finding in sporadic fused in sarcoma proteinopathies, indicating a multisystem disorder...
  32. pmc Homozygosity for the C9orf72 GGGGCC repeat expansion in frontotemporal dementia
    Pietro Fratta
    Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK
    Acta Neuropathol 126:401-9. 2013
    ..Our findings have implications for genetic counselling, highlighting the need to use genetic tests that distinguish C9orf72 homozygosity. ..
  33. ncbi request reprint DJ-1 (PARK7) is associated with 3R and 4R tau neuronal and glial inclusions in neurodegenerative disorders
    Ravindran Kumaran
    Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, 1, Wakefield Street, WC1N 1PJ, UK
    Neurobiol Dis 28:122-32. 2007
    ..Our observations confirm previous findings that DJ-1 is present in a subpopulation of glial and neuronal tau inclusions in tau diseases and associated with both 3R and 4R tau isoforms...
  34. ncbi request reprint Familial Danish dementia: a novel form of cerebral amyloidosis associated with deposition of both amyloid-Dan and amyloid-beta
    Janice L Holton
    Department of Molecular Pathogenesis, Queen Square Brain Bank, London, United Kingdom
    J Neuropathol Exp Neurol 61:254-67. 2002
    ..The significance of concurrent ADan and Abeta deposition in FDD is under further investigation...
  35. doi request reprint Conventional magnetic resonance imaging in confirmed progressive supranuclear palsy and multiple system atrophy
    Luke A Massey
    Sara Koe PSP Research Centre, UCL Institute of Neurology, University College London, London, United Kingdom
    Mov Disord 27:1754-62. 2012
    ..However, the low sensitivity of these and macroscopic findings at autopsy suggest a need for imaging techniques sensitive to microstructural abnormalities without regional atrophy...
  36. ncbi request reprint Relationships between age and late progression of Parkinson's disease: a clinico-pathological study
    Peter A Kempster
    Reta Lila Weston Institute of Neurological Studies, University College London, 1 Wakefield Street, London WC1N 1PJ, UK
    Brain 133:1755-62. 2010
    ..The chief effects of age on the rate of progression are seen over the early-middle part of the disease. An exponential curve for clinical progression provides the best explanation for these observations about age and the disease course...
  37. pmc Clinical and neuroanatomical signatures of tissue pathology in frontotemporal lobar degeneration
    Jonathan D Rohrer
    Dementia Research Centre, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK
    Brain 134:2565-81. 2011
    ....
  38. doi request reprint The genetics of Parkinson's syndromes: a critical review
    John Hardy
    Reta Lila Weston Institute and Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, England, UK
    Curr Opin Genet Dev 19:254-65. 2009
    ....
  39. doi request reprint MM2 subtype of sporadic Creutzfeldt-Jakob disease may underlie the clinical presentation of progressive supranuclear palsy
    Igor N Petrovic
    Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, 1 Wakefield St, London, WC1N 1PJ, UK
    J Neurol 260:1031-6. 2013
    ..This case and the literature support the notion that biochemical properties of the prion protein can influence the clinical presentation of sCJD...
  40. doi request reprint Regional differences in the severity of Lewy body pathology across the olfactory cortex
    Laura Silveira-Moriyama
    Reta Lila Weston Institute for Neurological Studies, UCL Institute of Neurology, London, UK
    Neurosci Lett 453:77-80. 2009
    ....
  41. ncbi request reprint Neuropathological findings in benign tremulous parkinsonism
    Marianna Selikhova
    Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom
    Mov Disord 28:145-52. 2013
    ....
  42. doi request reprint Testing an aetiological model of visual hallucinations in Parkinson's disease
    David A Gallagher
    Institute of Neurology, University College London, UK
    Brain 134:3299-309. 2011
    ..These clinical data are supported by the pathological study, in which higher overall cortical Lewy body counts, and in particular areas implicated in visuoperception and executive function, were associated with visual hallucinations...
  43. doi request reprint Does corticobasal degeneration exist? A clinicopathological re-evaluation
    Helen Ling
    Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, University College London, 1 Wakefield Street, London WC1N 1PJ, UK
    Brain 133:2045-57. 2010
    ..Despite these diagnostic difficulties we conclude that corticobasal degeneration is a discrete clinicopathological entity but with a broader clinical spectrum than was originally proposed...
  44. ncbi request reprint Characteristics of two distinct clinical phenotypes in pathologically proven progressive supranuclear palsy: Richardson's syndrome and PSP-parkinsonism
    David R Williams
    The Queen Square Brain Bank for Neurological Disorders, University College London, UK
    Brain 128:1247-58. 2005
    ..The different tau isoform deposition in the basal pons suggests that this may ultimately prove to be a discrete nosological entity...
  45. pmc Glucocerebrosidase mutations in clinical and pathologically proven Parkinson's disease
    Juliane Neumann
    Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK
    Brain 132:1783-94. 2009
    ....
  46. ncbi request reprint Magnetic resonance imaging signatures of tissue pathology in frontotemporal dementia
    Jennifer L Whitwell
    Dementia Research Centre, Institute of Neurology, University College London, England
    Arch Neurol 62:1402-8. 2005
    ..The pathologic substrates of frontotemporal dementia (FTD) are difficult to predict in vivo...
  47. pmc FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration
    Hazel Urwin
    UCL Institute of Neurology, London, UK
    Acta Neuropathol 120:33-41. 2010
    ..We identified three FTLD-UPS cases, which are negative for CHMP2B mutation, suggesting that the full complement of FTLD pathologies is yet to be elucidated...
  48. doi request reprint Globular glial tauopathies (GGT) presenting with motor neuron disease or frontotemporal dementia: an emerging group of 4-repeat tauopathies
    Zeshan Ahmed
    Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, 1 Wakefield Street, London, WC1N 1PJ, UK
    Acta Neuropathol 122:415-28. 2011
    ..We, therefore, propose the term globular glial tauopathy as an encompassing term to classify this emerging class of 4R tauopathy...
  49. pmc Tau acts as an independent genetic risk factor in pathologically proven PD
    Gavin Charlesworth
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK
    Neurobiol Aging 33:838.e7-11. 2012
    ..Using only neuropathologically proven PD, we show that the MAPT association remains and is independent of the PSP Association...
  50. pmc Genetic variability at the PARK16 locus
    Arianna Tucci
    Department of Molecular Neuroscience and Reta Lila Weston Institute, UCL Institute of Neurology, London, UK
    Eur J Hum Genet 18:1356-9. 2010
    ....
  51. ncbi request reprint Difference in MSA phenotype distribution between populations: genetics or environment?
    Tetsutaro Ozawa
    Queen Square Brain Bank for Neurological Disorders, UCL Institute of Neurology, Queen Square, University College London, London, UK
    J Parkinsons Dis 2:7-18. 2012
    ..Further investigations are needed to determine the environmental, genetic, and epigenetic factors that account for the differences in clinicopathological phenotype of MSA among different populations...
  52. pmc Pantothenate kinase-associated neurodegeneration is not a synucleinopathy
    Abi Li
    Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK Queen Square Brain Bank, UCL Institute of Neurology, London, UK Department of Pediatrics, University of Maryland, Baltimore, MD, USA Rita Lila Weston Institute of Neurological Studies, London, UK
    Neuropathol Appl Neurobiol . 2012
    ..2012 The Authors. Neuropathology and Applied Neurobiology © 2012 British Neuropathological Society...
  53. doi request reprint Genetic analysis of inherited leukodystrophies: genotype-phenotype correlations in the CSF1R gene
    Rita Guerreiro
    Reta Lilla Weston Laboratories, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, England
    JAMA Neurol 70:875-82. 2013
    ..The detection of mutations in this gene in cases diagnosed with different clinical entities further demonstrated the difficulties in the clinical diagnosis of HDLS...
  54. doi request reprint The effect of drug treatment on neurogenesis in Parkinson's disease
    Sean S O'Sullivan
    Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom
    Mov Disord 26:45-50. 2011
    ..Our findings suggest a positive impact of chronic L-dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases...
  55. ncbi request reprint Neuronal intranuclear inclusion disease: report on a case originally diagnosed as dopa-responsive dystonia with Lewy bodies
    Dominic C Paviour
    The Sara Koe Progressive Supranuclear Palsy Research Centre, Institute of Neurology, University College London, London, United Kingdom
    Mov Disord 20:1345-9. 2005
    ..This rare condition, which may be diagnosed in life with a full thickness rectal biopsy, needs to be considered in the differential diagnosis of any case presenting as progressive juvenile parkinsonism (JP) or dystonia...
  56. doi request reprint Impulsive-compulsive spectrum behaviors in pathologically confirmed progressive supranuclear palsy
    Sean S O'Sullivan
    Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, University College London, London, United Kingdom
    Mov Disord 25:638-42. 2010
    ..Pathological comparisons between these three cases and other case series of progressive supranuclear palsy are made...
  57. ncbi request reprint Adult-onset neurodegeneration with brain iron accumulation and cortical alpha-synuclein and tau pathology: a distinct clinicopathological entity
    George K Tofaris
    Department of Clinical Neurology, National Hospital for Neurology and Neurosurgery, Institute of Child Health and Great Ormond Street Hospital, London, England, UK
    Arch Neurol 64:280-2. 2007
    ..Familial cases with mutations in the pantothenate kinase gene are associated with a specific phenotype. In contrast, sporadic cases are heterogeneous in their clinical presentation...
  58. ncbi request reprint The spectrum of pathological involvement of the striatonigral and olivopontocerebellar systems in multiple system atrophy: clinicopathological correlations
    Tetsutaro Ozawa
    Queen Square Brain Bank, Department of Molecular Neuroscience, Institute of Neurology, Queen Square, UCL, London, UK
    Brain 127:2657-71. 2004
    ....
  59. pmc Duplication of amyloid precursor protein (APP), but not prion protein (PRNP) gene is a significant cause of early onset dementia in a large UK series
    Daniel McNaughton
    MRC Prion Unit, Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK
    Neurobiol Aging 33:426.e13-21. 2012
    ..The recognized phenotype may be expanded to include the possibility of early seizures and apparently sporadic disease which, in part, may be due to different mutational mechanisms. The pros and cons of our screening method are discussed...
  60. ncbi request reprint Altered cleavage and localization of PINK1 to aggresomes in the presence of proteasomal stress
    Miratul M K Muqit
    Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK
    J Neurochem 98:156-69. 2006
    ..These observations provide valuable insights into the mechanisms of LB formation in PD that should lead to a better understanding of PD pathogenesis...
  61. ncbi request reprint UCHL-1 gene in multiple system atrophy: a haplotype tagging approach
    Daniel G Healy
    Department of Molecular Neuroscience, Institute of Neurology, Queen Square, London United Kingdom
    Mov Disord 20:1338-43. 2005
    ..This search included the S18Y variant of UCHL-1, which has been reported to be protective in Parkinson's disease...
  62. ncbi request reprint Genetic variation at the tau locus and clinical syndromes associated with progressive supranuclear palsy
    David R Williams
    The Queen Square Brain Bank for Neurological Disorders, Institute of Neurology, Queen Square, London, United Kingdom
    Mov Disord 22:895-7. 2007
    ..No mutations were found in 75 patients (21 PSP-P), and H1c was associated with both Richardson's syndrome and PSP-P compared with controls. Routine screening for MAPT mutations in atypical PSP is not recommended...
  63. ncbi request reprint Sporadic and familial dementia with ubiquitin-positive tau-negative inclusions: clinical features of one histopathological abnormality underlying frontotemporal lobar degeneration
    Alison K Godbolt
    Dementia Research Centre, Institute of Neurology, University College London, England
    Arch Neurol 62:1097-101. 2005
    ..Familial disease occurs in up to 50% of frontotemporal lobar degeneration cases. One of several underlying histopathological abnormalities is of ubiquitin-positive tau-negative inclusions, similar to those in motor neuron disease...
  64. ncbi request reprint Tau exon 10 +16 mutation FTDP-17 presenting clinically as sporadic young onset PSP
    H R Morris
    National Hospital for Neurology and Neurosurgery, Queen Square, London, UK
    Neurology 61:102-4. 2003
    ..An age at onset younger than 50 years combined with the absence of early falls may indicate the possibility of a tau mutation in clinically diagnosed PSP...
  65. ncbi request reprint An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies
    Rohan de Silva
    Reta Lila Weston Institute of Neurological Studies, University College London, Windeyer Building, 46 Cleveland St, W1T 4JF, London, UK
    Acta Neuropathol 111:329-40. 2006
    ..The use of such tau isoform specific antibodies may refine pathological criteria underpinning FTLD...
  66. ncbi request reprint Mutations in TTBK2, encoding a kinase implicated in tau phosphorylation, segregate with spinocerebellar ataxia type 11
    Henry Houlden
    Department of Molecular Neuroscience, Institute of Neurology and The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
    Nat Genet 39:1434-6. 2007
    ..Affected brain tissue showed substantial cerebellar degeneration and tau deposition. These data suggest that TTBK2 is important in the tau cascade and in spinocerebellar degeneration...
  67. ncbi request reprint Down-regulation of the dopamine receptor D2 in mice lacking ataxin 1
    Robert Goold
    UCL Institute of Child Health, University College London, UK
    Hum Mol Genet 16:2122-34. 2007
    ..Therefore, this study identifies novel molecular targets that are regulated by Atxn1 which might contribute to the motor deficits in SCA1, and provides new insights into the mechanisms by which Atxn1 co-regulates transcription...
  68. pmc Primary diffuse leptomeningeal gliomatosis simulating tuberculous meningitis
    J H Rees
    University Department of Clinical Neurology, Institute of Neurology, Queen Square, London WC1N 3BG, UK
    J Neurol Neurosurg Psychiatry 70:120-2. 2001
    ..These cases emphasise the need for repeated reassessment in patients with culture negative lymphocytic meningitis. In addition, this is the first report of FDG-PET scanning in leptomeningeal gliomatosis...
  69. ncbi request reprint A multidisciplinary team approach to skull base chondrosarcomas
    H A Crockard
    Department of Surgical Neurology, The National Hospital for Neurology and Neurosurgery, London, United Kingdom
    J Neurosurg 95:184-9. 2001
    ..The authors review their experience with treating skull base chondrosarcomas, which are much rarer than skull base chordomas and differ from them in prognosis and treatment...
  70. ncbi request reprint Mixed glioneuronal tumour of the fourth ventricle with prominent rosette formation
    T S Jacques
    Division of Neuropathology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, UK
    Neuropathol Appl Neurobiol 32:217-20. 2006
    ..However, the clinical data available including the cases presented here, along with the histological features, suggest that these are low grade tumours with a good prognosis after surgical resection...
  71. ncbi request reprint A multidisciplinary team approach to skull base chordomas
    H A Crockard
    Department of Surgical Neurology, The National Hospital for Neurology and Neurosurgery, London, United Kingdom
    J Neurosurg 95:175-83. 2001
    ..A multidisciplinary team devised a protocol for long-term care of patients with skull base chordomas. In this study they describe their approach...
  72. ncbi request reprint Brain biopsy in dementia
    J D Warren
    Dementia Research Centre, Institute of Neurology, London, UK
    Brain 128:2016-25. 2005
    ....
  73. doi request reprint Neuropathology of primary adult-onset dystonia
    J L Holton
    Queen Square Brain Bank, Department of Molecular Neuroscience, University College London Institute of Neurology, Queen Square, London WC1N 3BG, UK
    Neurology 70:695-9. 2008
    ..However, it was unclear whether these changes are characteristic of these particular disorders or an epiphenomenon of dystonic conditions in general...
  74. pmc Pathological substrate for regional distribution of increased atrophy rates in progressive supranuclear palsy
    D C Paviour
    The Sara Koe PSP Research Centre, Institute of Neurology UCL, London, UK
    J Neurol Neurosurg Psychiatry 75:1772-5. 2004
    ..MRI features described previously in PSP correspond to regions of pathological involvement demonstrated in separate studies, but serial MRI with pathological follow up has not been undertaken...
  75. ncbi request reprint Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies
    R De Silva
    Reta Lila Weston Institute of Neurological Studies, University College London, and Department of Molecular Neuroscience and Neuropathology, Institute of Neurology, UK
    Neuropathol Appl Neurobiol 29:288-302. 2003
    ..These new isoform-specific antibodies are useful tools for analysing tau isoform expression and distribution as well as pathological changes in the human brain...
  76. ncbi request reprint Frontotemporal lobar degeneration with ubiquitin-only-immunoreactive neuronal changes: broadening the clinical picture to include progressive supranuclear palsy
    D C Paviour
    The Sara Koe PSP Research Centre, Institute of Neurology, London, UK
    Brain 127:2441-51. 2004
    ..FTLD-U or FTLD-MND should be considered in the differential diagnosis of progressive frontal dementia with an akinetic rigid syndrome and supranuclear gaze palsy or Steele-Richardson-Olszewski disease...
  77. pmc Hippocampal layers on high resolution magnetic resonance images: real or imaginary?
    U C Wieshmann
    NSE Epilepsy Research MRI Unit, Chalfont St Peter, Bucks, UK
    J Anat 195:131-5. 1999
    ..469 x 0.469 x 2 mm or lower) is not sufficient for the detection of all hippocampal layers. For the reliable detection of all hippocampal layers on MR images an increase by a factor of approximately 20 would be necessary...
  78. pmc Expression of BRI2 mRNA and protein in normal human brain and familial British dementia: its relevance to the pathogenesis of disease
    T Lashley
    Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, London, UK
    Neuropathol Appl Neurobiol 34:492-505. 2008
    ....
  79. doi request reprint Targeting of the pedunculopontine nucleus by an MRI-guided approach: a cadaver study
    Ludvic Zrinzo
    Unit of Functional Neurosurgery, Box 146, Institute of Neurology and National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK
    J Neural Transm 118:1487-95. 2011
    ..The results support the accuracy of the described specific MR imaging protocol...
  80. ncbi request reprint Clinicopathological investigation of vascular parkinsonism, including clinical criteria for diagnosis
    Jan C M Zijlmans
    Queen Square Brain Bank for Neurological Disorders, Institute of Neurology Queen Square, London, United Kingdom
    Mov Disord 19:630-40. 2004
    ..New clinical criteria for a diagnosis of VP are proposed based on the clinicopathological findings of this study...
  81. ncbi request reprint The genetic and pathological classification of familial frontotemporal dementia
    H R Morris
    Neurogenetics Section, Institute of Neurology, University College London, England
    Arch Neurol 58:1813-6. 2001
    ..Furthermore, these data suggest that there are at least 2 additional genes to be identified among families with autosomal dominant FTD...
  82. doi request reprint Diagnostic implications of histological analysis of neurosurgical aspirate in addition to routine resections
    Gelareh Zadeh
    Division of Neurosurgery, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada
    Neuropathology 32:44-50. 2012
    ..Collection of surgical aspirate also generates additional archival material which can be microdissected and used for tissue microarrays or for molecular studies...
  83. ncbi request reprint Influence of target size on vertical gaze palsy in a pathologically proven case of progressive supranuclear palsy
    Barry M Seemungal
    The Academic Department of Neuro Otology, Division of Neurosciences and Psychological Medicine, Imperial College Faculty of Medicine, Charing Cross Hospital, London, United Kingdom
    Mov Disord 18:818-22. 2003
    ....
  84. ncbi request reprint Somatic and germline mosaicism in sporadic early-onset Alzheimer's disease
    Jonathan A Beck
    MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology UCL, Queen Square, London, UK
    Hum Mol Genet 13:1219-24. 2004
    ..This finding has important implications for the aetiology of sporadic AD, and for other apparently sporadic neurodegenerative diseases such as Parkinson's disease, motor neuron disease and Creutzfeldt-Jakob disease...
  85. ncbi request reprint Molecular chaperons, amyloid and preamyloid lesions in the BRI2 gene-related dementias: a morphological study
    T Lashley
    Queen Square Brain Bank, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, UK
    Neuropathol Appl Neurobiol 32:492-504. 2006
    ..The presence of AAPs in the preamyloid lesions supports the notion that chaperon molecules may play a role in the early steps of fibrillogenesis...
  86. ncbi request reprint Neuropathologic variation in frontotemporal dementia due to the intronic tau 10(+16) mutation
    P L Lantos
    Department of Neuropathology, Institute of Psychiatry, King s College London, UK
    Neurology 58:1169-75. 2002
    ..An increasing number of recently described tau mutations show considerable clinical heterogeneity. The assessment of this phenotypic variation is of vital importance in the differential diagnosis of neurodegenerative diseases...
  87. pmc Sequence analysis of tau in familial and sporadic progressive supranuclear palsy
    H R Morris
    University Department of Clinical Neurology, Institute of Neurology, Queen Square, London WC1NBG, UK
    J Neurol Neurosurg Psychiatry 72:388-90. 2002
    ..This suggests that usually FTDP-17 and PSP, including the rare familial form of PSP, are likely to be separate conditions and that usually PSP and typical PSP-like syndromes are not due to mutations in tau...
  88. ncbi request reprint Hippocampal, but not parahippocampal, damage in a case of dense retrograde amnesia: a pathological study
    Dennis Chan
    Dementia Research Group, Department of Clinical Neurology, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
    Neurosci Lett 329:61-4. 2002
    ..T. is therefore not consistent with the postulated role of the hippocampus as a temporary memory store and suggests instead that the hippocampus is involved in the storage of remote memories as well as recent memories...
  89. ncbi request reprint A common LRRK2 mutation in idiopathic Parkinson's disease
    William P Gilks
    Department of Molecular Neuroscience, Institute of Neurology and National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
    Lancet 365:415-6. 2005
    ..We suggest that testing for this mutation will be important in the management and genetic counselling of patients with Parkinson's disease...
  90. ncbi request reprint Cervical spine chordoid meningioma. Case report
    Ahmed Ibrahim
    Victor Horsley Departments of Neurosurgery and Neuropathology, The National Hospital for Neurology and Neurosurgery, London, United Kingdom
    J Neurosurg Spine 2:195-8. 2005
    ..The authors describe a rare case of chordoid meningioma in the cervical spinal region...
  91. ncbi request reprint The phagocytic capacity of neurones
    Samantha Bowen
    Neuroscience Centre and Pathology Group, Queen Mary s School of Medicine and Dentistry, Institute of Pathology, Royal London Hospital, London, UK
    Eur J Neurosci 25:2947-55. 2007
    ....
  92. ncbi request reprint Analysis of tau haplotypes in Pick's disease
    H R Morris
    Neurogenetics, Institute of Neurology, Reta Lila Weston Institute of Neurological Research, University College London, UK
    Neurology 59:443-5. 2002
    ..There was no difference between the tau H2 haplotype or H2H2 genotype frequency in PiD cases and control subjects. No tau mutations were identified in pathologically typical cases of PiD, with antibody 12-E8-negative Pick bodies...
  93. ncbi request reprint Clinical features of frontotemporal dementia due to the intronic tau 10(+16) mutation
    J C Janssen
    Dementia Research Group, Institute of Neurology, London, UK
    Neurology 58:1161-8. 2002
    ..To describe the clinical features of nine British families with neuropathologically verified frontotemporal dementia (FTD) due to the intronic tau exon 10(+16) mutation...
  94. pmc The heritability and genetics of frontotemporal lobar degeneration
    J D Rohrer
    Dementia Research Centre, Institute of Neurology, Queen Square, London WC1N 3BG, UK
    Neurology 73:1451-6. 2009
    ..Frontotemporal lobar degeneration (FTLD) is a genetically and pathologically heterogeneous neurodegenerative disorder...
  95. ncbi request reprint PINK1 protein in normal human brain and Parkinson's disease
    S Gandhi
    Department of Molecular Neuroscience, Institute of Neurology University College London, London, UK
    Brain 129:1720-31. 2006
    ....
  96. ncbi request reprint Pathological, clinical and genetic heterogeneity in progressive supranuclear palsy
    H R Morris
    Department of Molecular Pathogenesis, Institute of Neurology, Queen Square, London, UK
    Brain 125:969-75. 2002
    ....
  97. ncbi request reprint Knight's move thinking? Mild cognitive impairment in a chess player
    H A Archer
    The Dementia Research Centre, The National Hospital for Neurology and Neurosurgery, London, UK
    Neurocase 11:26-31. 2005
    ....
  98. doi request reprint Clinical outcomes of progressive supranuclear palsy and multiple system atrophy
    S S O'Sullivan
    Reta Lila Weston Institute of Neurological Studies, University College London, London, UK
    Brain 131:1362-72. 2008
    ..The time to the first clinical milestone is a useful prognostic predictor for survival. We confirm that RS had a less favourable course than PSP-P, and that early autonomic failure in MSA is associated with shorter survival...
  99. doi request reprint A clinico-pathological study of subtypes in Parkinson's disease
    M Selikhova
    Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College, London, UK
    Brain 132:2947-57. 2009
    ..Although neuropathological examination failed to distinguish the other subtypes, the classification scheme was supported by an analysis of clinical data that were independent of the basic subgroup definitions...
  100. ncbi request reprint Osteosarcoma and fibrosarcoma caused by postoperative radiotherapy for a pituitary adenoma. Case report
    Kanna K Gnanalingham
    Department of Neurosurgery, National Hospital for Neurology and Neurosurgery, London, United Kingdom
    J Neurosurg 96:960-3. 2002
    ..The authors report on what they believe to be the first case in which fibrosarcoma and, later, osteosarcoma developed during a 14-year period following surgery and radiotherapy for a nonsecreting pituitary macroadenoma...
  101. pmc Microarray analysis of pediatric ependymoma identifies a cluster of 112 candidate genes including four transcripts at 22q12.1-q13.3
    Blanca Suarez-Merino
    Department of Molecular Neuroscience, Institute of Neurology, National Hospital for Neurology and Neurosurgery, University College London, London, UK
    Neuro Oncol 7:20-31. 2005
    ..3, respectively. These genes represent candidate genes involved in ependymoma tumorigenesis. To the authors' knowledge, this is the first time microarray analysis and Q-PCR have been linked to identify heterozygous/homozygous deletions...