David M A Mann

Summary

Affiliation: University of Manchester
Country: UK

Publications

  1. ncbi request reprint Brain distribution of dipeptide repeat proteins in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9ORF72
    Yvonne S Davidson
    Clinical and Cognitive Sciences Research Group, Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Salford Royal Hospital, Salford M6 8HD, UK
    Acta Neuropathol Commun 2:70. 2014
  2. pmc TDP-43 protein in plasma may index TDP-43 brain pathology in Alzheimer's disease and frontotemporal lobar degeneration
    Penelope Foulds
    Division of Biomedical and Life Sciences, School of Health and Medicine, University of Lancaster, Lancaster, UK
    Acta Neuropathol 116:141-6. 2008
  3. pmc Heterogeneity of ubiquitin pathology in frontotemporal lobar degeneration: classification and relation to clinical phenotype
    Ian R A Mackenzie
    Department of Pathology, Vancouver General Hospital, V5Z 1M9, Vancouver, BC, Canada
    Acta Neuropathol 112:539-49. 2006
  4. doi request reprint TDP-43 pathological changes in early onset familial and sporadic Alzheimer's disease, late onset Alzheimer's disease and Down's syndrome: association with age, hippocampal sclerosis and clinical phenotype
    Yvonne S Davidson
    Mental Health and Neurodegeneration Research Group, Salford Royal Foundation Trust, University of Manchester, Salford M6 8HD, UK
    Acta Neuropathol 122:703-13. 2011
  5. pmc Phosphorylated TDP-43 pathology and hippocampal sclerosis in progressive supranuclear palsy
    Osamu Yokota
    Greater Manchester Neurosciences Centre, Hope Hospital, University of Manchester, Salford, UK
    Acta Neuropathol 120:55-66. 2010
  6. doi request reprint Frequency and clinical characteristics of progranulin mutation carriers in the Manchester frontotemporal lobar degeneration cohort: comparison with patients with MAPT and no known mutations
    Stuart M Pickering-Brown
    Clinical Neuroscience Research Group, Faculty of Medical and Human Sciences, University of Manchester, Oxford Rd, Manchester M13 9PT, UK
    Brain 131:721-31. 2008
  7. ncbi request reprint Ubiquitinated pathological lesions in frontotemporal lobar degeneration contain the TAR DNA-binding protein, TDP-43
    Yvonne Davidson
    Clinical Neuroscience Research Group, Division of Medicine and Neuroscience, Greater Manchester Neurosciences Centre, Hope Hospital, University of Manchester, Salford, M6 8HD, UK
    Acta Neuropathol 113:521-33. 2007
  8. ncbi request reprint TDP-43 in ubiquitinated inclusions in the inferior olives in frontotemporal lobar degeneration and in other neurodegenerative diseases: a degenerative process distinct from normal ageing
    Yvonne Davidson
    Clinical Neuroscience Research Group, Faculty of Medical and Human Sciences, Greater Manchester Neurosciences Centre, School of Translational Medicine, Hope Hospital, University of Manchester, Salford, M6 8HD, UK
    Acta Neuropathol 118:359-69. 2009
  9. pmc Ubiquitin associated protein 1 is a risk factor for frontotemporal lobar degeneration
    Sara Rollinson
    Clinical Neurosciences, Faculty of Human and Medical Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, UK
    Neurobiol Aging 30:656-65. 2009
  10. doi request reprint Classification and pathology of primary progressive aphasia
    Jennifer M Harris
    From the Manchester Academic Health Sciences Centre J M H, C G, J C T, A M T R, D N, D d P, P P, D M A M, J S S, M J, Cerebral Function Unit, Greater Manchester Neuroscience Centre, Salford Royal NHS Foundation Trust, Salford and Institute of Brain, Behaviour and Mental Health J M H, D N, D M A M, J S S, M J, University of Manchester, UK
    Neurology 81:1832-9. 2013

Collaborators

Detail Information

Publications30

  1. ncbi request reprint Brain distribution of dipeptide repeat proteins in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9ORF72
    Yvonne S Davidson
    Clinical and Cognitive Sciences Research Group, Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Salford Royal Hospital, Salford M6 8HD, UK
    Acta Neuropathol Commun 2:70. 2014
    ....
  2. pmc TDP-43 protein in plasma may index TDP-43 brain pathology in Alzheimer's disease and frontotemporal lobar degeneration
    Penelope Foulds
    Division of Biomedical and Life Sciences, School of Health and Medicine, University of Lancaster, Lancaster, UK
    Acta Neuropathol 116:141-6. 2008
    ..As a predictive test, plasma TDP-43 level may have great practical value in directing therapeutic strategies aimed at preventing or removing tau or TDP-43 pathological changes from the brain in FTLD and AD...
  3. pmc Heterogeneity of ubiquitin pathology in frontotemporal lobar degeneration: classification and relation to clinical phenotype
    Ian R A Mackenzie
    Department of Pathology, Vancouver General Hospital, V5Z 1M9, Vancouver, BC, Canada
    Acta Neuropathol 112:539-49. 2006
    ....
  4. doi request reprint TDP-43 pathological changes in early onset familial and sporadic Alzheimer's disease, late onset Alzheimer's disease and Down's syndrome: association with age, hippocampal sclerosis and clinical phenotype
    Yvonne S Davidson
    Mental Health and Neurodegeneration Research Group, Salford Royal Foundation Trust, University of Manchester, Salford M6 8HD, UK
    Acta Neuropathol 122:703-13. 2011
    ..005), but this association disappeared when TDP-43-positive cases were excluded from the analysis. TDP-43 may, after all, be integral to the pathology of AD, and to some extent determine the clinical phenotype present...
  5. pmc Phosphorylated TDP-43 pathology and hippocampal sclerosis in progressive supranuclear palsy
    Osamu Yokota
    Greater Manchester Neurosciences Centre, Hope Hospital, University of Manchester, Salford, UK
    Acta Neuropathol 120:55-66. 2010
    ..These findings suggest that (1) although PSP is nominally a tauopathy, pathological TDP-43 can accumulate in the limbic system in some cases, and (2) TDP-43 pathology may be concurrent with HS...
  6. doi request reprint Frequency and clinical characteristics of progranulin mutation carriers in the Manchester frontotemporal lobar degeneration cohort: comparison with patients with MAPT and no known mutations
    Stuart M Pickering-Brown
    Clinical Neuroscience Research Group, Faculty of Medical and Human Sciences, University of Manchester, Oxford Rd, Manchester M13 9PT, UK
    Brain 131:721-31. 2008
    ..These findings complement recent clinico-pathological findings in suggesting identifiable associations between clinical phenotype and genotype in FTLD...
  7. ncbi request reprint Ubiquitinated pathological lesions in frontotemporal lobar degeneration contain the TAR DNA-binding protein, TDP-43
    Yvonne Davidson
    Clinical Neuroscience Research Group, Division of Medicine and Neuroscience, Greater Manchester Neurosciences Centre, Hope Hospital, University of Manchester, Salford, M6 8HD, UK
    Acta Neuropathol 113:521-33. 2007
    ..We conclude that the UBQ-ir lesions of FTLD and MND are defined by the presence of TDP-43, and that these disorders can be subsumed into a single disease entity under the umbrella of TDP-43 proteinopathy...
  8. ncbi request reprint TDP-43 in ubiquitinated inclusions in the inferior olives in frontotemporal lobar degeneration and in other neurodegenerative diseases: a degenerative process distinct from normal ageing
    Yvonne Davidson
    Clinical Neuroscience Research Group, Faculty of Medical and Human Sciences, Greater Manchester Neurosciences Centre, School of Translational Medicine, Hope Hospital, University of Manchester, Salford, M6 8HD, UK
    Acta Neuropathol 118:359-69. 2009
    ..The pathophysiological mechanism leading to their formation, and any consequences their presence may have on nerve cell function, remain unknown...
  9. pmc Ubiquitin associated protein 1 is a risk factor for frontotemporal lobar degeneration
    Sara Rollinson
    Clinical Neurosciences, Faculty of Human and Medical Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, UK
    Neurobiol Aging 30:656-65. 2009
    ..Our data for the first time identifies UBAP1 as a genetic risk factor for FTLD and suggests a mechanistic relationship between this protein and TDP-43...
  10. doi request reprint Classification and pathology of primary progressive aphasia
    Jennifer M Harris
    From the Manchester Academic Health Sciences Centre J M H, C G, J C T, A M T R, D N, D d P, P P, D M A M, J S S, M J, Cerebral Function Unit, Greater Manchester Neuroscience Centre, Salford Royal NHS Foundation Trust, Salford and Institute of Brain, Behaviour and Mental Health J M H, D N, D M A M, J S S, M J, University of Manchester, UK
    Neurology 81:1832-9. 2013
    ..We aimed to determine the extent to which patients with progressive language impairment conform to 2011 primary progressive aphasia (PPA) classification and to examine clinicopathologic correlations within PPA variants...
  11. ncbi request reprint The most common type of FTLD-FUS (aFTLD-U) is associated with a distinct clinical form of frontotemporal dementia but is not related to mutations in the FUS gene
    Julie S Snowden
    Mental Health and Neurodegeneration Research Group, Faculty of Human and Medical Sciences, University of Manchester, Manchester, UK
    Acta Neuropathol 122:99-110. 2011
    ..Whether mutations in the FUS gene cause some cases of FTLD remains unresolved...
  12. pmc Granular expression of prolyl-peptidyl isomerase PIN1 is a constant and specific feature of Alzheimer's disease pathology and is independent of tau, Aβ and TDP-43 pathology
    Ayoub Dakson
    Mental Health and Neurodegeneration Research Group, School of Community Based Medicine, Faculty of Medical and Human Sciences, Hope Hospital, Greater Manchester Neurosciences Centre, University of Manchester, Stott Lane, Salford, M6 8HD, UK
    Acta Neuropathol 121:635-49. 2011
    ..Present findings indicate that PIN1 changes are a constant feature of AD pathology and could serve as a biomarker of the onset or spread of AD neuropathology independent of tau or Aβ...
  13. doi request reprint Analysis of the hexanucleotide repeat in C9ORF72 in Alzheimer's disease
    Sara Rollinson
    Mental Health and Neurodegeneration Research Group, Faculty of Human and Medical Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, UK
    Neurobiol Aging 33:1846.e5-6. 2012
    ..A normal range of repeats was found in all cases. We conclude that the hexanucleotide repeat expansion is specific to the FTLD/ALS disease spectrum...
  14. ncbi request reprint Dementia lacking distinctive histology (DLDH) revisited
    Ian R A Mackenzie
    Department of Pathology, Vancouver General Hospital, Vancouver, BC, Canada
    Acta Neuropathol 112:551-9. 2006
    ..Hence, we conclude that DLDH is a very rare disorder, and that lack of sensitivity for UBQ immunostaining is likely responsible for the failure to disclose this pathology and to provide a diagnosis of FTLD-U...
  15. doi request reprint The clinical diagnosis of early-onset dementias: diagnostic accuracy and clinicopathological relationships
    Julie S Snowden
    Cerebral Function Unit, Greater Manchester Neuroscience Centre, Salford Royal NHS Foundation Trust, Salford M6 8HD, UK
    Brain 134:2478-92. 2011
    ..Moreover, careful clinical phenotyping allows prediction of histopathological subtype of frontotemporal lobar degeneration. The principles guiding diagnosis provide the foundation for future prospective studies...
  16. ncbi request reprint Apolipoprotein E epsilon4 allele frequency and age at onset of Alzheimer's disease
    Yvonne Davidson
    Clinical Neuroscience Research Group, Division of Medicine and Neuroscience, University of Manchester, Greater Manchester Neurosciences Centre, Hope Hospital, Salford, UK
    Dement Geriatr Cogn Disord 23:60-6. 2007
    ..44, was highest in the 60-69 years age class, progressively decreasing either side of this age group. APOE epsilon4 allele therefore has its maximum impact between onset ages of between 60 and 70 years...
  17. doi request reprint No association of PGRN 3'UTR rs5848 in frontotemporal lobar degeneration
    Sara Rollinson
    Clinical Neurosciences Research Group, Faculty of Human and Medical Sciences, University of Manchester, Oxford Road, Manchester, M13 9PT, UK
    Neurobiol Aging 32:754-5. 2011
    ..No association of rs5848 with FTLD was observed in any individual cohort nor was any observed when the data was combined. These data argue that rs5848 is not a risk factor for FTLD...
  18. ncbi request reprint TDP-43 gene analysis in frontotemporal lobar degeneration
    Sara Rollinson
    Division of Regenerative Medicine, Department of Medicine, University of Manchester, Oxford Road, Manchester M13 9PT, UK
    Neurosci Lett 419:1-4. 2007
    ..We found no evidence of TDP-43 variation increasing risk for FTLD in this cohort. These data suggest that TDP-43 accumulation is a consequence of the disease process underlying FTLD...
  19. pmc Nuclear Carrier and RNA Binding Proteins in Frontotemporal Lobar Degeneration associated with Fused in Sarcoma (FUS) pathological changes
    Yvonne S Davidson
    Mental Health and Neurodegeneration Research Group, Faculty of Human and Medical Sciences, University of Manchester, Manchester, UK Northwestern CNADC Neuropathology Core, Northwestern University Feinberg School of Medicine, Chicago, USA Department of Neuropathology, Walton Centre for Neurology and Neurosurgery, Liverpool, UK Neuropathology Cellular Pathology, Royal Victoria Infirmary, Newcastle upon Tyne, UK Institute for Ageing and Health, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, UK Departments of Neurology and Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA Cerebral Function Unit, Greater Manchester Neuroscience Centre, Salford Royal Foundation Trust, UK
    Neuropathol Appl Neurobiol . 2012
    ..2012 The Authors. Neuropathology and Applied Neurobiology © 2012 British Neuropathological Society...
  20. doi request reprint Progressive anomia revisited: focal degeneration associated with progranulin gene mutation
    Julie S Snowden
    School of Translational Medicine, University of Manchester, Hope Hospital, Salford, UK
    Neurocase 13:366-77. 2007
    ..The case exemplifies the heterogeneity of clinical expression of FTLD and contributes to understanding of primary progressive aphasia...
  21. doi request reprint Effect of topographical distribution of α-synuclein pathology on TDP-43 accumulation in Lewy body disease
    Osamu Yokota
    Greater Manchester Neurosciences Centre, Hope Hospital, University of Manchester, Salford, UK
    Acta Neuropathol 120:789-801. 2010
    ..In the amygdala, TDP-43 was often colocalized with α-synuclein or tau. Given these findings, we suggest that α-synuclein pathology is associated with TDP-43 accumulation in LBD cases...
  22. doi request reprint No interaction between tau and TDP-43 pathologies in either Frontotemporal Lobar Degeneration or Motor Neurone Disease
    Andrew C Robinson
    Clinical and Cognitive Sciences Research Group, Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Salford Royal Hospital, Salford, M6 8HD, UK
    Neuropathol Appl Neurobiol . 2014
    ..While such a classification implies only a single type of protein should be present, recent studies have demonstrated dual tau and TDP-43 proteinopathy can occur, particularly in inherited FTLD...
  23. pmc A longitudinal study on α-synuclein in blood plasma as a biomarker for Parkinson's disease
    Penelope G Foulds
    Division of Biomedical and Life Sciences, Faculty of Health and Medicine, University of Lancaster, Lancaster, LA1 4AY, UK
    Sci Rep 3:2540. 2013
    ..012). Overall, we conclude that the plasma level of phosphorylated α-synuclein has potential value as a diagnostic tool, whereas the level of total α-synuclein could act as a surrogate marker for the progression of PD. ..
  24. doi request reprint Detection of elevated levels of soluble alpha-synuclein oligomers in post-mortem brain extracts from patients with dementia with Lewy bodies
    Katerina E Paleologou
    Division of Biomedical and Life Sciences, School of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK
    Brain 132:1093-101. 2009
    ..Furthermore, these findings establish FILA-1 as a very sensitive tool for the detection of oligomeric forms of alpha-syn in human brain lysates...
  25. doi request reprint Development of a proteolytically stable retro-inverso peptide inhibitor of beta-amyloid oligomerization as a potential novel treatment for Alzheimer's disease
    Mark Taylor
    Division of Biomedical and Life Sciences, School of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK
    Biochemistry 49:3261-72. 2010
    ..Thus, RI-OR2 represents a strong candidate for further development as a novel treatment for Alzheimer's disease...
  26. ncbi request reprint Histopathological changes underlying frontotemporal lobar degeneration with clinicopathological correlation
    Jing Shi
    Clinical Neuroscience Research Group, University of Manchester, Greater Manchester Neurosciences Centre, Hope Hospital, Stott Lane, Salford M6 8HD, UK
    Acta Neuropathol 110:501-12. 2005
    ....
  27. pmc Plasma phosphorylated-TDP-43 protein levels correlate with brain pathology in frontotemporal lobar degeneration
    Penelope G Foulds
    Division of Biomedical and Life Sciences, School of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK
    Acta Neuropathol 118:647-58. 2009
    ....
  28. doi request reprint Histone deacetylase class II and acetylated core histone immunohistochemistry in human brains with Huntington's disease
    Hsin Hsien Yeh
    Wolfson Molecular Imaging Centre, School of Cancer and enabling Sciences, University of Manchester, Manchester, UK
    Brain Res 1504:16-24. 2013
    ....
  29. ncbi request reprint A 3'-UTR polymorphism in the oxidized LDL receptor 1 gene increases Abeta40 load as cerebral amyloid angiopathy in Alzheimer's disease
    Jing Shi
    Clinical Neuroscience Research Group, University of Manchester, Hope Hospital, Salford, M6 8HD, UK
    Acta Neuropathol 111:15-20. 2006
    ....