Manuela Neumann

Summary

Affiliation: University of Munich
Country: Germany

Publications

  1. ncbi Missense mutations in the progranulin gene linked to frontotemporal lobar degeneration with ubiquitin-immunoreactive inclusions reduce progranulin production and secretion
    Sunita S Shankaran
    Munich Center for Integrated Protein Science and Adolf Butenandt Institute, Department of Biochemistry, Laboratory for Neurodegenerative Disease Research, Schillerstrasse 44, 80336 Munich, Germany
    J Biol Chem 283:1744-53. 2008
  2. ncbi TDP-43 proteinopathy in frontotemporal lobar degeneration and amyotrophic lateral sclerosis: protein misfolding diseases without amyloidosis
    Manuela Neumann
    Center for Neuropathology and Prion Research, Ludwig Maximilians University of Munich, Feodor Lynen Strasse 23, 81377 Muenchen, Germany
    Arch Neurol 64:1388-94. 2007
  3. ncbi TDP-43-positive white matter pathology in frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Manuela Neumann
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neuropathol Exp Neurol 66:177-83. 2007
  4. ncbi Absence of heterogeneous nuclear ribonucleoproteins and survival motor neuron protein in TDP-43 positive inclusions in frontotemporal lobar degeneration
    Manuela Neumann
    Center for Neuropathology and Prion Research, Ludwig Maximilians University, Feodor Lynen Str 23, 81377 Munich, Germany
    Acta Neuropathol 113:543-8. 2007
  5. pmc Enrichment of C-terminal fragments in TAR DNA-binding protein-43 cytoplasmic inclusions in brain but not in spinal cord of frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Lionel M Igaz
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce St, 3rd Floor, Maloney Bldg, Philadelphia, PA 19104, USA
    Am J Pathol 173:182-94. 2008
  6. ncbi Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Manuela Neumann
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Science 314:130-3. 2006
  7. pmc Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies
    Kunihiro Uryu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neuropathol Exp Neurol 67:555-64. 2008
  8. pmc Requirements for stress granule recruitment of fused in sarcoma (FUS) and TAR DNA-binding protein of 43 kDa (TDP-43)
    Eva Bentmann
    Adolf Butenandt Institute, Biochemistry, Ludwig Maximilians University, Munchen, Germany
    J Biol Chem 287:23079-94. 2012
  9. ncbi TDP-43 pathologic lesions and clinical phenotype in frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Murray Grossman
    Department of Neurology, University of Pennsylvania School of Medicine, 2 Gibson, 3400 Spruce St, Philadelphia, PA 19104 4283, USA
    Arch Neurol 64:1449-54. 2007
  10. pmc Clinical and pathological continuum of multisystem TDP-43 proteinopathies
    Felix Geser
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Arch Neurol 66:180-9. 2009

Detail Information

Publications46

  1. ncbi Missense mutations in the progranulin gene linked to frontotemporal lobar degeneration with ubiquitin-immunoreactive inclusions reduce progranulin production and secretion
    Sunita S Shankaran
    Munich Center for Integrated Protein Science and Adolf Butenandt Institute, Department of Biochemistry, Laboratory for Neurodegenerative Disease Research, Schillerstrasse 44, 80336 Munich, Germany
    J Biol Chem 283:1744-53. 2008
    ..Upon reduction of progranulin, neither a major redistribution of TDP-43 nor proteolytic processing to disease-characterizing C-terminal fragments could be observed...
  2. ncbi TDP-43 proteinopathy in frontotemporal lobar degeneration and amyotrophic lateral sclerosis: protein misfolding diseases without amyloidosis
    Manuela Neumann
    Center for Neuropathology and Prion Research, Ludwig Maximilians University of Munich, Feodor Lynen Strasse 23, 81377 Muenchen, Germany
    Arch Neurol 64:1388-94. 2007
  3. ncbi TDP-43-positive white matter pathology in frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Manuela Neumann
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neuropathol Exp Neurol 66:177-83. 2007
    ..Taken together, these results expand the spectrum of TDP-43 pathology in FTLD-U, suggesting that white matter pathology might contribute to the neurodegenerative process and clinical symptoms in FTLD-U...
  4. ncbi Absence of heterogeneous nuclear ribonucleoproteins and survival motor neuron protein in TDP-43 positive inclusions in frontotemporal lobar degeneration
    Manuela Neumann
    Center for Neuropathology and Prion Research, Ludwig Maximilians University, Feodor Lynen Str 23, 81377 Munich, Germany
    Acta Neuropathol 113:543-8. 2007
    ..These results argue against a role of these binding partners in the pathogenesis of FTLD-U and emphasize the specificity of TDP-43 as marker for FTLD-U pathology...
  5. pmc Enrichment of C-terminal fragments in TAR DNA-binding protein-43 cytoplasmic inclusions in brain but not in spinal cord of frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Lionel M Igaz
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce St, 3rd Floor, Maloney Bldg, Philadelphia, PA 19104, USA
    Am J Pathol 173:182-94. 2008
    ..Therefore, regionally different pathogenic processes may underlie the development of abnormal TDP-43 proteinopathies...
  6. ncbi Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Manuela Neumann
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Science 314:130-3. 2006
    ..TDP-43 represents the common pathologic substrate linking these neurodegenerative disorders...
  7. pmc Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies
    Kunihiro Uryu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neuropathol Exp Neurol 67:555-64. 2008
    ..These findings provide further insight into the burden and clinical significance of TDP-43 pathology in disorders other than FTLD-U and amyotrophic lateral sclerosis...
  8. pmc Requirements for stress granule recruitment of fused in sarcoma (FUS) and TAR DNA-binding protein of 43 kDa (TDP-43)
    Eva Bentmann
    Adolf Butenandt Institute, Biochemistry, Ludwig Maximilians University, Munchen, Germany
    J Biol Chem 287:23079-94. 2012
    ....
  9. ncbi TDP-43 pathologic lesions and clinical phenotype in frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Murray Grossman
    Department of Neurology, University of Pennsylvania School of Medicine, 2 Gibson, 3400 Spruce St, Philadelphia, PA 19104 4283, USA
    Arch Neurol 64:1449-54. 2007
    ..TDP-43 is a major ubiquitinated disease protein in the pathologic condition of frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U)...
  10. pmc Clinical and pathological continuum of multisystem TDP-43 proteinopathies
    Felix Geser
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Arch Neurol 66:180-9. 2009
    ....
  11. pmc Arginine methylation next to the PY-NLS modulates Transportin binding and nuclear import of FUS
    Dorothee Dormann
    Adolf Butenandt Institute, Biochemistry, Ludwig Maximilians University, Munich, Germany
    EMBO J 31:4258-75. 2012
    ....
  12. pmc Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 Proteinopathies
    Lionel M Igaz
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, USA
    J Biol Chem 284:8516-24. 2009
    ..Thus, our results show that TDP-43 CTF expression recapitulates key biochemical features of pathological TDP-43 and support the hypothesis that the generation of TDP-43 CTFs is an important step in the pathogenesis of FTLD-U and ALS...
  13. ncbi Clinical, genetic, and pathologic characteristics of patients with frontotemporal dementia and progranulin mutations
    Vivianna M Van Deerlin
    Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Arch Neurol 64:1148-53. 2007
    ..Patients with frontotemporal dementia due to mutation of progranulin may have a distinct phenotype...
  14. pmc Pathological heterogeneity of frontotemporal lobar degeneration with ubiquitin-positive inclusions delineated by ubiquitin immunohistochemistry and novel monoclonal antibodies
    Deepak M Sampathu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce St, 3rd Floor Maloney Bldg, Philadelphia, PA 19104, USA
    Am J Pathol 169:1343-52. 2006
    ..Identification of the disease proteins recognized by these mAbs will further advance understanding of molecular substrates of FTLD-U neurodegenerative pathways...
  15. pmc Misfolded proteinase K-resistant hyperphosphorylated alpha-synuclein in aged transgenic mice with locomotor deterioration and in human alpha-synucleinopathies
    Manuela Neumann
    Department of Neuropathology, Ludwig Maximilians University, Munich, Germany
    J Clin Invest 110:1429-39. 2002
    ..The transgenic mice showed a progressive deterioration of locomotor function. Thus, misfolding and hyperphosphorylation of alphaS may cause dysfunction of affected brain regions...
  16. pmc TDP-43 mediates degeneration in a novel Drosophila model of disease caused by mutations in VCP/p97
    Gillian P Ritson
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 30:7729-39. 2010
    ..We suggest that these findings are likely relevant to the pathogenic mechanism of a broad array of TDP-43 proteinopathies, including frontotemporal lobar degeneration and amyotrophic lateral sclerosis...
  17. pmc Two German kindreds with familial amyotrophic lateral sclerosis due to TARDBP mutations
    Peter Kühnlein
    Center for Neuropathology and Prion Research, Ludwig Maximilians University, Munich, Feodor Lynen Strasse 23, 81377 Munich, Germany
    Arch Neurol 65:1185-9. 2008
    ..This makes TARDBP, the gene encoding for TDP-43, a candidate for genetic screening in ALS...
  18. pmc TARDBP mutations in amyotrophic lateral sclerosis with TDP-43 neuropathology: a genetic and histopathological analysis
    Vivianna M Van Deerlin
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
    Lancet Neurol 7:409-16. 2008
    ..Our aim was to investigate whether TARDBP is a candidate disease gene for familial ALS that is not associated with mutations in superoxide dismutase 1 (SOD1)...
  19. ncbi Regional distribution of proteinase K-resistant alpha-synuclein correlates with Lewy body disease stage
    Manuela Neumann
    Institute of Neuropathology, Laboratory of Alzheimer s and Parkinson s Disease Research, Ludwig Maximilians University, Munich, Germany
    J Neuropathol Exp Neurol 63:1225-35. 2004
    ..Variable amounts of neuritic PK-resistant alphaSYN were found in the striatum of all cases. Thus, PK resistance of alphaSYN may be useful for the development of biomarkers of LB diseases...
  20. ncbi TDP-43 proteinopathy: the neuropathology underlying major forms of sporadic and familial frontotemporal lobar degeneration and motor neuron disease
    Linda K Kwong
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, HUP, Philadelphia, PA, 19104 4283, USA
    Acta Neuropathol 114:63-70. 2007
    ....
  21. pmc Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions
    Vivianna M Van Deerlin
    1 Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA 2 These authors contributed equally to this work
    Nat Genet 42:234-9. 2010
    ..TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism...
  22. ncbi TDP-43 in the ubiquitin pathology of frontotemporal dementia with VCP gene mutations
    Manuela Neumann
    Center for Neuropathology and Prion Research, Ludwig Maximilians University, Munich, Germany
    J Neuropathol Exp Neurol 66:152-7. 2007
    ..TDP-43 is a common pathologic substrate linking a variety of distinct patterns of FTLD-U pathology caused by different genetic alterations...
  23. ncbi Pathological properties of the Parkinson's disease-associated protein DJ-1 in alpha-synucleinopathies and tauopathies: relevance for multiple system atrophy and Pick's disease
    Manuela Neumann
    Institute of Neuropathology, Ludwig Maximilians University of Munich, Munich, Germany
    Acta Neuropathol 107:489-96. 2004
    ..Our results suggest that DJ-1 is up-regulated in reactive astrocytes as well as in neuronal and glial cells with specific alpha-synucleinopathy and tauopathy...
  24. doi TDP-43-negative FTLD-U is a significant new clinico-pathological subtype of FTLD
    Sigrun Roeber
    Center for Neuropathology and Prion Research, Ludwig Maximilians University Munich, Feodor Lynen Str 23, 81377, Munich, Germany
    Acta Neuropathol 116:147-57. 2008
    ..The highly consistent clinical and neuropathological phenotype supports the concept that TDP-43-negative FTLD-U should be considered as a new clinicopathological FTLD entity...
  25. pmc Transactive response DNA-binding protein 43 burden in familial Alzheimer disease and Down syndrome
    Carol F Lippa
    Drexel University College of Medicine Philadelphia, Philadelphia, Pennsylvania 19102, USA
    Arch Neurol 66:1483-8. 2009
    ..To assess the transactive response DNA-binding protein 43 (TDP-43) burden in familial forms of Alzheimer disease (FAD) and Down syndrome (DS) to determine whether TDP-43 inclusions are also present...
  26. ncbi TDP-43 immunoreactivity in anoxic, ischemic and neoplastic lesions of the central nervous system
    Edward B Lee
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Acta Neuropathol 115:305-11. 2008
    ..These findings expand our knowledge of the distribution and localization of TDP-43, and indicate that the TDP-43 inclusions seen in frontotemporal dementias and motor neuron diseases are specific to a neurodegenerative process...
  27. ncbi hnRNP A3 binds to GGGGCC repeats and is a constituent of p62-positive/TDP43-negative inclusions in the hippocampus of patients with C9orf72 mutations
    Kohji Mori
    Adolf Butenandt Institute, Biochemistry, Ludwig Maximilians University, Schillerstr 44, 80336, Munich, Germany
    Acta Neuropathol 125:413-23. 2013
    ..Thus, we have identified one protein component of these pathognomonic inclusions...
  28. ncbi Novel G335V mutation in the tau gene associated with early onset familial frontotemporal dementia
    Manuela Neumann
    Center for Neuropathology and Prion Research, Ludwig Maximilians University, Munich, Germany
    Neurogenetics 6:91-5. 2005
    ....
  29. ncbi Cerebral gene expression profiles in sporadic Creutzfeldt-Jakob disease
    Wei Xiang
    Center for Neuropathology and Prion Research, Ludwig Maximilians University Munich, Munich, Germany
    Ann Neurol 58:242-57. 2005
    ..Conspicuously, sCJD brains showed a great similarity with ageing human brains, both in the global expression patterns and in the identified differentially expressed genes...
  30. doi Dopaminergic midbrain neurons are the prime target for mitochondrial DNA deletions
    Andreas Bender
    Dept of Neurology, Mitochondrial Neurogenetics, University of Munich, Marchioninistr 15, 81377, Munich, Germany
    J Neurol 255:1231-5. 2008
    ..01; ANOVA). This data shows that there is a specific susceptibility of dopaminergic SN neurons to accumulate substantial amounts of mtDNA deletions, regardless of the underlying clinical phenotype...
  31. pmc TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions
    Michael D Gallagher
    Cell and Molecular Biology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
    Acta Neuropathol 127:407-18. 2014
    ....
  32. ncbi Structure/function of alpha-synuclein in health and disease: rational development of animal models for Parkinson's and related diseases
    Philipp J Kahle
    Department of Biochemistry, Ludwig Maximilians University, Munich, Germany
    J Neurochem 82:449-57. 2002
  33. ncbi Proteolytic processing of TAR DNA binding protein-43 by caspases produces C-terminal fragments with disease defining properties independent of progranulin
    Dorothee Dormann
    Deutsches Zentrum für Neurodegenerative Erkrankungen and Adolf Butenandt Institute, Department of Biochemistry, Ludwig Maximilians University, Munich, Germany
    J Neurochem 110:1082-94. 2009
    ..Our findings therefore suggest that caspase-mediated processing generates CTFs of similar biochemical properties as those occurring in nuclear and cytoplasmic deposits of FTLD-U patients independent of PGRN levels...
  34. ncbi Creutzfeldt-Jakob disease in a patient with an R208H mutation of the prion protein gene (PRNP) and a 17-kDa prion protein fragment
    Sigrun Roeber
    Center for Neuropathology and Prion Research, Ludwig Maximilians Universitat Munchen, Feodor Lynen Srasse 23, 81377, Munchen, Germany
    Acta Neuropathol 109:443-8. 2005
    ..Neuropathological examination of the post mortem brain revealed tau pathology in the hippocampus and entorhinal cortex, as well as ballooned neurons in the cortex, hippocampus and subcortical gray matter...
  35. pmc Hyperphosphorylation and insolubility of alpha-synuclein in transgenic mouse oligodendrocytes
    Philipp J Kahle
    Laboratory for Alzheimer s and Parkinson s Disease Research, Department of Biochemistry, Ludwig Maximilians University, D 80336 Munich, Germany
    EMBO Rep 3:583-8. 2002
    ..Thus, ectopic expression alpha SYN in OLs might initiate salient features of MSA pathology...
  36. pmc Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration
    Nigel J Cairns
    Department of Neurology, Washington University School of Medicine, Campus Box 8118, 660 South Euclid Avenue, St Louis, MO, 63110, USA
    Acta Neuropathol 114:5-22. 2007
    ..These criteria will be of value to the practicing neuropathologist and provide a foundation for clinical, clinico-pathologic, mechanistic studies and in vivo models of pathogenesis of FTLD...
  37. pmc TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions
    Nigel J Cairns
    MRCPath, Department of Pathology and Immunology, Washington University School of Medicine, Campus Box 8118, St Louis, MO 63110, USA
    Am J Pathol 171:227-40. 2007
    ....
  38. ncbi Microglial activation mediates neurodegeneration related to oligodendroglial alpha-synucleinopathy: implications for multiple system atrophy
    Nadia Stefanova
    Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria
    Mov Disord 22:2196-203. 2007
    ....
  39. doi Neurodegeneration and motor dysfunction in a conditional model of Parkinson's disease
    Silke Nuber
    Department of Medical Genetics, University of Tuebingen, D 72076 Tuebingen, Germany
    J Neurosci 28:2471-84. 2008
    ..Furthermore, alpha-syn-associated cytotoxicity is independent of filamentous inclusion body formation in our conditional mouse model...
  40. pmc Oxidative stress in transgenic mice with oligodendroglial alpha-synuclein overexpression replicates the characteristic neuropathology of multiple system atrophy
    Nadia Stefanova
    Clinical Department of Neurology, Innsbruck Medical University, Anichstrasse 35 A 6020, Innsbruck, Austria
    Am J Pathol 166:869-76. 2005
    ..Our results indicate that combined mitochondrial inhibition and overexpression of oligodendroglial alpha-SYN generates a novel model of MSA that may be useful for evaluating both pathogenesis and treatment strategies...
  41. ncbi Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations
    Ian R A Mackenzie
    Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
    Ann Neurol 61:427-34. 2007
    ..We recently identified TDP-43 as the major pathological protein in sporadic ALS. In this study, we investigated TDP-43 in a larger series of ALS cases (n = 111), including familial cases with and without SOD1 mutations...
  42. ncbi Tau protein, Abeta42 and S-100B protein in cerebrospinal fluid of patients with dementia with Lewy bodies
    Brit Mollenhauer
    Department of Neurology, Georg August University Gottingen, Gottingen, Germany
    Dement Geriatr Cogn Disord 19:164-70. 2005
    ..We conclude that more specific markers have to be established for the differentiation of these diseases...
  43. ncbi Age-dependent cognitive decline and amygdala pathology in alpha-synuclein transgenic mice
    Christian Freichel
    Pharma Research, F Hoffmann La Roche Ltd, 4070 Basel, Switzerland
    Neurobiol Aging 28:1421-35. 2007
    ..Thus, age-dependent fibrillization of alphaSYN in specific cortical regions concomitant with cognitive decline may reflect dementia with Lewy bodies in a transgenic mouse model...
  44. ncbi 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...
  45. ncbi The amyloid-beta (Abeta) peptide pattern in cerebrospinal fluid in Alzheimer's disease: evidence of a novel carboxyterminally elongated Abeta peptide
    Piotr Lewczuk
    Department of Psychiatry and Psychotherapy, University of Erlangen Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany
    Rapid Commun Mass Spectrom 17:1291-6. 2003
    ..We conclude that SELDI-TOF offers a promising tool for dementia expression pattern profiling using a minute amount of a biological sample...
  46. ncbi Frontotemporal lobar degeneration: demographic characteristics of 353 patients
    Julene K Johnson
    Department of Neurology, Memory and Aging Center, University of California, San Francisco, 94117, USA
    Arch Neurol 62:925-30. 2005
    ..The publication of consensus criteria for FTLD, however, prompted systematic studies. The criteria categorize FTLD into 3 subgroups: frontotemporal dementia, semantic dementia, and progressive nonfluent aphasia...