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Title:
Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration | Acta Neuropathologica
Description:
The aim of this study was to improve the neuropathologic recognition and provide criteria for the pathological diagnosis in the neurodegenerative diseases grouped as frontotemporal lobar degeneration (FTLD); revised criteria are proposed. Recent advances in molecular genetics, biochemistry, and neuropathology of FTLD prompted the Midwest Consortium for Frontotemporal Lobar Degeneration and experts at other centers to review and revise the existing neuropathologic diagnostic criteria for FTLD. The proposed criteria for FTLD are based on existing criteria, which include the tauopathies [FTLD with Pick bodies, corticobasal degeneration, progressive supranuclear palsy, sporadic multiple system tauopathy with dementia, argyrophilic grain disease, neurofibrillary tangle dementia, and FTD with microtubule-associated tau (MAPT) gene mutation, also called FTD with parkinsonism linked to chromosome 17 (FTDP-17)]. The proposed criteria take into account new disease entities and include the novel molecular pathology, TDP-43 proteinopathy, now recognized to be the most frequent histological finding in FTLD. TDP-43 is a major component of the pathologic inclusions of most sporadic and familial cases of FTLD with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Mutations in valosin-containing protein (VCP) gene are present in rare familial forms of FTD, and some families with FTD and/or MND have been linked to chromosome 9p, and both are types of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. In addition to genetic heterogeneity amongst the TDP-43 proteinopathies, there is also neuropathologic heterogeneity and there is a close relationship between genotype and FTLD-U subtype. In addition to these recent significant advances in the neuropathology of FTLD-U, novel FTLD entities have been further characterized, including neuronal intermediate filament inclusion disease. The proposed criteria incorporate up-to-date neuropathology of FTLD in the light of recent immunohistochemical, biochemical, and genetic advances. 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.
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google, scholar, pubmed, article, frontotemporal, cas, dementia, degeneration, disease, lobar, pathology, neurol, neuropathol, university, cairns, mann, criteria, neuropathologic, mackenzie, dickson, neuropathology, neurology, department, trojanowski, school, medicine, acta, inclusions, ubiquitin, research, lee, gene, tdp, mutations, clinical, neary, usa, halliday, ftld, tau, ubiquitinpositive, pickeringbrown, snowden, brain, bigio, diagnosis, alzheimer, van, neumann, white,

Topics {✒️}

inclusion body myopathy tar dna-binding protein ubiquitin-positive tau-negative inclusions month download article/chapter variant creutzfeldt–jakob disease ubiquitin-positive intraneuronal inclusions ubiquitin-positive inclusions delineated neocortical ubiquitin-immunoreactive inclusions tau-negative inclusions caused chromosome 9p-linked als-ftd alzheimer disease-related lesions steele-richardson-olszewski syndrome glenda halliday primary progressive aphasia motor neuron disease neuropsychological profile full article pdf familial tdp-43 proteinopathy author information authors van der zee extra-motor cortices privacy choices/manage cookies tau-negative inclusions neurodegenerative disease research frontotemporal lobar degeneration related subjects protein gene mutations ubiquitin-positive inclusions lea tenenholz grinberg neurodegenerative diseases grouped check access instant access sporadic 4-repeat tauopathy amyotrophic lateral sclerosis amyotrophic-lateral-sclerosis ubiquitin proteasome system de deyn pp ubiquitin immunoreactive structures disease research center disease-related pathology argyrophilic grain disease tau protein heterogeneous degeneration involving faculdade de medicina rare familial forms progressive supranuclear palsy tangle predominant form tdp-43 proteinopathy author correspondence van den broeck

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         headline:Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration
         description:The aim of this study was to improve the neuropathologic recognition and provide criteria for the pathological diagnosis in the neurodegenerative diseases grouped as frontotemporal lobar degeneration (FTLD); revised criteria are proposed. Recent advances in molecular genetics, biochemistry, and neuropathology of FTLD prompted the Midwest Consortium for Frontotemporal Lobar Degeneration and experts at other centers to review and revise the existing neuropathologic diagnostic criteria for FTLD. The proposed criteria for FTLD are based on existing criteria, which include the tauopathies [FTLD with Pick bodies, corticobasal degeneration, progressive supranuclear palsy, sporadic multiple system tauopathy with dementia, argyrophilic grain disease, neurofibrillary tangle dementia, and FTD with microtubule-associated tau (MAPT) gene mutation, also called FTD with parkinsonism linked to chromosome 17 (FTDP-17)]. The proposed criteria take into account new disease entities and include the novel molecular pathology, TDP-43 proteinopathy, now recognized to be the most frequent histological finding in FTLD. TDP-43 is a major component of the pathologic inclusions of most sporadic and familial cases of FTLD with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Mutations in valosin-containing protein (VCP) gene are present in rare familial forms of FTD, and some families with FTD and/or MND have been linked to chromosome 9p, and both are types of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. In addition to genetic heterogeneity amongst the TDP-43 proteinopathies, there is also neuropathologic heterogeneity and there is a close relationship between genotype and FTLD-U subtype. In addition to these recent significant advances in the neuropathology of FTLD-U, novel FTLD entities have been further characterized, including neuronal intermediate filament inclusion disease. The proposed criteria incorporate up-to-date neuropathology of FTLD in the light of recent immunohistochemical, biochemical, and genetic advances. 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.
         datePublished:2007-06-20T00:00:00Z
         dateModified:2007-06-20T00:00:00Z
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            Frontotemporal dementia
            Semantic dementia
            Progressive non-fluent aphasia
            Frontotemporal lobar degeneration
            Motor neuron disease
            Tauopathy
            Ubiquitin
            TDP-43 proteinopathy
            Progranulin
            Valosin-containing protein
            Charged multivesicular body protein 2B
            Neuronal intermediate filament inclusion disease
            Neuropathologic diagnosis
            Pathology
            Neurosciences
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                        name:Department of Pathology and Immunology, Washington University School of Medicine, St Louis, USA
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                     name:Northwestern University Feinberg School of Medicine
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                        name:Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, USA
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                        name:Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, USA
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               name:Virginia M.-Y. Lee
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                        name:Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, USA
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               name:Kimmo J. Hatanpaa
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      headline:Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration
      description:The aim of this study was to improve the neuropathologic recognition and provide criteria for the pathological diagnosis in the neurodegenerative diseases grouped as frontotemporal lobar degeneration (FTLD); revised criteria are proposed. Recent advances in molecular genetics, biochemistry, and neuropathology of FTLD prompted the Midwest Consortium for Frontotemporal Lobar Degeneration and experts at other centers to review and revise the existing neuropathologic diagnostic criteria for FTLD. The proposed criteria for FTLD are based on existing criteria, which include the tauopathies [FTLD with Pick bodies, corticobasal degeneration, progressive supranuclear palsy, sporadic multiple system tauopathy with dementia, argyrophilic grain disease, neurofibrillary tangle dementia, and FTD with microtubule-associated tau (MAPT) gene mutation, also called FTD with parkinsonism linked to chromosome 17 (FTDP-17)]. The proposed criteria take into account new disease entities and include the novel molecular pathology, TDP-43 proteinopathy, now recognized to be the most frequent histological finding in FTLD. TDP-43 is a major component of the pathologic inclusions of most sporadic and familial cases of FTLD with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Mutations in valosin-containing protein (VCP) gene are present in rare familial forms of FTD, and some families with FTD and/or MND have been linked to chromosome 9p, and both are types of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. In addition to genetic heterogeneity amongst the TDP-43 proteinopathies, there is also neuropathologic heterogeneity and there is a close relationship between genotype and FTLD-U subtype. In addition to these recent significant advances in the neuropathology of FTLD-U, novel FTLD entities have been further characterized, including neuronal intermediate filament inclusion disease. The proposed criteria incorporate up-to-date neuropathology of FTLD in the light of recent immunohistochemical, biochemical, and genetic advances. 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.
      datePublished:2007-06-20T00:00:00Z
      dateModified:2007-06-20T00:00:00Z
      pageStart:5
      pageEnd:22
      sameAs:https://doi.org/10.1007/s00401-007-0237-2
      keywords:
         Frontotemporal dementia
         Semantic dementia
         Progressive non-fluent aphasia
         Frontotemporal lobar degeneration
         Motor neuron disease
         Tauopathy
         Ubiquitin
         TDP-43 proteinopathy
         Progranulin
         Valosin-containing protein
         Charged multivesicular body protein 2B
         Neuronal intermediate filament inclusion disease
         Neuropathologic diagnosis
         Pathology
         Neurosciences
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                     name:Department of Pathology and Immunology, Washington University School of Medicine, St Louis, USA
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                  name:Washington University School of Medicine
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            name:Charles L. White
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            name:Lea Tenenholz Grinberg
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            name:Ida E. Holm
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