Clinicopathological correlations in behavioural variant frontotemporal dementia
Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting challenge for clinicians but will be critical for the success of disease-modifying therapies. We sought to improve pathological prediction by explori...
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| Published in: | Brain (London, England : 1878) Vol. 140; no. 12; p. 3329 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
England
01.12.2017
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| ISSN: | 1460-2156, 1460-2156 |
| Online Access: | Get more information |
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| Abstract | Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting challenge for clinicians but will be critical for the success of disease-modifying therapies. We sought to improve pathological prediction by exploring clinicopathological correlations in a large bvFTD cohort. Among 438 patients in whom bvFTD was either the top or an alternative possible clinical diagnosis, 117 had available autopsy data, including 98 with a primary pathological diagnosis of frontotemporal lobar degeneration (FTLD), 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerative disease-related pathology outside of the motor system. Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. Alzheimer's disease was uncommon (6%) among patients whose only top diagnosis during follow-up was bvFTD. Seventy-nine per cent of FTLD-tau, 86% of FTLD-TDP, and 88% of FTLD-FUS met at least 'possible' bvFTD diagnostic criteria at first presentation. The frequency of the six core bvFTD diagnostic features was similar in FTLD-tau and FTLD-TDP, suggesting that these features alone cannot be used to separate patients by major molecular class. Voxel-based morphometry revealed that nearly all pathological subgroups and even individual patients share atrophy in anterior cingulate, frontoinsula, striatum, and amygdala, indicating that degeneration of these regions is intimately linked to the behavioural syndrome produced by these diverse aetiologies. In addition to these unifying features, symptom profiles also differed among pathological subtypes, suggesting distinct anatomical vulnerabilities and informing a clinician's prediction of pathological diagnosis. Data-driven classification into one of the 10 most common pathological diagnoses was most accurate (up to 60.2%) when using a combination of known predictive factors (genetic mutations, motor features, or striking atrophy patterns) and the results of a discriminant function analysis that incorporated clinical, neuroimaging, and neuropsychological data. |
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| AbstractList | Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting challenge for clinicians but will be critical for the success of disease-modifying therapies. We sought to improve pathological prediction by exploring clinicopathological correlations in a large bvFTD cohort. Among 438 patients in whom bvFTD was either the top or an alternative possible clinical diagnosis, 117 had available autopsy data, including 98 with a primary pathological diagnosis of frontotemporal lobar degeneration (FTLD), 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerative disease-related pathology outside of the motor system. Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. Alzheimer's disease was uncommon (6%) among patients whose only top diagnosis during follow-up was bvFTD. Seventy-nine per cent of FTLD-tau, 86% of FTLD-TDP, and 88% of FTLD-FUS met at least 'possible' bvFTD diagnostic criteria at first presentation. The frequency of the six core bvFTD diagnostic features was similar in FTLD-tau and FTLD-TDP, suggesting that these features alone cannot be used to separate patients by major molecular class. Voxel-based morphometry revealed that nearly all pathological subgroups and even individual patients share atrophy in anterior cingulate, frontoinsula, striatum, and amygdala, indicating that degeneration of these regions is intimately linked to the behavioural syndrome produced by these diverse aetiologies. In addition to these unifying features, symptom profiles also differed among pathological subtypes, suggesting distinct anatomical vulnerabilities and informing a clinician's prediction of pathological diagnosis. Data-driven classification into one of the 10 most common pathological diagnoses was most accurate (up to 60.2%) when using a combination of known predictive factors (genetic mutations, motor features, or striking atrophy patterns) and the results of a discriminant function analysis that incorporated clinical, neuroimaging, and neuropsychological data.Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting challenge for clinicians but will be critical for the success of disease-modifying therapies. We sought to improve pathological prediction by exploring clinicopathological correlations in a large bvFTD cohort. Among 438 patients in whom bvFTD was either the top or an alternative possible clinical diagnosis, 117 had available autopsy data, including 98 with a primary pathological diagnosis of frontotemporal lobar degeneration (FTLD), 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerative disease-related pathology outside of the motor system. Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. Alzheimer's disease was uncommon (6%) among patients whose only top diagnosis during follow-up was bvFTD. Seventy-nine per cent of FTLD-tau, 86% of FTLD-TDP, and 88% of FTLD-FUS met at least 'possible' bvFTD diagnostic criteria at first presentation. The frequency of the six core bvFTD diagnostic features was similar in FTLD-tau and FTLD-TDP, suggesting that these features alone cannot be used to separate patients by major molecular class. Voxel-based morphometry revealed that nearly all pathological subgroups and even individual patients share atrophy in anterior cingulate, frontoinsula, striatum, and amygdala, indicating that degeneration of these regions is intimately linked to the behavioural syndrome produced by these diverse aetiologies. In addition to these unifying features, symptom profiles also differed among pathological subtypes, suggesting distinct anatomical vulnerabilities and informing a clinician's prediction of pathological diagnosis. Data-driven classification into one of the 10 most common pathological diagnoses was most accurate (up to 60.2%) when using a combination of known predictive factors (genetic mutations, motor features, or striking atrophy patterns) and the results of a discriminant function analysis that incorporated clinical, neuroimaging, and neuropsychological data. Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting challenge for clinicians but will be critical for the success of disease-modifying therapies. We sought to improve pathological prediction by exploring clinicopathological correlations in a large bvFTD cohort. Among 438 patients in whom bvFTD was either the top or an alternative possible clinical diagnosis, 117 had available autopsy data, including 98 with a primary pathological diagnosis of frontotemporal lobar degeneration (FTLD), 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerative disease-related pathology outside of the motor system. Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. Alzheimer's disease was uncommon (6%) among patients whose only top diagnosis during follow-up was bvFTD. Seventy-nine per cent of FTLD-tau, 86% of FTLD-TDP, and 88% of FTLD-FUS met at least 'possible' bvFTD diagnostic criteria at first presentation. The frequency of the six core bvFTD diagnostic features was similar in FTLD-tau and FTLD-TDP, suggesting that these features alone cannot be used to separate patients by major molecular class. Voxel-based morphometry revealed that nearly all pathological subgroups and even individual patients share atrophy in anterior cingulate, frontoinsula, striatum, and amygdala, indicating that degeneration of these regions is intimately linked to the behavioural syndrome produced by these diverse aetiologies. In addition to these unifying features, symptom profiles also differed among pathological subtypes, suggesting distinct anatomical vulnerabilities and informing a clinician's prediction of pathological diagnosis. Data-driven classification into one of the 10 most common pathological diagnoses was most accurate (up to 60.2%) when using a combination of known predictive factors (genetic mutations, motor features, or striking atrophy patterns) and the results of a discriminant function analysis that incorporated clinical, neuroimaging, and neuropsychological data. |
| Author | Vossel, Keith A Matthews, Brandy R Ossenkoppele, Rik Trujillo, Andrew Kramer, Joel H Tartaglia, Maria Carmela Nana, Alissa L Perry, David C Datta, Samir Vargas, Jose Norberto S Kornak, John Lee, Suzee E Radke, Anneliese Coppola, Giovanni Grinberg, Lea T Brown, Alainna B Sidhu, Manu Karydas, Anna Gaus, Stephanie E Seeley, William W Sturm, Virginia E Trojanowski, John Q Miller, Bruce L Brown, Jesse A Miller, Zachary A Geschwind, Daniel Huang, Eric J Rankin, Katherine P Hwang, Ji-Hye L Kao, Aimee W Boxer, Adam L Rabinovici, Gil D Sias, Ana C Gorno-Tempini, Maria Luisa Seo, Sang Won De May, Mary Rosen, Howard J Possin, Katherine L |
| Author_xml | – sequence: 1 givenname: David C surname: Perry fullname: Perry, David C organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 2 givenname: Jesse A surname: Brown fullname: Brown, Jesse A organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 3 givenname: Katherine L surname: Possin fullname: Possin, Katherine L organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 4 givenname: Samir surname: Datta fullname: Datta, Samir organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 5 givenname: Andrew surname: Trujillo fullname: Trujillo, Andrew organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 6 givenname: Anneliese surname: Radke fullname: Radke, Anneliese organization: University of California Davis, Davis, CA, USA – sequence: 7 givenname: Anna surname: Karydas fullname: Karydas, Anna organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 8 givenname: John surname: Kornak fullname: Kornak, John organization: Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA – sequence: 9 givenname: Ana C surname: Sias fullname: Sias, Ana C organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 10 givenname: Gil D surname: Rabinovici fullname: Rabinovici, Gil D organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 11 givenname: Maria Luisa surname: Gorno-Tempini fullname: Gorno-Tempini, Maria Luisa organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 12 givenname: Adam L surname: Boxer fullname: Boxer, Adam L organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 13 givenname: Mary surname: De May fullname: De May, Mary organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 14 givenname: Katherine P surname: Rankin fullname: Rankin, Katherine P organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 15 givenname: Virginia E surname: Sturm fullname: Sturm, Virginia E organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 16 givenname: Suzee E surname: Lee fullname: Lee, Suzee E organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 17 givenname: Brandy R surname: Matthews fullname: Matthews, Brandy R organization: Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA – sequence: 18 givenname: Aimee W surname: Kao fullname: Kao, Aimee W organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 19 givenname: Keith A surname: Vossel fullname: Vossel, Keith A organization: Department of Neurology, University of Minnesota, Minneapolis, MN, USA – sequence: 20 givenname: Maria Carmela surname: Tartaglia fullname: Tartaglia, Maria Carmela organization: Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Canada – sequence: 21 givenname: Zachary A surname: Miller fullname: Miller, Zachary A organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 22 givenname: Sang Won surname: Seo fullname: Seo, Sang Won organization: Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, South Korea – sequence: 23 givenname: Manu surname: Sidhu fullname: Sidhu, Manu organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 24 givenname: Stephanie E surname: Gaus fullname: Gaus, Stephanie E organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 25 givenname: Alissa L surname: Nana fullname: Nana, Alissa L organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 26 givenname: Jose Norberto S surname: Vargas fullname: Vargas, Jose Norberto S organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 27 givenname: Ji-Hye L surname: Hwang fullname: Hwang, Ji-Hye L organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 28 givenname: Rik surname: Ossenkoppele fullname: Ossenkoppele, Rik organization: Department of Neurology and Alzheimer Center, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands – sequence: 29 givenname: Alainna B surname: Brown fullname: Brown, Alainna B organization: University of Washington School of Medicine, Seattle, WA, USA – sequence: 30 givenname: Eric J surname: Huang fullname: Huang, Eric J organization: Department of Pathology and Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA – sequence: 31 givenname: Giovanni surname: Coppola fullname: Coppola, Giovanni organization: Neurogenetics program, Department of Neurology, and Semel Institute for Neuroscience and Human Behaviour, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA – sequence: 32 givenname: Howard J surname: Rosen fullname: Rosen, Howard J organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 33 givenname: Daniel surname: Geschwind fullname: Geschwind, Daniel organization: Neurogenetics program, Department of Neurology, and Semel Institute for Neuroscience and Human Behaviour, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA – sequence: 34 givenname: John Q surname: Trojanowski fullname: Trojanowski, John Q organization: Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA – sequence: 35 givenname: Lea T surname: Grinberg fullname: Grinberg, Lea T organization: Department of Pathology and Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA – sequence: 36 givenname: Joel H surname: Kramer fullname: Kramer, Joel H organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 37 givenname: Bruce L surname: Miller fullname: Miller, Bruce L organization: Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA – sequence: 38 givenname: William W surname: Seeley fullname: Seeley, William W organization: Department of Pathology and Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29053860$$D View this record in MEDLINE/PubMed |
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| Keywords | frontotemporal dementia Alzheimer’s disease corticobasal degeneration Pick’s disease frontotemporal lobar degeneration |
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| Snippet | Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting... |
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| SubjectTerms | Adult Aged Aged, 80 and over Alzheimer Disease - diagnostic imaging Alzheimer Disease - pathology Alzheimer Disease - psychology Amyotrophic Lateral Sclerosis - diagnostic imaging Amyotrophic Lateral Sclerosis - pathology Amyotrophic Lateral Sclerosis - psychology Autopsy Brain - diagnostic imaging Brain - pathology Female Frontotemporal Dementia - diagnostic imaging Frontotemporal Dementia - pathology Frontotemporal Dementia - psychology Frontotemporal Lobar Degeneration - diagnostic imaging Frontotemporal Lobar Degeneration - pathology Frontotemporal Lobar Degeneration - psychology Humans Magnetic Resonance Imaging Male Middle Aged Organ Size Pick Disease of the Brain - diagnostic imaging Pick Disease of the Brain - pathology Pick Disease of the Brain - psychology Supranuclear Palsy, Progressive - diagnostic imaging Supranuclear Palsy, Progressive - pathology Supranuclear Palsy, Progressive - psychology |
| Title | Clinicopathological correlations in behavioural variant frontotemporal dementia |
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