Clinical marker for Alzheimer disease pathology in logopenic primary progressive aphasia

To determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia (PPA). We performed a retrospective case-control study of 34 patients with PPA with available autopsy tissue. We compared baseline and longitudinal clin...

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Vydané v:	Neurology Ročník 88; číslo 24; s. 2276
Hlavní autori:	Giannini, Lucia A A, Irwin, David J, McMillan, Corey T, Ash, Sharon, Rascovsky, Katya, Wolk, David A, Van Deerlin, Vivianna M, Lee, Edward B, Trojanowski, John Q, Grossman, Murray
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 13.06.2017
Predmet:	Aged Alzheimer Disease - diagnosis Alzheimer Disease - pathology Alzheimer Disease - psychology Aphasia, Primary Progressive - diagnosis Aphasia, Primary Progressive - pathology Aphasia, Primary Progressive - psychology Brain - diagnostic imaging Brain - pathology Cost of Illness Female Follow-Up Studies Frontotemporal Lobar Degeneration - diagnosis Frontotemporal Lobar Degeneration - pathology Frontotemporal Lobar Degeneration - psychology Humans Language Tests Longitudinal Studies Magnetic Resonance Imaging Male Neuropsychological Tests Phonetics Retrospective Studies
ISSN:	1526-632X, 1526-632X
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Abstract	To determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia (PPA). We performed a retrospective case-control study of 34 patients with PPA with available autopsy tissue. We compared baseline and longitudinal clinical features in patients with primary AD neuropathology to those with primary non-AD pathologies. We analyzed regional neuroanatomic disease burden in pathology-defined groups using postmortem neuropathologic data. A total of 19/34 patients had primary AD pathology and 15/34 had non-AD pathology (13 frontotemporal lobar degeneration, 2 Lewy body disease). A total of 16/19 (84%) patients with AD had a logopenic spectrum phenotype; 5 met published criteria for the logopenic variant (lvPPA), 8 had additional grammatical or semantic deficits (lvPPA+), and 3 had relatively preserved sentence repetition (lvPPA-). Sentence repetition was impaired in 68% of patients with PPA with AD pathology; forward digit span (DF) was impaired in 90%, substantially higher than in non-AD PPA (33%, < 0.01). Lexical retrieval difficulty was common in all patients with PPA and did not discriminate between groups. Compared to non-AD, PPA with AD pathology had elevated microscopic neurodegenerative pathology in the superior/midtemporal gyrus, angular gyrus, and midfrontal cortex ( < 0.01). Low DF scores correlated with high microscopic pathologic burden in superior/midtemporal and angular gyri ( ≤ 0.03). Phonologic loop dysfunction is a central feature of AD-associated PPA and specifically correlates with temporoparietal neurodegeneration. Quantitative measures of phonologic loop function, combined with modified clinical lvPPA criteria, may help discriminate AD-associated PPA.
AbstractList	To determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia (PPA).OBJECTIVETo determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia (PPA).We performed a retrospective case-control study of 34 patients with PPA with available autopsy tissue. We compared baseline and longitudinal clinical features in patients with primary AD neuropathology to those with primary non-AD pathologies. We analyzed regional neuroanatomic disease burden in pathology-defined groups using postmortem neuropathologic data.METHODSWe performed a retrospective case-control study of 34 patients with PPA with available autopsy tissue. We compared baseline and longitudinal clinical features in patients with primary AD neuropathology to those with primary non-AD pathologies. We analyzed regional neuroanatomic disease burden in pathology-defined groups using postmortem neuropathologic data.A total of 19/34 patients had primary AD pathology and 15/34 had non-AD pathology (13 frontotemporal lobar degeneration, 2 Lewy body disease). A total of 16/19 (84%) patients with AD had a logopenic spectrum phenotype; 5 met published criteria for the logopenic variant (lvPPA), 8 had additional grammatical or semantic deficits (lvPPA+), and 3 had relatively preserved sentence repetition (lvPPA-). Sentence repetition was impaired in 68% of patients with PPA with AD pathology; forward digit span (DF) was impaired in 90%, substantially higher than in non-AD PPA (33%, p < 0.01). Lexical retrieval difficulty was common in all patients with PPA and did not discriminate between groups. Compared to non-AD, PPA with AD pathology had elevated microscopic neurodegenerative pathology in the superior/midtemporal gyrus, angular gyrus, and midfrontal cortex (p < 0.01). Low DF scores correlated with high microscopic pathologic burden in superior/midtemporal and angular gyri (p ≤ 0.03).RESULTSA total of 19/34 patients had primary AD pathology and 15/34 had non-AD pathology (13 frontotemporal lobar degeneration, 2 Lewy body disease). A total of 16/19 (84%) patients with AD had a logopenic spectrum phenotype; 5 met published criteria for the logopenic variant (lvPPA), 8 had additional grammatical or semantic deficits (lvPPA+), and 3 had relatively preserved sentence repetition (lvPPA-). Sentence repetition was impaired in 68% of patients with PPA with AD pathology; forward digit span (DF) was impaired in 90%, substantially higher than in non-AD PPA (33%, p < 0.01). Lexical retrieval difficulty was common in all patients with PPA and did not discriminate between groups. Compared to non-AD, PPA with AD pathology had elevated microscopic neurodegenerative pathology in the superior/midtemporal gyrus, angular gyrus, and midfrontal cortex (p < 0.01). Low DF scores correlated with high microscopic pathologic burden in superior/midtemporal and angular gyri (p ≤ 0.03).Phonologic loop dysfunction is a central feature of AD-associated PPA and specifically correlates with temporoparietal neurodegeneration. Quantitative measures of phonologic loop function, combined with modified clinical lvPPA criteria, may help discriminate AD-associated PPA.CONCLUSIONSPhonologic loop dysfunction is a central feature of AD-associated PPA and specifically correlates with temporoparietal neurodegeneration. Quantitative measures of phonologic loop function, combined with modified clinical lvPPA criteria, may help discriminate AD-associated PPA. To determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia (PPA). We performed a retrospective case-control study of 34 patients with PPA with available autopsy tissue. We compared baseline and longitudinal clinical features in patients with primary AD neuropathology to those with primary non-AD pathologies. We analyzed regional neuroanatomic disease burden in pathology-defined groups using postmortem neuropathologic data. A total of 19/34 patients had primary AD pathology and 15/34 had non-AD pathology (13 frontotemporal lobar degeneration, 2 Lewy body disease). A total of 16/19 (84%) patients with AD had a logopenic spectrum phenotype; 5 met published criteria for the logopenic variant (lvPPA), 8 had additional grammatical or semantic deficits (lvPPA+), and 3 had relatively preserved sentence repetition (lvPPA-). Sentence repetition was impaired in 68% of patients with PPA with AD pathology; forward digit span (DF) was impaired in 90%, substantially higher than in non-AD PPA (33%, < 0.01). Lexical retrieval difficulty was common in all patients with PPA and did not discriminate between groups. Compared to non-AD, PPA with AD pathology had elevated microscopic neurodegenerative pathology in the superior/midtemporal gyrus, angular gyrus, and midfrontal cortex ( < 0.01). Low DF scores correlated with high microscopic pathologic burden in superior/midtemporal and angular gyri ( ≤ 0.03). Phonologic loop dysfunction is a central feature of AD-associated PPA and specifically correlates with temporoparietal neurodegeneration. Quantitative measures of phonologic loop function, combined with modified clinical lvPPA criteria, may help discriminate AD-associated PPA.
Author	Grossman, Murray Giannini, Lucia A A Wolk, David A Van Deerlin, Vivianna M Irwin, David J McMillan, Corey T Rascovsky, Katya Lee, Edward B Trojanowski, John Q Ash, Sharon
Author_xml	– sequence: 1 givenname: Lucia A A surname: Giannini fullname: Giannini, Lucia A A organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 2 givenname: David J surname: Irwin fullname: Irwin, David J organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 3 givenname: Corey T surname: McMillan fullname: McMillan, Corey T organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 4 givenname: Sharon surname: Ash fullname: Ash, Sharon organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 5 givenname: Katya surname: Rascovsky fullname: Rascovsky, Katya organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 6 givenname: David A surname: Wolk fullname: Wolk, David A organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 7 givenname: Vivianna M surname: Van Deerlin fullname: Van Deerlin, Vivianna M organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 8 givenname: Edward B surname: Lee fullname: Lee, Edward B organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 9 givenname: John Q surname: Trojanowski fullname: Trojanowski, John Q organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia – sequence: 10 givenname: Murray surname: Grossman fullname: Grossman, Murray email: mgrossma@mail.med.upenn.edu organization: From the Department of Neurology (L.A.A.G.), University Medical Center Groningen, University of Groningen, the Netherlands; Penn Frontotemporal Degeneration Center, Department of Neurology (L.A.A.G., D.J.I., C.T.M., S.A., K.R., M.G.), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (D.J.I., V.M.V.D., J.Q.T.), Alzheimer's Disease Center (D.A.W.), Department of Neurology, and Translational Pathology Laboratory, Perelman School of Medicine (E.B.L.), University of Pennsylvania, Philadelphia. mgrossma@mail.med.upenn.edu
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Snippet	To determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia (PPA). We... To determine whether logopenic features of phonologic loop dysfunction reflect Alzheimer disease (AD) neuropathology in primary progressive aphasia...
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SubjectTerms	Aged Alzheimer Disease - diagnosis Alzheimer Disease - pathology Alzheimer Disease - psychology Aphasia, Primary Progressive - diagnosis Aphasia, Primary Progressive - pathology Aphasia, Primary Progressive - psychology Brain - diagnostic imaging Brain - pathology Cost of Illness Female Follow-Up Studies Frontotemporal Lobar Degeneration - diagnosis Frontotemporal Lobar Degeneration - pathology Frontotemporal Lobar Degeneration - psychology Humans Language Tests Longitudinal Studies Magnetic Resonance Imaging Male Neuropsychological Tests Phonetics Retrospective Studies
Title	Clinical marker for Alzheimer disease pathology in logopenic primary progressive aphasia
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