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September 27, 2016; 87 (13) Article

Aphasic variant of Alzheimer disease

Clinical, anatomic, and genetic features

Emily Rogalski, Jaiashre Sridhar, Benjamin Rader, Adam Martersteck, Kewei Chen, Derin Cobia, Cynthia K. Thompson, Sandra Weintraub, Eileen H. Bigio, M.-Marsel Mesulam
First published August 26, 2016, DOI: https://doi.org/10.1212/WNL.0000000000003165
Emily Rogalski
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Jaiashre Sridhar
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Benjamin Rader
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Adam Martersteck
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Kewei Chen
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Derin Cobia
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Cynthia K. Thompson
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Sandra Weintraub
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Eileen H. Bigio
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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M.-Marsel Mesulam
From the Cognitive Neurology and Alzheimer's Disease Center (E.R., J.S., B.R., A.M., C.K.T., S.W., M.-M.M.) and Departments of Psychiatry and Behavioral Sciences (D.C., S.W.), Neurology (C.K.T., M.-M.M.), and Pathology (E.H.B.), Northwestern University Feinberg School of Medicine, Chicago, IL; Banner Alzheimer's Institute (K.C.), Phoenix, AZ; and Department of Communication Sciences Disorders (C.K.T.), Northwestern University, Evanston, IL.
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Citation
Aphasic variant of Alzheimer disease
Clinical, anatomic, and genetic features
Emily Rogalski, Jaiashre Sridhar, Benjamin Rader, Adam Martersteck, Kewei Chen, Derin Cobia, Cynthia K. Thompson, Sandra Weintraub, Eileen H. Bigio, M.-Marsel Mesulam
Neurology Sep 2016, 87 (13) 1337-1343; DOI: 10.1212/WNL.0000000000003165

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Abstract

Objective: To identify features of primary progressive aphasia (PPA) associated with Alzheimer disease (AD) neuropathology. A related objective was to determine whether logopenic PPA is a clinical marker for AD.

Methods: A total of 139 prospectively enrolled participants with a root diagnosis of PPA constituted the reference set. Those with autopsy or biomarker evidence of AD, and who had been evaluated at mild disease stages (Aphasia Quotient ≥85), were included (n = 19). All had quantitative language testing and APOE genotyping. Fifteen had MRI morphometry.

Results: Impaired word-finding was the universal presenting complaint in the aphasic AD group. PPA clinical subtype was logopenic (n = 13) and agrammatic (n = 6). Fluency, repetition, naming, and grammaticality ranged from preserved to severely impaired. All had relative preservation of word comprehension. Eight of the 15 aphasic participants with AD showed no appreciable cortical atrophy at the individual level on MRI. As a group, atrophy was asymmetrically concentrated in the left perisylvian cortex. APOE ε4 frequency was not elevated.

Conclusions: There is a close, but not obligatory, association between logopenic PPA and AD. No language measure, with the possible exception of word comprehension, can confirm or exclude AD in PPA. Biomarkers are therefore essential for diagnosis. Asymmetry of cortical atrophy and normal APOE ε4 prevalence constitute deviations from typical AD. These and additional neuropathologic features suggest that AD has biological subtypes, one of which causes PPA. Better appreciation of this fact should promote the inclusion of individuals with PPA and positive AD biomarkers into relevant clinical trials.

GLOSSARY

AD=
Alzheimer disease;
AQ=
aphasia quotient;
FDR=
false discovery rate;
FTLD=
frontotemporal lobar degeneration;
NAT=
Northwestern Anagram Test;
NAVS-SPPT=
Sentence Production Priming Test of the Northwestern Assessment of Verbs and Sentences;
NFT=
neurofibrillary tangles;
PPA=
primary progressive aphasia;
PPA-G=
primary progressive aphasia agrammatic subtype;
PPA-L=
primary progressive aphasia logopenic subtype;
PPA-S=
primary progressive aphasia semantic subtype;
SOB=
sum of boxes;
WAB-R=
Western Aphasia Battery–Revised;
WPM=
words per minute

Footnotes

  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

  • Supplemental data at Neurology.org

  • Received March 7, 2016.
  • Accepted in final form June 13, 2016.
  • © 2016 American Academy of Neurology
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