Varying degrees of temporoparietal hypometabolism on FDG-PET reveal amyloid-positive logopenic primary progressive aphasia is not a homogeneous clinical entity

Kamini Krishnan, Mary Margaret Machulda, Jennifer Lynn Whitwell, Alissa Butts, Joseph R. Duffy, Edythe A. Strand, Matthew L. Senjem, Anthony J. Spychalla, Clifford R Jr. Jack, Val Lowe, Keith Anthony Josephs

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Abstract

Background: The logopenic variant of primary progressive aphasia (lvPPA) manifests due to a breakdown of the language network with prominent hypometabolism of the left temporoparietal region. LvPPA is strongly associated with amyloid deposition, yet there is question as to whether it is a homogeneous clinical entity. Objective: This study investigated whether differences in temporoparietal metabolic patterns on 18F fludeoxyglucose positron emission tomography (FDG-PET) could elucidate brain regions preferentially affected in lvPPA. Method: We used differences in FDG-PET metabolic z-scores relative to controls for means of left lateral temporal, left inferior parietal, and left superior parietal regions to classify 53 amyloid-positive lvPPA patients into temporal, parietal, or temporoparietal predominate groups. Clinical features and FDG-PET regions of hypometabolism outside of the temporoparietal region were then compared across the three groups; the latter using statistical parametric mapping. Results: Of the 53 lvPPA patients, 15 were classified as temporal, 14 as temporoparietal, and 22 as parietal predominate. There were no significant differences between the groups on demographic measures, language evaluation, or apolipoprotein E genotype. Compared to the other two groups, individuals with the parietal predominate pattern had extensive hypometabolism in left frontal lobe and the precuneus. Furthermore, this group had greater behavioral dyscontrol and deficits in executive function, visuospatial skills, visual memory retention, working memory, and cognitive flexibility (Bonferronip < 0.05). Conclusions: This study demonstrates that there is clinical heterogeneity within amyloid-positive lvPPA. Patients with lvPPA with predominant parietal hypometabolism, unlike those with temporal or temporoparietal predominant hypometabolism, demonstrated widespread cognitive and behavioral changes.

Original languageEnglish (US)
Pages (from-to)1019-1029
Number of pages11
JournalJournal of Alzheimer's Disease
Volume55
Issue number3
DOIs
StatePublished - 2017

Fingerprint

Primary Progressive Aphasia
Amyloid
Positron-Emission Tomography
Parietal Lobe
Language
Executive Function
Frontal Lobe
Apolipoproteins E
Short-Term Memory
Genotype
Demography
Brain

Keywords

  • F fludeoxyglucose
  • Amyloid-β
  • executive function
  • positron emission tomography
  • primary progressive aphasia
  • visuospatial deficit
  • working memory

ASJC Scopus subject areas

  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

Cite this

@article{dabcece6f0f1459aa02b8cc21bce73ac,
title = "Varying degrees of temporoparietal hypometabolism on FDG-PET reveal amyloid-positive logopenic primary progressive aphasia is not a homogeneous clinical entity",
abstract = "Background: The logopenic variant of primary progressive aphasia (lvPPA) manifests due to a breakdown of the language network with prominent hypometabolism of the left temporoparietal region. LvPPA is strongly associated with amyloid deposition, yet there is question as to whether it is a homogeneous clinical entity. Objective: This study investigated whether differences in temporoparietal metabolic patterns on 18F fludeoxyglucose positron emission tomography (FDG-PET) could elucidate brain regions preferentially affected in lvPPA. Method: We used differences in FDG-PET metabolic z-scores relative to controls for means of left lateral temporal, left inferior parietal, and left superior parietal regions to classify 53 amyloid-positive lvPPA patients into temporal, parietal, or temporoparietal predominate groups. Clinical features and FDG-PET regions of hypometabolism outside of the temporoparietal region were then compared across the three groups; the latter using statistical parametric mapping. Results: Of the 53 lvPPA patients, 15 were classified as temporal, 14 as temporoparietal, and 22 as parietal predominate. There were no significant differences between the groups on demographic measures, language evaluation, or apolipoprotein E genotype. Compared to the other two groups, individuals with the parietal predominate pattern had extensive hypometabolism in left frontal lobe and the precuneus. Furthermore, this group had greater behavioral dyscontrol and deficits in executive function, visuospatial skills, visual memory retention, working memory, and cognitive flexibility (Bonferronip < 0.05). Conclusions: This study demonstrates that there is clinical heterogeneity within amyloid-positive lvPPA. Patients with lvPPA with predominant parietal hypometabolism, unlike those with temporal or temporoparietal predominant hypometabolism, demonstrated widespread cognitive and behavioral changes.",
keywords = "F fludeoxyglucose, Amyloid-β, executive function, positron emission tomography, primary progressive aphasia, visuospatial deficit, working memory",
author = "Kamini Krishnan and Machulda, {Mary Margaret} and Whitwell, {Jennifer Lynn} and Alissa Butts and Duffy, {Joseph R.} and Strand, {Edythe A.} and Senjem, {Matthew L.} and Spychalla, {Anthony J.} and Jack, {Clifford R Jr.} and Val Lowe and Josephs, {Keith Anthony}",
year = "2017",
doi = "10.3233/JAD-160614",
language = "English (US)",
volume = "55",
pages = "1019--1029",
journal = "Journal of Alzheimer's Disease",
issn = "1387-2877",
publisher = "IOS Press",
number = "3",

}

TY - JOUR

T1 - Varying degrees of temporoparietal hypometabolism on FDG-PET reveal amyloid-positive logopenic primary progressive aphasia is not a homogeneous clinical entity

AU - Krishnan, Kamini

AU - Machulda, Mary Margaret

AU - Whitwell, Jennifer Lynn

AU - Butts, Alissa

AU - Duffy, Joseph R.

AU - Strand, Edythe A.

AU - Senjem, Matthew L.

AU - Spychalla, Anthony J.

AU - Jack, Clifford R Jr.

AU - Lowe, Val

AU - Josephs, Keith Anthony

PY - 2017

Y1 - 2017

N2 - Background: The logopenic variant of primary progressive aphasia (lvPPA) manifests due to a breakdown of the language network with prominent hypometabolism of the left temporoparietal region. LvPPA is strongly associated with amyloid deposition, yet there is question as to whether it is a homogeneous clinical entity. Objective: This study investigated whether differences in temporoparietal metabolic patterns on 18F fludeoxyglucose positron emission tomography (FDG-PET) could elucidate brain regions preferentially affected in lvPPA. Method: We used differences in FDG-PET metabolic z-scores relative to controls for means of left lateral temporal, left inferior parietal, and left superior parietal regions to classify 53 amyloid-positive lvPPA patients into temporal, parietal, or temporoparietal predominate groups. Clinical features and FDG-PET regions of hypometabolism outside of the temporoparietal region were then compared across the three groups; the latter using statistical parametric mapping. Results: Of the 53 lvPPA patients, 15 were classified as temporal, 14 as temporoparietal, and 22 as parietal predominate. There were no significant differences between the groups on demographic measures, language evaluation, or apolipoprotein E genotype. Compared to the other two groups, individuals with the parietal predominate pattern had extensive hypometabolism in left frontal lobe and the precuneus. Furthermore, this group had greater behavioral dyscontrol and deficits in executive function, visuospatial skills, visual memory retention, working memory, and cognitive flexibility (Bonferronip < 0.05). Conclusions: This study demonstrates that there is clinical heterogeneity within amyloid-positive lvPPA. Patients with lvPPA with predominant parietal hypometabolism, unlike those with temporal or temporoparietal predominant hypometabolism, demonstrated widespread cognitive and behavioral changes.

AB - Background: The logopenic variant of primary progressive aphasia (lvPPA) manifests due to a breakdown of the language network with prominent hypometabolism of the left temporoparietal region. LvPPA is strongly associated with amyloid deposition, yet there is question as to whether it is a homogeneous clinical entity. Objective: This study investigated whether differences in temporoparietal metabolic patterns on 18F fludeoxyglucose positron emission tomography (FDG-PET) could elucidate brain regions preferentially affected in lvPPA. Method: We used differences in FDG-PET metabolic z-scores relative to controls for means of left lateral temporal, left inferior parietal, and left superior parietal regions to classify 53 amyloid-positive lvPPA patients into temporal, parietal, or temporoparietal predominate groups. Clinical features and FDG-PET regions of hypometabolism outside of the temporoparietal region were then compared across the three groups; the latter using statistical parametric mapping. Results: Of the 53 lvPPA patients, 15 were classified as temporal, 14 as temporoparietal, and 22 as parietal predominate. There were no significant differences between the groups on demographic measures, language evaluation, or apolipoprotein E genotype. Compared to the other two groups, individuals with the parietal predominate pattern had extensive hypometabolism in left frontal lobe and the precuneus. Furthermore, this group had greater behavioral dyscontrol and deficits in executive function, visuospatial skills, visual memory retention, working memory, and cognitive flexibility (Bonferronip < 0.05). Conclusions: This study demonstrates that there is clinical heterogeneity within amyloid-positive lvPPA. Patients with lvPPA with predominant parietal hypometabolism, unlike those with temporal or temporoparietal predominant hypometabolism, demonstrated widespread cognitive and behavioral changes.

KW - F fludeoxyglucose

KW - Amyloid-β

KW - executive function

KW - positron emission tomography

KW - primary progressive aphasia

KW - visuospatial deficit

KW - working memory

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U2 - 10.3233/JAD-160614

DO - 10.3233/JAD-160614

M3 - Article

C2 - 27802232

AN - SCOPUS:85005966820

VL - 55

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JO - Journal of Alzheimer's Disease

JF - Journal of Alzheimer's Disease

SN - 1387-2877

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