Neuroinflammation in frontotemporal lobar degeneration revealed by 11C-PBR28 PET

Min Jeong Kim; Meghan McGwier; Kimberly J. Jenko; Joseph Snow; Cheryl Morse; Sami S. Zoghbi; Victor W. Pike; Robert B. Innis; William C. Kreisl

doi:10.1002/acn3.50802

Neuroinflammation in frontotemporal lobar degeneration revealed by ¹¹C-PBR28 PET

Min Jeong Kim
, Meghan McGwier
, Kimberly J. Jenko
, Joseph Snow
, Cheryl Morse
, Sami S. Zoghbi
, Victor W. Pike
, Robert B. Innis
, William C. Kreisl

Psychiatry

National Institutes of Health
Columbia University

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

This study used ¹¹C-PBR28 positron emission tomography (PET) imaging to determine whether levels of 18-kDa translocator protein (TSPO), an inflammation-specific biomarker, are increased in frontotemporal lobar degeneration (FTLD) patients. ¹¹C-PBR28, ¹⁸F-FDG, and ¹¹C-PIB brain PET scans, as well as magnetic resonance imaging (MRI), were conducted in four FTLD patients and 22 healthy controls. ¹¹C-PBR28 scans revealed that all FTLD patients showed increased TSPO binding versus controls. Significantly greater increases in TSPO were observed in the frontal, lateral temporal, parietal, and occipital cortices, topographically consistent with individual clinical phenotypes and with brain MRI and ¹⁸F-FDG PET. Amyloid burden was not increased.

Original language	English
Pages (from-to)	1327-1331
Number of pages	5
Journal	Annals of Clinical and Translational Neurology
Volume	6
Issue number	7
DOIs	https://doi.org/10.1002/acn3.50802
State	Published - Jul 2019

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title = "Neuroinflammation in frontotemporal lobar degeneration revealed by 11C-PBR28 PET",

abstract = "This study used 11C-PBR28 positron emission tomography (PET) imaging to determine whether levels of 18-kDa translocator protein (TSPO), an inflammation-specific biomarker, are increased in frontotemporal lobar degeneration (FTLD) patients. 11C-PBR28, 18F-FDG, and 11C-PIB brain PET scans, as well as magnetic resonance imaging (MRI), were conducted in four FTLD patients and 22 healthy controls. 11C-PBR28 scans revealed that all FTLD patients showed increased TSPO binding versus controls. Significantly greater increases in TSPO were observed in the frontal, lateral temporal, parietal, and occipital cortices, topographically consistent with individual clinical phenotypes and with brain MRI and 18F-FDG PET. Amyloid burden was not increased.",

author = "Kim, \{Min Jeong\} and Meghan McGwier and Jenko, \{Kimberly J.\} and Joseph Snow and Cheryl Morse and Zoghbi, \{Sami S.\} and Pike, \{Victor W.\} and Innis, \{Robert B.\} and Kreisl, \{William C.\}",

note = "Publisher Copyright: {\textcopyright} Published 2019. This article is a U.S. Government work and is in the public domain in the USA. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.",

year = "2019",

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doi = "10.1002/acn3.50802",

language = "English",

volume = "6",

pages = "1327--1331",

journal = "Annals of Clinical and Translational Neurology",

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T1 - Neuroinflammation in frontotemporal lobar degeneration revealed by 11C-PBR28 PET

AU - Kim, Min Jeong

AU - McGwier, Meghan

AU - Jenko, Kimberly J.

AU - Snow, Joseph

AU - Morse, Cheryl

AU - Zoghbi, Sami S.

AU - Pike, Victor W.

AU - Innis, Robert B.

AU - Kreisl, William C.

N1 - Publisher Copyright: © Published 2019. This article is a U.S. Government work and is in the public domain in the USA. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

PY - 2019/7

Y1 - 2019/7

N2 - This study used 11C-PBR28 positron emission tomography (PET) imaging to determine whether levels of 18-kDa translocator protein (TSPO), an inflammation-specific biomarker, are increased in frontotemporal lobar degeneration (FTLD) patients. 11C-PBR28, 18F-FDG, and 11C-PIB brain PET scans, as well as magnetic resonance imaging (MRI), were conducted in four FTLD patients and 22 healthy controls. 11C-PBR28 scans revealed that all FTLD patients showed increased TSPO binding versus controls. Significantly greater increases in TSPO were observed in the frontal, lateral temporal, parietal, and occipital cortices, topographically consistent with individual clinical phenotypes and with brain MRI and 18F-FDG PET. Amyloid burden was not increased.

AB - This study used 11C-PBR28 positron emission tomography (PET) imaging to determine whether levels of 18-kDa translocator protein (TSPO), an inflammation-specific biomarker, are increased in frontotemporal lobar degeneration (FTLD) patients. 11C-PBR28, 18F-FDG, and 11C-PIB brain PET scans, as well as magnetic resonance imaging (MRI), were conducted in four FTLD patients and 22 healthy controls. 11C-PBR28 scans revealed that all FTLD patients showed increased TSPO binding versus controls. Significantly greater increases in TSPO were observed in the frontal, lateral temporal, parietal, and occipital cortices, topographically consistent with individual clinical phenotypes and with brain MRI and 18F-FDG PET. Amyloid burden was not increased.

UR - https://www.scopus.com/pages/publications/85069772821

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SN - 2328-9503

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JO - Annals of Clinical and Translational Neurology

JF - Annals of Clinical and Translational Neurology

IS - 7

ER -

Neuroinflammation in frontotemporal lobar degeneration revealed by ¹¹C-PBR28 PET

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