Open AccessNeuroinflammation in frontotemporal lobar degeneration revealed by 11 C‐PBR28 PET
Author(s) -
Kim Min-Jeong,
McGwier Meghan,
Jenko Kimberly J.,
Snow Joseph,
Morse Cheryl,
Zoghbi Sami S.,
Pike Victor W.,
Innis Robert B.,
Kreisl William C.
Publication year - 2019
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.50802
Subject(s) - translocator protein , frontotemporal lobar degeneration , medicine , positron emission tomography , neuroinflammation , magnetic resonance imaging , biomarker , pathology , neuroimaging , frontotemporal dementia , nuclear medicine , dementia , radiology , disease , psychiatry , biology , biochemistry
This study used 11 C‐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. 11 C‐PBR28, 18 F‐FDG, and 11 C‐PIB brain PET scans, as well as magnetic resonance imaging (MRI), were conducted in four FTLD patients and 22 healthy controls. 11 C‐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 18 F‐FDG PET. Amyloid burden was not increased.