Neuroinflammation in frontotemporal lobar degeneration revealed by (11)C‐PBR28 PET

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...

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Detalles Bibliográficos
Autores principales: Kim, Min-Jeong, McGwier, Meghan, Jenko, Kimberly J., Snow, Joseph, Morse, Cheryl, Zoghbi, Sami S., Pike, Victor W., Innis, Robert B., Kreisl, William C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Brief Communications
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6649481/
https://www.ncbi.nlm.nih.gov/pubmed/31353865
http://dx.doi.org/10.1002/acn3.50802
Descripción
Sumario: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.

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