Distinct patterns of increased translocator protein in posterior cortical atrophy and amnestic Alzheimer's disease

We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 1...

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Published in	Neurobiology of aging Vol. 51; pp. 132 - 140
Main Authors	Kreisl, William C., Lyoo, Chul Hyoung, Liow, Jeih-San, Snow, Joseph, Page, Emily, Jenko, Kimberly J., Morse, Cheryl L., Zoghbi, Sami S., Pike, Victor W., Turner, R. Scott, Innis, Robert B.
Format	Journal Article
Language	English
Published	United States Elsevier Inc 01.03.2017
Subjects	Aged Alzheimer Disease - diagnostic imaging Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid - metabolism Atrophy Female Glucose - metabolism Humans Internal Medicine Male Microglia - pathology Middle Aged Nerve Degeneration Neuroinflammation Neurology Occipital Lobe - diagnostic imaging Occipital Lobe - metabolism Occipital Lobe - pathology PET imaging Positron-Emission Tomography Protein Binding Receptors, GABA - metabolism PET imaging Neuroinflammation Alzheimer's disease
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Abstract	We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with 11C-PBR28 to measure translocator protein 18 kDa. PCA patients showed greater 11C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater 11C-PBR28 binding in inferior and medial temporal cortex. Increased 11C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD.
AbstractList	We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with C-PBR28 to measure translocator protein 18 kDa. PCA patients showed greater C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater C-PBR28 binding in inferior and medial temporal cortex. Increased C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD. Abstract We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with11 C-PBR28 to measure translocator protein 18 kDa. PCA patients showed greater11 C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater11 C-PBR28 binding in inferior and medial temporal cortex. Increased11 C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD. We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa (TSPO), a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer’s disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with 11 C-PBR28 to measure TSPO. PCA patients showed greater 11 C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater 11 C-PBR28 binding in inferior and medial temporal cortex. Increased 11 C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD. We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with 11C-PBR28 to measure translocator protein 18 kDa. PCA patients showed greater 11C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater 11C-PBR28 binding in inferior and medial temporal cortex. Increased 11C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD. We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with 11C-PBR28 to measure translocator protein 18 kDa. PCA patients showed greater 11C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater 11C-PBR28 binding in inferior and medial temporal cortex. Increased 11C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD.We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of microglial activation, that is distinct from that in patients with amnestic presentation of Alzheimer's disease (AD). Eleven PCA patients, 11 amnestic AD patients, and 15 age-matched controls underwent positron emission tomography with 11C-PBR28 to measure translocator protein 18 kDa. PCA patients showed greater 11C-PBR28 binding than controls in occipital, posterior parietal, and temporal regions. In contrast, amnestic AD patients showed greater 11C-PBR28 binding in inferior and medial temporal cortex. Increased 11C-PBR28 binding overlapped with reduced cortical volume for both PCA and amnestic AD patients, and with areas of reduced glucose metabolism in PCA patients. While both patient groups showed diffuse amyloid binding, PCA patients showed greater binding than amnestic AD patients in bilateral occipital cortex. These results suggest that microglial activation is closely associated with neurodegeneration across different subtypes of AD.
Author	Zoghbi, Sami S. Kreisl, William C. Turner, R. Scott Morse, Cheryl L. Liow, Jeih-San Jenko, Kimberly J. Innis, Robert B. Lyoo, Chul Hyoung Page, Emily Pike, Victor W. Snow, Joseph
AuthorAffiliation	b Office of the Clinical Director, National Institute of Mental Health, Bethesda, MD a Molecular Imaging Branch, National Institute of Mental Health, Bethesda, MD c Memory Disorders Program, Georgetown University, Washington, DC
AuthorAffiliation_xml	– name: a Molecular Imaging Branch, National Institute of Mental Health, Bethesda, MD – name: b Office of the Clinical Director, National Institute of Mental Health, Bethesda, MD – name: c Memory Disorders Program, Georgetown University, Washington, DC
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Snippet	We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of... Abstract We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a... We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa, a marker of... We sought to determine whether patients with posterior cortical atrophy (PCA) demonstrate a pattern of binding to translocator protein 18 kDa (TSPO), a marker...
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SubjectTerms	Aged Alzheimer Disease - diagnostic imaging Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid - metabolism Atrophy Female Glucose - metabolism Humans Internal Medicine Male Microglia - pathology Middle Aged Nerve Degeneration Neuroinflammation Neurology Occipital Lobe - diagnostic imaging Occipital Lobe - metabolism Occipital Lobe - pathology PET imaging Positron-Emission Tomography Protein Binding Receptors, GABA - metabolism
Title	Distinct patterns of increased translocator protein in posterior cortical atrophy and amnestic Alzheimer's disease
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