This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (23)  • Contact me when this article is cited  Related Content  • Related article  • Similar articles in this journal  Topic Collections  • Alzheimer Disease  • Lewy Body Disease  • Movement Disorders  • Neurology, Other  • Alert me on articles by topic

A Case Report

Brian J. Bacskai, PhD; Matthew P. Frosch, MD, PhD; Stefanie H. Freeman, MD; Scott B. Raymond, BS; Jean C. Augustinack, PhD; Keith A. Johnson, MD; Michael C. Irizarry, MD; William E. Klunk, MD, PhD; Chester A. Mathis, PhD; Steven T. DeKosky, MD; Steven M. Greenberg, MD, PhD; Bradley T. Hyman, MD, PhD; John H. Growdon, MD

Arch Neurol. 2007;64(3):431-434.

Objective  To determine the correspondence between uptake of Pittsburgh Compound B (PiB) in life and measures of β-amyloid (Aβ) in postmortem tissue analysis.

Patient  A 76-year-old man with a clinical diagnosis of dementia with Lewy bodies underwent fluorodeoxyglucose ¹⁸F and PiB positron emission tomographic brain scans. Imaging revealed marked region specific binding of PiB and abnormal fluorodeoxyglucose uptake.

Intervention  Autopsy was performed 3 months after the PiB scan.

Results  Autopsy confirmed the clinical diagnosis; in addition, there was severe cerebral amyloid angiopathy and only moderate numbers of parenchymal Aβ plaques. Biochemical measures revealed a positive correlation between Aβ levels and regional PiB binding.

Conclusion  This report confirms that PiB detects Aβ in the living patient and demonstrates that amyloid deposited as cerebral amyloid angiopathy can be the dominant source of signal.

Author Affiliations: MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Charlestown, Mass (Drs Bacskai, Frosch, Irizarry, Greenberg, Hyman, and Growdon and Mr Raymond); C. S. Kubik Laboratory for Neuropathology (Drs Frosch and Freeman) and Department of Radiology (Drs Augustinack and Johnson), Massachusetts General Hospital, Boston; and Departments of Psychiatry (Drs Klunk and Mathis) and Neurology (Dr DeKosky), University of Pittsburgh, Pittsburgh, Pa. Dr Irizarry is now with GlaxoSmithKline, Research Triangle Park, NC.

RELATED ARTICLE

Pittsburgh Compound B Retention and Verification of Amyloid Deposition

Arch Neurol. ;64():315-316.
FULL TEXT  

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Assessment of {beta}-Amyloid in a Frontal Cortical Brain Biopsy Specimen and by Positron Emission Tomography With Carbon 11-Labeled Pittsburgh Compound B
Leinonen et al.
Arch Neurol 2008;0:65.10.noc80013-6.
ABSTRACT | FULL TEXT  

PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease
Koivunen et al.
Brain 2008;131:1845-1853.
ABSTRACT | FULL TEXT  

Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease
Ikonomovic et al.
Brain 2008;131:1630-1645.
ABSTRACT | FULL TEXT  

Carbon 11-Labeled Pittsburgh Compound B Positron Emission Tomographic Amyloid Imaging in Patients With APP Locus Duplication
Remes et al.
Arch Neurol 2008;65:540-544.
ABSTRACT | FULL TEXT  

11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment
Jack et al.
Brain 2008;131:665-680.
ABSTRACT | FULL TEXT  

PIB is a non-specific imaging marker of amyloid-beta (A{beta}) peptide-related cerebral amyloidosis
Lockhart et al.
Brain 2007;130:2607-2615.
ABSTRACT | FULL TEXT  

A{beta} amyloid deposition in the language system and how the brain responds
Nelissen et al.
Brain 2007;130:2055-2069.
ABSTRACT | FULL TEXT  

Pittsburgh Compound B Retention and Verification of Amyloid Deposition
Holtzman
Arch Neurol 2007;64:315-316.
FULL TEXT