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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.

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