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David M. Holtzman, MD

Arch Neurol. 2007;64(3):315-316.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Making a definitive diagnosis of Alzheimer disease (AD), or more specifically determining whether the presence of amyloid plaques in the central nervous system may be contributing to the clinical phenotype in a patient with dementia, was previously possible only with brain biopsy or at autopsy. The recent development of amyloid imaging with compounds such as carbon 11 (¹¹C)–labeled Pittsburgh Compound B (PiB) and positron emission tomography (PET) scanning is likely to ultimately change the way physicians diagnose and treat disorders in which the aggregation of β-amyloid (Aβ) plays a role.¹ It has been shown in human tissue ex vivo that the amount of PiB binding correlates strongly with the amount of Aβ present as measured biochemically.^2-3 Further, in tissue sections from human brain² as well as in vivo in a transgenic mouse model with Aβ deposition,⁴ it appears that PiB binds to Aβ if it . . . [Full Text of this Article]

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