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 (2)  • Contact me when this article is cited  Related Content  • Related article  • Similar articles in this journal  Topic Collections  • Alzheimer Disease  • Neurology, Other  • Alert me on articles by topic

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]

AUTHOR INFORMATION

RELATED ARTICLE

Molecular Imaging With Pittsburgh Compound B Confirmed at Autopsy: A Case Report
, , , , , , , , , , , , and
Arch Neurol. ;64():431-434.
FULL TEXT  

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

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