Nuclear Medicine and Biology
Volume 34, Issue 7 , Pages 809-822, October 2007

Impact of amyloid imaging on drug development in Alzheimer's disease☆

  • Chester A. Mathis

      Affiliations

    • Department of Radiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    • Corresponding Author InformationCorresponding author. PET Facility, B-938, University of Pittsburgh Medical Center Presbyterian Hospital, Pittsburgh, PA 15213, USA. Tel.: +1 412 647 0734; fax: +1 412 647 0700.
    • ,
  • Brian J. Lopresti

      Affiliations

    • Department of Radiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    • ,
  • William E. Klunk

      Affiliations

    • Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA

Received 19 June 2007; accepted 25 June 2007. published online 03 September 2007.

Abstract 

Imaging agents capable of assessing amyloid-beta (Aβ) content in vivo in the brains of Alzheimer's disease (AD) subjects likely will be important as diagnostic agents to detect Aβ plaques in the brain as well as to help test the amyloid cascade hypothesis of AD and as an aid to assess the efficacy of anti-amyloid therapeutics currently under development and in clinical trials. Positron emission tomography (PET) imaging studies of amyloid deposition in human subjects with several Aβ imaging agents are currently underway. We reported the first PET studies of the carbon 11-labeled thioflavin-T derivative Pittsburgh Compound B in 2004, and this work has subsequently been extended to include a variety of subject groups, including AD patients, mild cognitive impairment patients and healthy controls. The ability to quantify regional Aβ plaque load in the brains of living human subjects has provided a means to begin to apply this technology as a diagnostic agent to detect regional concentrations of Aβ plaques and as a surrogate marker of therapeutic efficacy in anti-amyloid drug trials.

Keywords: Amyloid imaging, Amyloid beta, Aβ, PiB, Alzheimer's disease, Anti-amyloid therapy

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

☆ GE Healthcare holds a license agreement with the University of Pittsburgh based on the [11C]PiB imaging technology described in this article but provided no financial support for the preparation of this article and had no role in the writing or interpretation of the information contained in this article. Drs. Mathis and Klunk are co-inventors of [11C]PiB and, as such, have a financial interest in this license agreement.

PII: S0969-8051(07)00177-1

doi:10.1016/j.nucmedbio.2007.06.015

Nuclear Medicine and Biology
Volume 34, Issue 7 , Pages 809-822, October 2007

Article Tools

* Image Usage & Resolution