Alzheimer's & Dementia: The Journal of the Alzheimer's Association
Volume 4, Issue 1, Supplement 1 , Pages S67-S76, January 2008

Differentiating Alzheimer’s disease from dementia with Lewy bodies and Parkinson’s disease with (+)-[11C]dihydrotetrabenazine positron emission tomography

  • Robert A. Koeppe

      Affiliations

    • Division of Nuclear Medicine, Department of Radiology, The University of Michigan, Ann Arbor, MI, USA
    • Corresponding Author InformationCorresponding author. Tel.: 734-763-9247; Fax: 734-764-2088.
    • ,
  • Sid Gilman

      Affiliations

    • Department of Neurology, The University of Michigan, Ann Arbor, MI, USA
    • ,
  • Larry Junck

      Affiliations

    • Department of Neurology, The University of Michigan, Ann Arbor, MI, USA
    • ,
  • Kris Wernette

      Affiliations

    • Division of Nuclear Medicine, Department of Radiology, The University of Michigan, Ann Arbor, MI, USA
    • Department of Neurology, The University of Michigan, Ann Arbor, MI, USA
    • ,
  • Kirk A. Frey

      Affiliations

    • Division of Nuclear Medicine, Department of Radiology, The University of Michigan, Ann Arbor, MI, USA
    • Department of Neurology, The University of Michigan, Ann Arbor, MI, USA

Abstract 

Background

Several progressive neurologic disorders begin with cognitive decline or parkinsonism, notably Alzheimer’s disease (AD), Parkinson’s disease (PD), and dementia with Lewy bodies (DLB). We used positron emission tomography (PET) in attempts to differentiate these disorders.

Methods

We performed PET with (+)-[11C]dihydrotetrabenazine ([11C]DTBZ) to examine blood-to-brain ligand transport (K1) and striatal monoaminergic presynaptic binding (distribution volume [DV]) in 25 DLB, 30 PD, and 25 AD patients and 57 elderly controls (NC).

Results

[11C]DTBZ DV was decreased significantly in caudate nucleus, anterior putamen, and posterior putamen in DLB and PD compared with AD and NC. DLB and PD groups showed an anterior-to-posterior gradient of binding loss relative to NC, least in caudate nucleus and largest in posterior putamen. The gradient was significantly steeper in PD than DLB. Both PD and DLB showed significantly greater interhemispheric striatal binding asymmetry than NC, and PD had greater asymmetry than DLB. Cerebral cortical [11C]DTBZ K1 was decreased diffusely by 4% to 8% in PD. Larger K1 deficits occurred in AD and DLB temporoparietal and prefrontal association cortices and posterior cingulate cortex. Greater reduction of K1 occurred in occipital cortex in DLB than AD. Receiver operating characteristic curve analyses distinguished DLB from AD more effectively on the basis of striatal DV than occipital K1 and distinguished DLB from PD more effectively on the basis of cerebral cortical K1 than striatal DV patterns. Overall, 90% of cases were properly classified by combining these measures.

Conclusions

PET with [11C]DTBZ can differentiate DLB from both PD and AD in a single neuroimaging study.

Keywords: Dementia with Lewy bodies, Alzheimer’s disease, Parkinson’s disease, Nigrostriatal projection, Vesicular monoamine transporter type-2, Positron emission tomography, Dihydrotetrabenazine

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 30.00 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.
 

PII: S1552-5260(07)00657-7

doi:10.1016/j.jalz.2007.11.016

Alzheimer's & Dementia: The Journal of the Alzheimer's Association
Volume 4, Issue 1, Supplement 1 , Pages S67-S76, January 2008

Article Tools

* Image Usage & Resolution