Striatal monoaminergic terminals in Lewy body and Alzheimer's dementias

Authors

  • Masahiko Suzuki MD, PhD,

    1. Department of Radiology, (Nuclear Medicine) University of Michigan, Ann Arbor, MI
    2. Mental Health Research Institute, University of Michigan, Ann Arbor, MI
    3. Department of Neurology, Jikei University, School of Medicine, Tokyo, Japan
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  • Timothy J. Desmond MS,

    1. Mental Health Research Institute, University of Michigan, Ann Arbor, MI
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  • Roger L. Albin MD,

    1. Department of Neurology, University of Michigan, Ann Arbor, MI
    2. Geriatrics Research, Education and Clinical Center, Ann Arbor, MI
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  • Kirk A. Frey MD, PhD

    Corresponding author
    1. Department of Radiology, (Nuclear Medicine) University of Michigan, Ann Arbor, MI
    2. Department of Neurology, University of Michigan, Ann Arbor, MI
    3. Mental Health Research Institute, University of Michigan, Ann Arbor, MI
    • Room B1G-412/0028 AGH, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0028
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Abstract

Vesicular monoamine transporter type 2 and benzodiazepine binding site expressions were examined with quantitative autoradiography in postmortem striata from 19 patients with dementia with Lewy bodies, seven patients with dementia with Lewy bodies and Alzheimer's disease, 12 patients with Alzheimer's disease, and eight neurologically normal subjects. Striatal vesicular monoamine transporter type 2 expression in dementia with Lewy bodies and in dementia with Lewy bodies plus Alzheimer's disease was reduced significantly, indicating degeneration of nigrostriatal projections. Striatal benzodiazepine binding site expression was unchanged, indicating preserved intrinsic striatal neuropil. Vesicular monoamine transporter type 2 and benzodiazepine binding site expressions were each preserved in Alzheimer's disease striatum. We conclude that dementia with Lewy bodies may be distinguished from Alzheimer's disease by postmortem examination or by future in vivo measurements of the striatal vesicular monoamine transporter type 2.

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