Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography

Authors

  • David J. Brooks MD, DSc, FRCP, FMedSci

    Corresponding author
    1. MRC Clinical Sciences Centre and Division of Neuroscience, Imperial College, London, United Kingdom
    • Cyclotron Building, Hammersmith Hospital, Du Cane Road, London, W12 0NN, United Kingdom
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  • Potential conflicts of interest: David Brooks is the sole author of this work. He holds a part-time position as Head of Neurology with Medical Diagnostics, GE Healthcare, who owns the commercial rights to PIB but did not resource any of the studies quoted.

Abstract

Although Parkinson's disease with later dementia (PDD) and dementia with Lewy bodies (DLB) are pathologically characterized by the presence of intraneuronal Lewy inclusion bodies, amyloid deposition is also associated to varying degrees with both these disorders. Fibrillar amyloid load can now be quantitated in vivo with positron emission tomography (PET) using imaging biomarkers. Here the reported findings of 11C-PIB PET studies concerning the amyloid load associated with PD and its influence on dementia are reviewed. It is concluded that the presence of amyloid acts to accelerate the dementia process in Lewy body disorders, though has little influence on its nature. Anti-amyloid strategies could be a relevant approach for slowing dementia in a number of DLB and PDD cases. © 2009 Movement Disorder Society

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