14. Neuropathology of Dementia in Parkinson's Disease

  1. C. Warren Olanow MD, FRCPC4,5,6,
  2. Fabrizio Stocchi MD, PhD7 and
  3. Anthony E. Lang MD, FRCPC8,9,10
  1. Dennis W. Dickson MD1 and
  2. Carolyn F. Orr FRACP, PhD2,3

Published Online: 27 JUN 2011

DOI: 10.1002/9781444397970.ch14

Parkinson's Disease: Non-Motor and Non-Dopaminergic Features

Parkinson's Disease: Non-Motor and Non-Dopaminergic Features

How to Cite

Dickson, D. W. and Orr, C. F. (2011) Neuropathology of Dementia in Parkinson's Disease, in Parkinson's Disease: Non-Motor and Non-Dopaminergic Features (eds C. W. Olanow, F. Stocchi and A. E. Lang), Blackwell Publishing Ltd., Oxford, UK. doi: 10.1002/9781444397970.ch14

Editor Information

  1. 4

    Department of Neurology, Mount Sinai School of Medicine, New York, NY, USA

  2. 5

    Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA

  3. 6

    Robert and John M. Bendheim Parkinson's Disease Center, Mount Sinai School of Medicine, New York, NY, USA

  4. 7

    Parkinson's Disease and Movement Disorders Research Centre, Institute for Research and Medical Care, IRCCS San Raffaele Pisana, Rome, Italy

  5. 8

    Division of Neurology, University of Toronto, Toronto, ON, Canada

  6. 9

    Parkinson's Disease Research, University of Toronto, Toronto, ON, Canada

  7. 10

    Movement Disorder Centre, Toronto Western Hospital, Toronto, ON, Canada

Author Information

  1. 1

    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA

  2. 2

    Department of Neurology, Mayo Clinic, Rochester, MN, USA

  3. 3

    Department of Neurology, Mayo Clinic, Rochester, NY, USA

Publication History

  1. Published Online: 27 JUN 2011
  2. Published Print: 29 JUL 2011

ISBN Information

Print ISBN: 9781405191852

Online ISBN: 9781444397970

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Keywords:

  • Aβ;
  • Lewy body;
  • Lewy neurites;
  • neurofibrillary tangles;
  • senile plaques;
  • synapses;
  • α-synuclein;
  • tau

Summary

The neuropathology of Parkinson's disease dementia (PDD), like Parkinson's disease (PD), is heterogeneous, but most cases have Lewy-related pathology as the major pathologic substrate of parkinsonism. Less common causes of the PDD clinical syndrome include progressive supranuclear palsy and corticobasal degeneration. Most cases of PDD have diffuse cortical Lewy bodies, medial temporal neurofibrillary degeneration, and neocortical diffuse amyloid deposits. In most cases, Alzheimer-type pathology is not sufficient to warrant a diagnosis of Alzheimer's disease (AD). A subset of cases have concurrent AD, multiple cerebrovascular lesions consistent with vascular dementia, or severe pathology of the isodendritic core of cortically projecting subcortical nuclei with Lewy-related pathology that is relatively restricted to brainstem or limbic areas. Comparable degrees of Lewy-related and Alzheimer-type pathology are sometimes detected in subjects with PD without dementia, which suggests that there are other, yet to be determined, factors that are more proximal causes of cognitive impairment in PDD, such as synaptic loss, deficiencies of neurotransmitters, or the presence of soluble toxic oligomers of Aβ, tau or α-synuclein that lead to neuronal dysfunction.