Mark S. Forman, Virginia M-Y. Lee, John Q. Trojanowski Neuron

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Synucleinopathies and Tauopathies

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Nosology of Parkinson’s Disease: Looking for the Way Out of a Quackmire Mark S. Forman, Virginia M-Y. Lee, John Q. Trojanowski Neuron Volume 47, Issue 4, Pages 479-482 (August 2005) DOI: 10.1016/j.neuron.2005.07.021 Copyright © 2005 Elsevier Inc. Terms and Conditions

Figure 1 Molecular Genetic Neuropathology of Parkinson’s Disease Algorithm for the neuropathologic differential diagnosis of patients with PD. Neuropathologic examination of the majority of patients with L-dopa-responsive parkinsonism reveals α-synuclein-positive Lewy body pathology (indicated in blue). However, neuropathologic evaluation cannot readily distinguish those patients with concurrent dementia (i.e., PDD or DLB). In addition, a subset of parkinsonian patients will have α-synuclein-positive glial cytoplasmic inclusions indicative of multiple system atrophy while other patients will have tau pathology (±senile plaques). There is limited neuropathologic data on patients with many of the newly described mutations. Moreover, this algorithm represents an oversimplification and does not reflect other disorders that may also present with parkinsonism. AD, Alzheimer’s disease; CBD, corticobasal degeneration; DLB, dementia with Lewy bodies; FTDP-17, frontotemporal dementia with parkinsonism linked to chromosome 17; GCI, glial cytoplasmic inclusions; LBVAD, Lewy body variant of Alzheimer’s disease; MSA, multiple system atrophy; PD, Parkinson’s disease; PDD, Parkinson’s disease dementia; PSP, progressive supranuclear palsy. Neuron 2005 47, 479-482DOI: (10.1016/j.neuron.2005.07.021) Copyright © 2005 Elsevier Inc. Terms and Conditions