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Acta Neuropathologica

, Volume 115, Issue 4, pp 377–378 | Cite as

Clarifying the pathological progression of Parkinson’s disease

  • Glenda HallidayEmail author
Editorial

Despite the main pathological features of Parkinson’s disease (PD) being identified by Lewy (Lewy bodies) and Tretiakoff (depigmention of the substantia nigra) nearly a century ago, it has been only in recent years that research momentum on its molecular pathogenesis has uncovered evidence of the progression of PD. This research momentum started a decade ago when the α-synuclein gene mutation was identified in a dominantly inherited form of the disease and the protein identified as the major constituent of Lewy bodies and Lewy neurites [3]. Using this molecular key, Braak et al. [1] carefully examined a large cross-section of the population and for the first time tackled the concept of the initiation and progression of PD pathology. Their hypothesis that PD pathology is initiated in peripheral mucosa and travels into the brain via the olfactory and vagus nerves [2] has energised the neurological community to focus on these still hypothetical preclinical disease stages.

In the current...

References

  1. 1.
    Braak H, Del Tredici K, Rub U, de Vos RA, Jansen Steur EN, Braak E (2003) Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol Aging 24:197–211PubMedCrossRefGoogle Scholar
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    Hawkes CH, Del Tredici K, Braak H (2007) Parkinson’s disease: a dual-hit hypothesis. Neuropathol Appl Neurobiol 33:599–614PubMedCrossRefGoogle Scholar
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    Spillantini MG, Schmidt ML, Lee VM, Trojanowski JQ, Jakes R, Goedert M (1997) Alpha-synuclein in Lewy bodies. Nature 388:839–840PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 2008

Authors and Affiliations

  1. 1.Prince of Wales Medical Research Institute and the University of New South WalesRandwickAustralia

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