Article

Molecular Neurobiology

, Volume 47, Issue 2, pp 495-508

The Lewy Body in Parkinson’s Disease and Related Neurodegenerative Disorders

  • Koichi WakabayashiAffiliated withDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine Email author 
  • , Kunikazu TanjiAffiliated withDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine
  • , Saori OdagiriAffiliated withDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine
  • , Yasuo MikiAffiliated withDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine
  • , Fumiaki MoriAffiliated withDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine
  • , Hitoshi TakahashiAffiliated withDepartment of Pathology, Brain Research Institute, University of Niigata

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Abstract

The histopathological hallmark of Parkinson’s disease (PD) is the presence of fibrillar aggregates referred to as Lewy bodies (LBs), in which α-synuclein is a major constituent. Pale bodies, the precursors of LBs, may serve the material for that LBs continue to expand. LBs consist of a heterogeneous mixture of more than 90 molecules, including PD-linked gene products (α-synuclein, DJ-1, LRRK2, parkin, and PINK-1), mitochondria-related proteins, and molecules implicated in the ubiquitin–proteasome system, autophagy, and aggresome formation. LB formation has been considered to be a marker for neuronal degeneration because neuronal loss is found in the predilection sites for LBs. However, recent studies have indicated that nonfibrillar α-synuclein is cytotoxic and that fibrillar aggregates of α-synuclein (LBs and pale bodies) may represent a cytoprotective mechanism in PD.

Keywords

α-Synuclein Lewy body Pale body Parkinson’s disease Presynapse