title: Accumulation of NACP/alpha-synuclein in lewy body disease and multiple system atrophy.
abstract: OBJECTIVE
  NACP/alpha-synuclein is an aetiological gene product in familial Parkinson's disease. To clarify the pathological role of NACP/alpha-synuclein in sporadic Parkinson's disease and other related disorders including diffuse Lewy body disease (DLBD) and multiple system atrophy (MSA), paraffin sections were examined immunocytochemically using anti-NACP/alpha-synuclein antibodies.
  
  
  METHODS
  A total of 58 necropsied brains, from seven patients with Parkinson's disease, five with DLBD, six with MSA, 12 with Alzheimer's disease, one with Down's syndrome, one with amyotrophic lateral sclerosis (ALS), three with ALS and dementia, one with Huntington's disease, two with progressive supranuclear palsy (PSP), one with Pick's disease, one with myotonic dystrophy, and three with late cerebellar cortical atrophy (LCCA), and 15 elderly normal controls were examined.
  
  
  RESULTS
  In addition to immunoreactive Lewy bodies, widespread accumulation of NACP/alpha-synuclein was found in neurons and astrocytes from the brainstem and basal ganglia to the cerebral cortices in Parkinson's disease/DLBD. NACP/alpha-synuclein accumulates in oligodendrocytes from the spinal cord, the brain stem to the cerebellar white matter, and inferior olivary neurons in MSA. These widespread accumulations were not seen in other types of dementia or spinocerebellar ataxia.
  
  
  CONCLUSIONS
  Completely different types of NACP/alpha-synuclein accumulation in Parkinson's disease/DLBD and MSA suggest that accumulation is a major step in the pathological cascade of both diseases and provides novel strategies for the development of therapies.
authors.affiliation: Department of Neurology, Gunma University School of Medicine, Japan. mshoji@akagi.sb.gunma-u.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Shoji
authors.forename: Y
authors.initials: Y
authors.lastname: Harigaya
authors.forename: A
authors.initials: A
authors.lastname: Sasaki
authors.forename: K
authors.initials: K
authors.lastname: Uéda
authors.forename: K
authors.initials: K
authors.lastname: Ishiguro
authors.forename: E
authors.initials: E
authors.lastname: Matsubara
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Ikeda
authors.forename: M
authors.initials: M
authors.lastname: Kanai
authors.forename: Y
authors.initials: Y
authors.lastname: Tomidokoro
authors.forename: M
authors.initials: M
authors.lastname: Shizuka
authors.forename: M
authors.initials: M
authors.lastname: Amari
authors.forename: K
authors.initials: K
authors.lastname: Kosaka
authors.forename: Y
authors.initials: Y
authors.lastname: Nakazato
authors.forename: K
authors.initials: K
authors.lastname: Okamoto
authors.forename: S
authors.initials: S
authors.lastname: Hirai
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001344:Autopsy; D001479:Basal Ganglia / Q000378:metabolism; D001933:Brain Stem / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D005260:Female; D006801:Humans; D016631:Lewy Bodies / Q000378:metabolism; D020961:Lewy Body Disease / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D019578:Multiple System Atrophy / Q000378:metabolism* / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D010300:Parkinson Disease / Q000378:metabolism* / Q000473:pathology; D051843:Synucleins; D014018:Tissue Distribution
chemical_list: D009419:Nerve Tissue Proteins; D051843:Synucleins