title: Prion disease causes less severe lesions in human hippocampus than other parts of brain.
abstract: OBJECTIVE
  The hippocampus can be very sensitive to damage in the scrapie-infected mouse, a well-established animal model of prion diseases. Terminally ill scrapie-infected animals exhibit nearly complete loss of cornu ammonis (CA) 1 pyramidal neurons, but few studies have focused on the neuropathological lesions of the human hippocampus in autopsied brain tissue; in particular, few findings on differences in severity of pathology between the hippocampal and parahippocampal formations have been obtained. The aim of the present paper is to evaluate the human hippocampus of prion disease through neuropathological examination.
  
  
  METHODS
  A systemic, detailed neuropathological study throughout the subdivisions of the hippocampus was carried out in 23 autopsied cases of prion diseases. Prion protein immunohistochemistry was performed in serial brain sections to determine the topography of prion deposits.
  
  
  RESULTS
  Compared to lesions in other brain regions, hippocampal lesions were mild, despite numerous prion deposits. The distribution of prion deposits did not appear to be correlated with neuropathological changes. The present findings differed from the hippocampal pathology observed in scrapie-infected mice. In addition, differences in neuropathological severity were observed within the hippocampal formation.
  
  
  CONCLUSIONS
  The human hippocampus may be protected from the neurotoxic effects of prion deposits.
authors.affiliation: Department of Neuropsychiatry, Shinshu University School of Medicine, Nagano, Japan.
authors.forename: Minoru
authors.initials: M
authors.lastname: Kaneko
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Sugiyama
authors.forename: Daimei
authors.initials: D
authors.lastname: Sasayama
authors.forename: Keiko
authors.initials: K
authors.lastname: Yamaoka
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Miyakawa
authors.forename: Kunimasa
authors.initials: K
authors.lastname: Arima
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Tsuchiya
authors.forename: Kazuko
authors.initials: K
authors.lastname: Hasegawa
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Washizuka
authors.forename: Tokiji
authors.initials: T
authors.lastname: Hanihara
authors.forename: Tokisi
authors.initials: T
authors.lastname: Hanihara
authors.forename: Naoji
authors.initials: N
authors.lastname: Amano
authors.forename: Saburo
authors.initials: S
authors.lastname: Yagishita
mesh_terms: D000328:Adult; D000368:Aged; D002540:Cerebral Cortex / Q000473:pathology; D007562:Creutzfeldt-Jakob Syndrome / Q000473:pathology; D004292:Dominance, Cerebral / Q000502:physiology; D018728:Entorhinal Cortex / Q000473:pathology; D005260:Female; D016098:Gerstmann-Straussler-Scheinker Disease / Q000235:genetics / Q000473:pathology; D005911:Gliosis / Q000473:pathology; D006624:Hippocampus / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000473:pathology; D020534:Parahippocampal Gyrus / Q000473:pathology*; D017096:Prion Diseases / Q000473:pathology*; D011328:Prions / Q000032:analysis / Q000235:genetics
chemical_list: D011328:Prions