title: Induction of amyloid-β(1-42) in the retina and optic nerve head of chronic ocular hypertensive monkeys.
abstract: OBJECTIVE
  Recent studies have indicated that accumulation of amyloid β(1-42) (Aβ(1-42)), which is associated with the progression of Alzheimer disease, may also be responsible for retinal ganglion cell death in glaucoma. The purpose of this study was to investigate the expression and localization of Aβ(1-42) in the retina and the optic nerve head (ONH) of monkeys with experimental glaucoma.
  
  
  METHODS
  Five cynomolgus monkeys with a glaucomatous left eye at 4, 9, 11, 15, and 24 weeks after laser photocoagulation treatment were studied by immunohistochemical methods. Another two cynomolgus monkeys with a glaucomatous left eye at 133 weeks after laser photocoagulation treatment were used to measure Aβ(1-42) concentrations in the retina by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  At 11 to 24 weeks after the laser photocoagulation treatment, Aβ(1-42) was upregulated in the nerve fiber layer (NFL) and the ganglion cell layer (GCL) of the retina and the ONH, but the expression of amyloid precursor protein decreased in the NFL and ONH from levels at 9 weeks. The localizations of Aβ(1-42) were merged in glial fibrillary acidic protein-positive astroglial cells but not phosphorylated neurofilament heavy- or nonphosphorylated neurofilament heavy-positive axons in the retina and the ONH. Likewise, Aβ(1-42) concentrations in the retina of monkeys increased in the chronic stage of glaucoma.
  
  
  CONCLUSIONS
  These findings indicate that the upregulation of Aβ(1-42) after an intraocular pressure elevation could apply to monkeys since the structure of the ONH is more similar to humans than that of rodents.
authors.affiliation: Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Ito
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Shimazawa
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Tsuruma
authors.forename: Chihiro
authors.initials: C
authors.lastname: Mayama
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Ishii
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Onoe
authors.forename: Makoto
authors.initials: M
authors.lastname: Aihara
authors.forename: Makoto
authors.initials: M
authors.lastname: Araie
authors.forename: Hideaki
authors.initials: H
authors.lastname: Hara
mesh_terms: D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D005901:Glaucoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D017075:Laser Coagulation / Q000009:adverse effects; D008252:Macaca fascicularis; D009412:Nerve Fibers / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D009798:Ocular Hypertension / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009898:Optic Disk / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D010446:Peptide Fragments / Q000235:genetics / Q000378:metabolism*; D012165:Retinal Ganglion Cells / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D015854:Up-Regulation
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)