Injections of okadaic acid, but not beta-amyloid peptide, induce Alz-50 immunoreactive dystrophic neurites in the cerebral cortex of sheep

P. T. Nelson, C. B. Saper

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

In an attempt to produce an animal model of neurofibrillary degeneration of the Alzheimer type, okadaic acid (a phosphatase inhibitor) and beta-amyloid peptide (1-40) were microinjected into the cerebral cortex of six adult sheep. After survivals varying from 1 day to 3 months, the injection sites and adjacent areas were evaluated using light microscopic immunocytochemistry. Near sites of implantation of crystalline okadaic acid, the Alz-50 monoclonal antibody stained twisted, dystrophic neurites. None of the beta-amyloid peptide injections caused neurofibrillary pathology. However, immunohistochemical analysis revealed no detectable beta-amyloid peptide remaining in the neuropil, even at 1 day, indicating rapid clearance of the beta-amyloid peptide. The induction of Alz-50 immunoreactive dystrophic neurites by okadaic acid in sheep represents a novel animal model of Alzheimer's neurofibrillary pathology.

Original languageEnglish
Pages (from-to)77-80
Number of pages4
JournalNeuroscience Letters
Volume208
Issue number2
DOIs
StatePublished - Apr 19 1996

Bibliographical note

Funding Information:
We thank Drs. Peter Davies, Dennis Selkoe, and R. Benoit for generously providing antisera for the current experiments; Drs. Alfredo Lorenzo and Bruce Yankner for flAP peptide; and Quan Hue Ha for excellent technical assistance. This work was supported by grants from the Fidelity Foundation and USPHS grant AG 12856.

Keywords

  • Alz-50
  • Alzheimer's disease
  • Tau
  • brain
  • neurofibrillary tangles
  • okadaic acid
  • sheep

ASJC Scopus subject areas

  • General Neuroscience

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