Format

Send to

Choose Destination
See comment in PubMed Commons below
Neurosci Lett. 1996 Apr 19;208(2):77-80.

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

Author information

1
Committee on Neurobiology, University of Chicago, IL 60637, USA.

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.

PMID:
8859894
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center