Intravenous administration of a transferrin receptor antibody-nerve growth factor conjugate prevents the degeneration of cholinergic striatal neurons in a model of Huntington disease

Jeffrey H. Kordower, Vinod Charles, Robert Bayer, Raymond T. Bartus, Scott Putney, Lee R. Walus, Phillip M. Friden

Research output: Contribution to journalArticlepeer-review

108 Scopus citations

Abstract

Intrastriatal injections of quinolinic acid induce a pattern of neuronal degeneration similar to that seen in Huntington disease. In the present study, nerve growth factor (NGF) crossed the blood-brain barrier in a dose- dependent fashion following intravenous infusion when conjugated to an antibody directed against the transferrin receptor (OX-26). Intravenous injections of the OX-26-NGF conjugate selectively prevented the loss of striatal choline acetyltransferase-immunoreactive neurons which normally occurs following quinolinic acid administration relative to control rats receiving vehicle or a nonconjugated mixture of OX-26 and NGF. These data demonstrate that a neurotrophic factor-antibody conjugate can prevent the degeneration of central NGF-responsive neurons following systemic administration.

Original languageEnglish (US)
Pages (from-to)9077-9080
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume91
Issue number19
DOIs
StatePublished - Sep 13 1994
Externally publishedYes

Keywords

  • choline acetyltransferase
  • quinolinic acid
  • striatum
  • transferrin receptor

ASJC Scopus subject areas

  • General

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