INTRAVENOUS ADMINISTRATION OF A TRANSFERRIN RECEPTOR ANTIBODY NERVE GROWTH-FACTOR CONJUGATE PREVENTS THE DEGENERATION OF CHOLINERGIC STRIATAL NEURONS IN A MODEL OF HUNTINGTON DISEASE
Jh. Kordower et al., INTRAVENOUS ADMINISTRATION OF A TRANSFERRIN RECEPTOR ANTIBODY NERVE GROWTH-FACTOR CONJUGATE PREVENTS THE DEGENERATION OF CHOLINERGIC STRIATAL NEURONS IN A MODEL OF HUNTINGTON DISEASE, Proceedings of the National Academy of Sciences of the United Statesof America, 91(19), 1994, pp. 9077-9080
Intrastriatal injections of quinolinic acid induce a pattern of neuron
al degeneration similar to that seen in Huntington disease. In the pre
sent study, nerve growth factor (NGF) crossed the blood-brain barrier
in a dose dependent fashion following intravenous infusion when conjug
ated to an antibody directed against the transferrin receptor (OX-26).
Intravenous injections of the OX-26-NGF conjugate selectively prevent
ed the loss of striatal choline acetyltransferase-immunoreactive neuro
ns which normally occurs following quinolinic acid administration rela
tive to control rats receiving vehicle or a nonconjugated mixture of O
X-26 and NGF. These data demonstrate that a neurotrophic factor-antibo
dy conjugate can prevent the degeneration of central NGF responsive ne
urons following systemic administration.