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Creatine kinase isozymes in duchenne dystrophy.

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cholinergic neurons to NGF. In either case, increasing the
amount of NGF available t o the cholinergic neurons should
produce beneficial effects. Unfortunately, NGF does not
cross the blood-brain barrier; also, only minimal amounts
of pure NGF are presently available. If further studies substantiate the effects of NGF o n central cholinergic neurons,
it would appear worthwhile t o attempt to develop synthetic
compounds which have functional properties similar to
N G F , but which can pass the blood-brain barrier. Chronic
application of such drugs might retard the loss of cholinergic neurons.
Department of Neurochemistry
Max-Planck Institute far Psychiatry
Martinsried, West G e m a n y
Supported by a fellowship from the Alexander von Humboldt
Stiftung, Bonn, West Germany.
I thank Drs H. Thoenen for support and encouragement and R.
Heumann for discussions regarding the presented topic.
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Creatine Kmase Isozymes
in Duchenne Dystrophy
A. D. Desai, MB, FRCP(E), and A. M. Varadkar, MSc
With reference to the article by Ionasescu et a1 entitled
“Alterations in Creatine Kinase in Fresh Muscle and Cell
Cultures in Duchenne Dystrophy” (Ann Neurol 9:394399, 198l), we would like to make the following observations based o n studies we performed of total creatine
kinase (CK) activity and its isozymes in fresh normal and
Duchenne muscular dystrophy (DMD) muscles as well as
in normal fetuses (16 to 18 weeks) (Karandikar et al, J
Postgrad Med 2653-67, 1980).
C K levels in D M D and fetal muscles were remarkably
similar and were significantly reduced compared with levels
in normal muscle. T h e CK isozyme pattern on polyacrylamide gel electrophoresis revealed the M M and MB
types of isozymes in normal, D M D , and fetal muscles. Unlike Ionasescu e t al, we did not detect BB isozyme in any of
these muscles, including fetal muscle. However, in accordance with their observations, we found a high MB : M M
ratio in D M D muscles. And similar to their observations,
an estimation of C K activity in culture medium that we carried out recently showed no difference in D M D culture
medium from normal controls (unpublished data).
Department of Neurosurgery
Seth G . S . Medicul College &
K. E. M . Hospital
Parel, Bombay 400 012, India
Victor Ionasescu, MD,” and Ronald Feld, P h D t
We thank Drs Desai and Varadkar for their comments.
Their study is interesting and is concordant with our conclusions for the main findings. T h e only difference is the
absence of CK-BB isozyme in D M D and fetal muscle. We
are wondering if this difference is not related to their technique. T h e presence of CK-BB isozyme in fetal and dystrophic muscle has been documented by several studies
[I-41, listed in our references.
Departments of “Pediatrics and ?Pathology
University of Iowa Hospitals & Clinics
Iowa City, IA 52242
1. Goto L, Nagamine M, Katsuki S: Creatine phosphokinase
isoenzyme in muscles-human fetus and patients. Arch Neurol
20:422-429, 1969
2. Lang H: Creatine Kinase Isoenzymes. Pathophysiology and
Clinical Application. Berlin and New York, Springer, 1981
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kinase et de I’aldolase du muscle fcctal et pathologique. Clin
Chim Acta 20:439-447, 1968
4. Somer H, Dubowitz V, Donner M: Creatine kinase isoenzymes
in neuromuscular diseases. J Neurol Sci 29:129-136, 1976
110 Annals of Neurology
Vol 13 No 1 January 1983
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creating, isozyme, duchenne, dystrophy, kinases
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