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CURRENT SCIENCE REVIEWS   by Joe Bruman   December 1996   p. 1 of

Lancet; 26 October 1996:1159 (news item):
Fetal neurons are used in graft therapy because they can diversify
in response to external cues, whereas adult ones generally cannot.
Now adult (rat) neurons have been found and cultured which can do
that. The use of autologous cells for transplants could eliminate
the present requirement for fetal ones, as well as the need for
immunosuppression. Further, if the desired cues for self-repair
could be found, surgical transplantation might become unnecessary.

Zhou F et al; J Neurosci 1996;6966-6974:
To succeed, a fetal transplant must not only survive, it must
replace the neural pathway that has failed in PD. In a rat model,
authors supplemented a transplant to the substantia nigra, with a
track of kainic acid that guided growth toward the corpus striatum,
restoring the lost motor function.

Winkler C et al; J Neurosci 1996;7206-7215:
In a rat model of PD, injection of glial-derived neurotrophic
factor (GDNF) near the substantia nigra gave long-term protection
to the damaged neurons, but they didn't reinnervate the corpus
striatum, nor was striatal dopamine function restored.

Mendez I et al; J Neurosci 1996;7216-7227:
In current practice, fetal substantia nigra cells are implanted,
not in the host substantia nigra but in the corpus striatum,
because the cells can't grow along the desired pathway. In a rat
model, authors found that simultaneous grafts in both the corpus
striatum and the substantia nigra resulted in rapid restoration of
the destroyed pathway and some recovery of function, by growing
toward each other.

Basso M et al; J Neurosci 1996;7308-7317: and
Basso M et al; J Neurosci 1996;7318-7330:
Hyperexcitable reflex blinks are a cardinal sign of PD. In two
related papers, authors describe a series of elegant experiments
(on rats) showing how the loss of dopamine from the substantia
nigra leads to this symptom. In the normal brain, reflex blink is
inhibited by a series of reactions passing through several
centers; from the substantia nigra via the superior colliculus to
the nucleus raphe magnus, and thence to the spinal trigeminal
neurons involved in the reflex blink circuit. This discovery
should lead to better understanding of PD cause and treatment.

Science News, 16 November 1996:316 (news item):
Apoptosis, a common natural mechanism by which organisms get rid
of damaged, aged, or unneeded cells, may become abnormal and
cause a number of disorders, including neurodegenerative diseases
such as ALS, AD, and Huntington's disease. While not mentioned,
PD is an obvious candidate for inclusion.

Polymeropoulos M et al; Science, 15 Nov 1996:1197-1199:
Tedious analysis of DNA from a 592-member family, including 60 with
PD, suggests that a single mutant gene, located in a short region
of chromosome 4, confers susceptibility to the disease. They
haven't found it yet, and in similar cases the final search has
taken from a few months to as long as 8 years. Success should help
to clarify the cause of PD, as well as a valuable diagnostic aid.