CURRENT SCIENCE REVIEWS   by Joe Bruman   October  1996   p.1 of 3

Bower H; BMJ 17 Aug 1996:381:
UK health authorities want control of alternative medicines adver-
tised on the Internet like that in effect for street advertising.
While these drugs may have genuine medical value they haven't run
the rigorous gantlet of approval, either as prescription or over-
counter drugs. Therefore they are marketed as dietary supplements,
often by mail order, with claims carefully phrased to avoid
government intervention. Products mentioned include DHEA,
Melatonin, Shark cartilage, Pycnogenol.

Knowlton B et al; Science, 6 Sep 1996:1399-1402:
PD patients and amnesiacs were given a gambling-type test where
they had to predict an outcome based on cues whose appearance was
random in order and variable in accuracy. The amnesiacs learned
to predict well, but forgot the training session; PD patients
recalled the training well but could not learn to predict. They
were at a fairly late stage (H-Y average 2.8) and under various
regimes of dopamine-enhancement therapy.

Robbins T; Science, 6 Sep 1996: 1263-1264:
PD impairs memory (as you always suspected). Declarative memory
(of events, facts, and images) resides in the temporal lobes and
is unaffected. Non-declarative memory, (the ability to learn
habits, skills, or judgement through repeated experience or
practice) seems to reside in the caudate and putamen, and is
impaired in PD patients. The effect of compensation for the loss
or of dopamine-enhancement therapy is still uncertain.

Science News, 7 Sep 1996:150 (news item):
Conventional wisdom, that memory loss in aging is due to death of
cells in the hippocampus (a formation within a ventricle of the
temporal lobe) is challenged by more careful counting technique
in rat brains. Aged rats, with or without memory impairment, had
the same number of hippocampal cells as young ones, suggesting
that the cells don't die, but only quit functioning. If that is
true, there is hope that various brain diseases may be easier to
treat. (In another development, workers found on autopsy that the
hippocampus of PD patients was on average 25% smaller than normal.
Whether that was a precursor to or a consequence of PD was not
determined.)

Mercer B; Arch Neur 1996;53:881-884:
PROPATH, a health management program for PD patients, consists of
a videocassette, a series of pamphlets, and regularly scheduled
questionnaires. It helped patients feel better but didn't change
their degree of satisfaction with treatment, and most physicians
didn't find it helpful.

Defebvre L et al; Arch Neur 1996;53:898-903:
Either thalamotomy or electrical stimulation of the ventral
intermediate nucleus is effective treatment for parkinsonian
tremor. Inspired by a single report of reduced gait disturbance
in a PD patient with the DBS implant, authors studied 7 others
but found no corresponding improvement.





CURRENT SCIENCE REVIEWS    By Joe Bruman   October 1996  p.2 of 3

Hutchinson M, Fazzini E; J Neur N'surg Psych 1996;61:324-325:
Although anticholinergics were accepted treatment for PD before
the widespread use of levodopa, authors tried tacrine, a drug
with the opposite effect, in 7 late-stage patients who also had
developed dementia. The dementia (hallucinations) was reduced,
and, unexpectedly, gait and rigidity symptoms improved as well.

Science News, 21 Sep 1996:180 (news item):
Failure of the mammal CNS to repair injury is due to suppression of
macrophages, immune cells that are essential to healing elsewhere
in the body. Workers speculate that the suppression is an evolved
defense against the macrophages, which themselves can cause
damage to the complex mammalian CNS. By first exposing the immune
cells to a rat's peripheral nerve tissue, and then placing them on
its severed optic nerve, researchers were able to stimulate some
regeneration, suggesting an eventual breakthrough in treatment of
various neurologic disorders.

Lancet, 21 Sep 1996:814 (editorial):
Review of diverse approaches to spinal cord repair at several
laboratories. They aim at persuading replacement neurons not only
to grow, but also to connect with the proper target cell, implying
a possible clue to future PD therapy.

Baron M et al; Ann Neur 1996;40:355-366:
Fifteen pallidotomy recipients were followed for a year, showing
improvement in all the cardinal PD motor signs as well as reduced
drug-induced motor fluctuations and dyskinesias. As currently
applied, pallidotomy is highly effective treatment for advanced
Parkinson's disease. (Useful reference for insurance claimants)

Olanow W; Ann Neur 1996;40:341-343:
Reviews history of pallidotomy since its discovery in 1952 and its
recent resurgence. Discusses remaining questions such as: who are
the best candidates; how do the benefits compare with those of
fetal transplants or deep-brain stimulation; how does pallidotomy
work. It is paradoxical that dyskinesia and parkinsonian motor
symptoms, due to opposing conditions in the subthalamic nucleus,
are improved simultaneously by pallidotomy.

Ann Neur 1996;40:344-345:
Review of transcranial magnetic stimulation as a clinical and
research tool. Brief mention of therapeutic use to reduce
bradykinesia in PD.

Yuen E, Mobley W; Ann Neur 1996;40:346:
There are many neurotrophic factors, having different effects on
neural development. One hypothesis is that developing neurons
compete for a limited supply of NTF emitted by target cells, and
the ones that fail to connect die. There is hope that some NTFs
may have a therapeutic effect, although there is no example of
disease caused by a lack of NTF.

Armon C et al; Neur 1996;47:626-635:
Valproate, useful against epilepsy, may cause reversible parkin-
sonism and cognitive impairment.



CURRENT SCIENCE REVIEWS    By Joe Bruman   October 1996   p.3 of 3

Wilson J et al; Neur 1996;47:718-726:
Postmortem studies compared diagnostic value of 5 different
neurochemical markers of striatal dopamine nerve terminals, against
data from FD PET scans in living PD patients, in the quest for
better diagnostic tools.

Thal L et al; Neur 1996;47:705-711:
Acetyl-L-Carnitine, which I believe has been mentioned as a diet
supplement, seems to improve neurotrophin levels, reduce cognitive
deficits, and exert a neuroprotective effect, in rats. A double-
blind trial in human Alzheimer's patients showed corresponding
benefits in early-onset subjects (under 65), but worsened
conditions in older ones.

Hellenbrand W et al; Neur 1996;47:636-643:
Questionnaires about food habits answered by 342 German PD patients
and 342 controls showed negative correlation for raw vegetables,
potatos, beer, spirits, coffee, but not wine or tea; no significant
difference for fruits or cooked vegetables, and positive correlation
for sweets, snacks, and raw meat.

Hellenbrand W et al; Neur 1996;47:644-650:
In the same study, responses about specific nutrients showed inverse
correlation for beta-carotene, ascorbic acid and niacin, no
difference for tocopherol, protein, or fat, and positive correlation
for monosaccharide and polysaccharide intake.

Waterhouse A et al: Lancet, 21 Sep 1996:834:
Chocolate and red wine are potent antioxidants, and when combined
may be both pleasant and good for you. Authors happen to be in the
Department of Viticulture and Enology, UC Davis, California.

Cheers,
Joe


J. R. Bruman (818) 789-3694
3527 Cody Road
Sherman Oaks CA 91403