Tina,
Thank kyou so much for what you do. It was so good to wake this morning and
have email of three positive findings in Parkiinson's. May I ask where you get
your information. How often do you post? This really seems like a good idea
to tell the membership about. It would almost be like getting a Wall Street
Journal at your front door every morning.
Together we make a difference,
Brenda Tucker, Co-Founder
PLWP, Inc.


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There are 3 messages in this issue.

Topics in this digest:

1. Potassium and Parkinson
From: tina_semal
2. Teva sats clinical trial of PDdrug successful
From: tina_semal
3. insecticide neurotoxicity yields clues to onset of PD
From: tina_semal


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Message: 1
Date: Fri, 28 Mar 2003 05:56:45 -0000
From: tina_semal
Subject: Potassium and Parkinson

CHICAGO (Ivanhoe Newswire) -- Researchers from Northwestern
University report symptoms of Parkinson's disease, a
neurodegenerative disease afflicting over 1 million people in the
United States, may be improved by blocking a specific potassium
channel in a select group of brain cells.


The common symptoms of Parkinson's disease, including resting tremor,
muscle rigidity and slowed movement, are the result of dopamine loss
from the cell. Researchers have found a mechanism that may lessen the
symptoms and slow progression of the disease.


Scientists say a potassium channel unique to the affected brain
regions controls the cellular mechanism responsible for Parkinson's
disease symptoms. The potassium channel, called Kv3.4, is found in a
subset of neurons outside the basal ganglia. The basal ganglia are
structures located deep in the brain that are responsible for normal
movement such as walking. Neurons in another region of the brain
contain high numbers of potassium channels that may account for the
symptoms in Parkinson's disease patients.


Current therapies to surgically destroy these neurons or employ
electrode stimulation to disrupt neuronal activity provide
symptomatic relief. They also cause unwanted side effects such as
uncontrolled movement. "The perfect therapy for Parkinson's disease
would be to prevent neurons from exhibiting the behavior that causes
the symptoms … without altering their 'good' behaviors," says
researcher James Surmeier.


Blocking potassium channels with the Kv3.4 subunit or eliminating the
subunit using gene therapy techniques are two possible therapeutic
options, the authors write. Surmeier says, "Doing so would eliminate
the 'bad' behavior but, importantly, preserve the 'good' behavior …
of these neurons."

Reported March 25, 2003






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Message: 2
Date: Fri, 28 Mar 2003 06:11:19 -0000
From: tina_semal
Subject: Teva sats clinical trial of PDdrug successful

Generic drug giant Teva Pharmaceuticals yesterday released two
positive announcements: the successful completion of the Rasagiline
phase III clinical program in Parkinson's disease; and U.S. approval
for its versions of a drug to reduce glucose in the bloodstream.


Teva and its drug testing partner, H. Lundbeck, yesterday said two
phase III clinical trials of Rasagiline in patients with advanced
Parkinson's disease had been successfully completed. Both trials
achieved statistically significant results, Teva said.


Each study, which compared single daily dosages of Rasagiline to a
placebo as an added treatment to Levodopa, demonstrated significant
reductions in the duration of the "off" time in which patients are
unable to function normally.


Rasagiline is now expected to be submitted for regulatory approval in
North America and Europe during the second half of 2003, Teva said in
its press release.


Rasagiline was developed by Teva based on the original research of
professors Moussa Youdim and John Finberg from the Haifa Technion
School of Medicine in Israel. Youdim heads the Eve Topf
Neurodegenerative Disease Research and Teaching Center at the Faculty
of Medicine at the Technion, where he develops drugs for
neurodegenerative conditions.


Under its agreement with Teva, Lundbeck will market Rasagiline in
Europe and other overseas markets in a joint effort with Teva, while
Teva retains exclusive marketing rights in the rest of the world,
including North America.


Meanwhile, Teva has received tentative U.S. Food and Drug
Administration approval to market Metformin HCl extended-release
tablets, in 50-mg dosage, the Israeli drugmaker announced yesterday.


The brand-name product sells for about $410 million a year, Teva
said. Metformin HCl Extended-Release Tablets are the AB-rated generic
equivalent of Bristol-Myers Squibb's antihyperglycemic drug,
Glucophage XR. The tablets are prescribed together with dietary
changes to lower blood glucose levels in patients with type two
diabetes. Teva did not disclose whether it filed for approval under
Paragraph four, which would grant it a six- month period of marketing
exclusivity.


Analyst Ori Hershkovitz of Leader&Co says Bristol-Myers' patent on
Glucophage expires in October 2003, after which Teva could start
marketing its generic version. If Teva gets exclusivity, Hershkovitz
estimates it could command revenues of $70 million in the first year,
with a 35-percent profit margin - meaning, it could increase Teva's
net by $25 million.


Without exclusivity, Hershkovitz estimates, its sales would increase
by $20-30 million, contributing $3-5 million profits in the first
year.


SOURCE: Ha'aretz Daily, Israel
http://www.haaretzdaily.com/hasen/pages/ShArt.jhtml?itemNo=277418&cont
rassID=2&subContrassID=2&sbSubContrassID=0&listSrc=Y
March 27, 2003 Adar2 23, 5763
By Ilan Mosnaim




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Message: 3
Date: Fri, 28 Mar 2003 07:26:34 -0000
From: tina_semal
Subject: insecticide neurotoxicity yields clues to onset of PD

BLACKSBURG, Va., March 24, 2003 -- A grant from the U.S. Army has led
Virginia Tech researchers to discover that exposure to some
insecticides may cause a cascade of chemical events in the brain that
could lead to Parkinson's Disease.


Jeffrey R. Bloomquist, a neurotoxicologist and associate professor in
the university's Department of Entomology, will describe his findings
as part of the International Award for Research in Agrochemicals, a
symposium honoring Robert M. Hollingworth, at the annual meeting of
the American Chemical Society in New Orleans this week.


"We found low-level exposures set in motion a process with an early
onset that develops slowly and is persistent," Bloomquist said. "More
surprising is that high-level exposures resulted in few immediate
effects that we could observe, but in the longer term there was a
delayed effect."


The Virginia Tech researchers studied the levels of dopamine,
dopamine transporter protein expression, and the levels of a synaptic
protein (alpha-synuclein) in mice exposed to various doses of the
insecticide permethrin. The increase in dopamine uptake indicated the
mouse's system was reacting to a neurochemical insult caused by the
presence of the insecticide. The slow response to high levels of
exposure to pesticides is caused, Bloomquist thinks, by the system
being overloaded and only after a period of a few weeks is it capable
of responding to the insult in the same way as low doses.


In some individuals, dopamine-producing neurons may be challenged by
genetic factors or by previous exposure to other neurotoxins. For
individuals with a genetic predisposition, exposure to permethrin may
trigger chemical events in the brain that result in an increased risk
for damage to the area of the brain that is selectively damaged in
Parkinson's disease.


The loss of motor skills, resulting in symptoms such as muscle
rigidity, shuffling gait, and a rhythmic tremor, has been linked to
the loss of dopamine production in the brain. That loss of dopamine
is the major neurochemical expression of Parkinson's Disease.


"Our studies have documented low-dose effects of permethrin, doses
below one-one thousandth of a lethal dose for a mouse, with effects
on those brain pathways involved in Parkinson's Disease," he said.
"We have found effects consistent with a pre-parkinsonsian condition,
but not yet full-blown parkinsonism."


Bloomquist also found permethrin exposure resulted in an
overproduction of the protein alpha-synuclein at low doses. The
accumulation of the protein is a major component of the formation of
the Lewy bodies, fibrous tangles observed in the brains of patients
with Parkinson's Disease.


The studies so far have concentrated on two-week exposures in mice.
Bloomquist hopes to continue the work, looking at longer-term
exposure. He is also studying the effects of another widely used
pesticide, chlorpyrifos.


Bloomquist and his co-investigator, Dr. Bradley Klein, are supported
by a five year, $584,558 grant from the United States Army Medical
Research and Materiel Command. One purpose of the Neurotoxin Exposure
Treatment Research Program, under which the project was funded, is to
determine if military operational and deployment exposures increase
risks for neurodegenerative disease and, if so, determine means of
protecting troops.


"Permethrin is used worldwide in agriculture and urban settings,"
Bloomquist said. "Widespread human exposure to this compound occurs,
so its effects are not limited to soldiers."


The talk, "Low-dose effects of insecticides to dopaminergic pathways
involved in parkinsonism" (AGRO 31) will be presented at 2 p.m.
Monday, March 24, in the Hampton Inn Convention Center Fulton room.






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