NEW YORK (Reuters Health) Aug 26 - Cell biologists are closing in on
the pathogenic processes that underlie the neurodegeneration
associated with familial Parkinson's disease (PD), according to a
report in the August 27th issue of Science.

In familial PD, mutated alpha-synuclein accumulates within the cell,
lead author Dr. Ana Maria Cuervo, of Albert Einstein College of
Medicine in Bronx, New York, told Reuters Health.

"We wanted to know why this protein accumulates and is not removed,"
she said. "We realized that not only is it not removed, it blocks the
removal of other proteins that are normally degraded within the
lysosome, and that is what eventually kills the neuron."

She explained that the lysosome has two pathways for degrading
damaged proteins, one called "chaperone-mediated autophagy" (CMA), in
which a chaperone-substrate complex binds to the lysosomal membrane
receptor. The substrate proteins, including wild-type alpha-
synuclein, are then translocated into the lumen of the lysosome for
enzymatic degradation.

Her group found that aberrant alpha-synuclein binds more tightly to
the lysosome receptors but is then poorly internalized. As a result,
other damaged cytosolic proteins that are normally taken up by the
lysosome and degraded cannot bind to the lysosomal membrane receptor.

Early in this process, another, less selective pathway that degrades
proteins, called macroautophagy, is activated. In this process, large
regions of cytosol are engulfed and degraded. The researchers found
that, although wild-type alpha-synuclein is not subject to
macroautophagy, the mutated forms are. Under these conditions,
however, macroautophagy cannot maintain normal rates of protein
degradation.

"When synuclein blocks one pathway, the other compensates for a
while, but over time it gets overwhelmed," Dr. Cuervo said. That is
one reason why patients "get worse and worse as they age."

"We hope that we can find a way to stimulate the removal system that
the mutant alpha-synuclein blocks," she concluded. "If we can do so
early enough in the disease process and prevent toxic protein
accumulation, hopefully we will ameliorate symptomatology of the
disease."

Science 2004;305:1292-1295.

Dee Shneiderman <dduck1947@...> wrote:Absolutely! And can we send it to
JAMA, etc.? Of
course, that wouldn't take care of the docs who don't
read journals...

BTW, I was at work when I sent the message, as I often
am and my son was on the computer last night. So no
instant message.

--- Gary Coplin wrote:

> Hi Dee:
> I would like to post this to all the tremor groups.
> Get wider reaction. Is that ok by you? Regards GaryC
>
>
> Hello,
>
> A message has been sent to the
> EssentialTremorForProfessionals2 group from
>
> dduck1947@...
>
> The message summary:
> --------------------
> FROM: dduck1947@...
> DATE: Mon, 30 Aug 2004 15:55:36 -0000
> SUBJECT: Misdiagnosis
>
> There seems to be a common thread through all the
> various
> tremor groups: the prevalence of what I call
> "arrogant
> misdiagnosis". When healthcare professionals
> diagnose a
> tremor as "nervousness", prescribe a tranquizer and
> tell the
> patient goodbye. It's amazing to me how many people
> get that
> response from their docs. Has anyone done any kind
> of study
> on this sort of thing?
>
> It's surprising that many patients were persistent
> enough to
> get a more helpful answer, but it's disturbing to
> think that



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One of the foods richest in antioxidant is carrot (beta-carotene). The trick is
getting enough of the vital substances without eating a mountain of vegetables.
I experiment with juicing recipes. Some are very tasty (can they be good for you
if they taste good?) Carrot is a good base, with beetroot to sweeten, try
broccoli or kale (borecole) for extra minerals and vitamins (and to make it look
like liquidised frog)and of course tomato (makes it look like the frog was
shot). Prepare the veggies as minimally as possible( wash off the dirt leave on
the skins) use raw, add small amounts of fruit such as apple or pear or citrus
juice to vary the flavour.

Important.... use a good juicer which spins the juice out and collects the pulp
in a separate container. Drink the juice fresh if possible or refrigerate in a
closed container for not more than a day.

Avoid foods which are rich in tannic acid (such as rhubarb and spinach) as the
acid locks up the good stuff. Then what to do with all the leftover pulp? You
can't eat it all but you can make some into veggie burgers, or use as a stuffing
for pancakes, or mix with mince to make a sort of bolognese. Regrettably, some
has to end up in the compost heap or maybe chook pen.

They tell me that juice shops are quite the rage in our yuppy city centres these
days. Don't have much call to go there, ain't got a mobile phone.

Oh, and there is one other highly concentrated source of antioxidants. Can't
remember the name but I will look it up and post it, it's made from powdered
seaweed, from Japan, it's bright green and make cool frog coloured milkshakes,
even better with yoghurt and ice cream as a smoothy.





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Can anyone help Barbara. If so email or call me direct. 713-721-3314 Regards
GaryC

AdvancedPDHelp@... wrote:Gary,

My mother is maxed out on PD drugs: I must keep digging as now she has been on
Comtan over a year and man if she becomes tolerant to that, she is in big time
trouble. Requip is too similar to Mirapex to switch her to. She has been taking
Mirapex since 12/98: when the neuro upped her from 1 mg X 3 day to 1.5 mg, it
helped for about a month and she slide back where she had been so I know she has
become tolerant to that.

I am hot on the track of this CEP-1347. I sent the below through twice to the no
borders Parkinson's online group but it never came through. I don't know what I
am doing wrong. If you belong to that group, would you copy and paste the below
in for me and send it and also the post about the great Medicare Card?

Let me know if you can do the above!

Barbara

Hi,

I sent through a Wall Street Journal article on a promising new Parkinson's drug
developed by Cephalon: CEH 1347. I did not see my post come across so maybe that
is because it is copyrighted and even for our group, you can't send it. The drug
is supposed to stop the dopamine producing cells from dying like they do in
Parkinson's do at least it does not get worse or as worse as it would if left on
present day PD drugs.

The clinical trials finished enrollment in March 2004 and it goes through 2006.
Anyone lucky enough to get in it?

Here is the link to the article and the part on this new drug (Phase II/III
Clinical Trial with 800 patients enrolled at 65 sites):

http://online.wsj.com/article/0,,SB108966833980761606,00.html

"...Levodopa replaces dopamine in the brain, it hasn't been proved to stop the
dopamine-producing cells from dying in the first place. That is where Cephalon
hopes CEP-1347 will come in. CEP-1347 has shown signs that it can protect brain
cells and stop them from dying, Dr. Blake said. Animal models of Parkinson's
disease have shown that CEP-1347 protects dopamine-producing neurons in the area
of the brain affected by the disease.
The Parkinson Study Group, a nonprofit group of physicians and other experts in
the disease, began conducting a Phase II/Phase III clinical trial of CEP-1347 in
2002 at 65 centers around North America. H. Lundbeck A/S, a Danish
pharmaceuticals company, is a partner with Cephalon in the study. Lundbeck has
European rights to the drug.

CEP-1347 isn't considered a potential cure for Parkinson's. Instead, it could
prolong a higher quality of life for patients, said Lucy Sargent, spokeswoman
for the Parkinson's Disease Foundation. There is no known cure for Parkinson's.

"If it works, I would say it's a huge breakthrough because it's the first
generation of a drug which is designed to act on dopamine cells, to stop
dopamine cells from killing themselves," said Michael Zigmond, a Parkinson's
researcher at the University of Pittsburgh..."

See also:

Cephalon and Lundbeck Initiate Clinical Program With CEP-1347 for Neurodegener

Clinical Trial: Safety and efficacy study of CEP-1347 in the treatment of Park

One can get this on a compassionate need basis. We have a family friend who is a
doctor who would go to work on trying to get my Mother in on a compassionate
need basis, but I don't know enough about it yet to lobby him on it.

My mother is 87 with advanced Parkinson's. She is in good health except for the
PD. She has had PD since 1987. She takes combined in one pill 3 times a day
Sinemet CR/Comtan and 3 X 1.5 mg Mirapex. She is maxed out on both.

Thanks!

Barbara




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August 5, 2004
E-MOVE reports from the 8th International Congress of Parkinson's
Disease and Movement Disorders, Rome June 14-17, 2004. Page (S) and
poster (P) numbers are from Movement Disorders 2004;19 (suppl 9)

1. Neuropsychiatric symptoms in Parkinson's disease patients
presenting for subthalamic stimulation
V Voon, JA Saint-Cyr, AM Lozano, E Moro, AE Lang
P1202, S410-411

Neuropsychiatric evaluation was conducted in 20 consecutive patients
presenting for DBS surgery. Initial screening excluded patients with
overt dementia or active disabling psychiatric symptoms. Despite
this, current or previous psychiatric disorders were identified in
90% of patients, including depressive disorders (60%), anxiety (55%),
psychotic symptoms (20%), and mania (15%). The Montgomery Asberg
Depression Rating Scale was more effective in identifying patients at
risk than the Beck Depression Inventory.


2. Mood, motivation, and personality in PD patients on subthalamic
stimulation
C Ardouin, P Krack, A Funkiewiez, A Batir, V Fraix, H Klinger, S
Chabardes, AL Benabid, P Pollak
P495, S176-177

Thirty-four patients undergoing STN DBS were prospectively evaluated
for changes in mood, motivation and personality, at baseline, 3
months, and 12 months after surgery. Mean patient age was 55, DBS-
induced motor improvement was 61%, and reduction in levodopa dose was
76%. Results from a battery of neuropsychological tests indicated no
change in cognition, improvement in mood at 3 months but not 12
months, no global change in personality, but a progressive worsening
of apathy. Starkstein apathy scores increased approximately 50% by 12
months. At baseline, no patients scored above a 14 on the Starkstein
scale, while 6 did at 12 months. Apathetic patients were more
depressed and had a greater decrease in levodopa dose compared to
nonapathetic patients. The authors indicate that apathy typically
responded to re-increase in dopaminergic therapy.


3. Suicide risk in patients with Parkinson's disease undergoing
subthalamic stimulation
V Voon, JA Saint-Cyr, AM Lozano, E Moro, K Dujardin, AE Lang
P941, S323-324

To determine the incidence and characteristics of suicide attempts
among patients undergoing STN DBS, the authors surveyed 16 surgical
centers and reviewed the published literature. Eight centers
responded, representing a total of 406 STN DBS patients, of whom 2
had completed suicide and 7 had attempted. Literature review revealed
an additional 4 attempts and 2 completions among 153 patients.
Completed suicides occurred from 3 months to 3 years after surgery;
attempts occurred from 2 months to 5 years after surgery. "Valid
predictive factors, including premorbid risk, have not yet been
identified," according to the authors.


4. Death by suicide after deep brain stimulation
PR Burkhard, FJ Vingerhoets, A Berney, J Bougosslavsky, JG Villemure,
J Ghika
P919, S316

Of 140 patients presenting for deep brain stimulation, 6 died by
suicide between 3 months and 7 years post-surgery. Patients included
4 with PD, 1 with essential tremor, and 1 with post-anoxic dystonia.
None had had recent changes in stimulation parameters. Four had a pre-
surgical history of depression, 2 had attempted suicide previously,
and 2 had planned suicide attempts.

August 21, 2004
Testosterone deficiency and apathy in Parkinson's disease: A pilot
study
RE Ready, J Friedman, J Grace, H Fernandez
J Neurol Neurosurg Psychiatry 2004;75:1323-1326

Forty-nine of 60 consecutive non-demented males with PD agreed to
complete three neurobehavioral scales and a measurement of serum
testosterone. Almost half the sample had low testosterone, defined as
less than 326 ng/dL. Score on the Frontal Systems Behavioral Scale of
apathy correlated significantly and negatively with testosterone. The
association was independent of disease severity. The authors suggest
that testosterone deficiency may exacerbate frontal systems
dysfunction, but note that further study is required to determine if
apathy is responsive to testosterone supplementation.


Sexual well-being in parkinsonian patients after deep brain
stimulation of the subthalamic nucleus
L Castelli, P Perozzo, ML Genesia, E Torre, M Pesare, A Cinquepalmi,
M Lanotte, B Bergamasco, L Lopiano
J Neurol Neurosurg Psychiatry 2004;75:1260-1264

Thirty-one consecutive PD patients (21 male, 10 female) underwent
bilateral STN DBS. At baseline while on medication, and 9-12 months
after surgery while on medication and stimulation, patients completed
a modified version of the Gollombok Rust Inventory of Sexual
Satisfaction, Beck Depression Inventory, and an anxiety scale.

Women showed no change on the GRISS as a result of surgery. In
men, "dissatisfaction" improved significantly (6.2 pre-op, 5.1 post-
op, p<0.05), but not infrequency, non-communication, avoidance, non-
sensuality, premature ejaculation, or impotence. In the subgroup of
males younger than 60, infrequency and avoidance were also
significantly improved. No correlations were found between sexual
satisfaction and depression, anxiety, or levodopa dose change as a
result of surgery.

August 21, 2004
Severe multivalvular heart disease: A new complication of ergot
derivative dopamine agonists
J Horvath, RD Fross, G Kleiner-Fisman, R Lerch, H Stalder, S Liaudat,
WJ Raskoff, KD Flachsbart, H Rakowski, JC Pache, PR Burkhard, AE Lang
Movement Disorders 2004;6:656-662

The authors report four new cases of valvular heart disease secondary
to long-term treatment with ergot-derived dopamine agonists.
--Patient 1, who received cabergoline for 20 months, developed
rapidly worsening shortness of breath due to "severe mitral, moderate
to severe aortic and tricuspid, and mild pulmonary regurgitation as
well as retraction and thickening of the free aspects of these
valves." Immediate discontinuation of cabergoline and replacement
with pramipexole led to slow and not entirely complete regression of
valve defects over the next two years.
--Patient 2, who received pergolide for 2 years, presented with
severe bipedal edema and abdominal swelling due to multivalvular
insufficiency. Pergolide was stopped, but no regression of valvular
damage was seen over 4 years.
--Patient 3, who received pergolide for 4 years, developed severe
tricuspid and mild mitral regurgitation and moderate, asymptomatic
coronary arteriopathy, requiring tricuspid valve replacement surgery.
--Patient 4 developed shortness of breath after 16 months on
pergolide. Her heart condition deteriorated over the next 9 months,
and required multiple valve repair surgery. The patient subsequently
experienced massive global heart failure and progressive valvular
insufficiency. Pergolide was stopped, and her condition improved over
the following 30 months.

The authors conclude, "These cases add to a rapidly growing and
worrying list of similar published reports, suggesting that we may
well be facing a novel, yet unrecognized, complication of this class
of agents…[W]e propose that an assessment of cardiac function be
performed before and in the course of long-term therapy with ergot
derivative dopamine agonists."

Diagnosis and management of pergolide-induced fibrosis
P Agarwal, S Fahn, J Frucht
Movement Disorders 2004;6:699-704

The authors report two cases of valvular disease secondary to
pergolide use, one in a patient with PD, and one in a patient with
restless legs syndrome. They propose that patients be counseled about
the risks, and that non-ergot agonists be used as first-line agents.
In patients who develop leg swelling, the recommend switching to a
non-ergot DA or to levodopa. Additional symptoms, such as dysuria or
dyspnea, are cause for initiation of a workup for serosal fibrosis,
including CT of the chest, abdomen, and pelvis.

August 21, 2004
Systemic exposure to proteasome inhibitors causes a progressive model
of Parkinson's disease
KSP McNaught, DP Perl, AL Brown, CW Olanow
Ann Neurol 2004;56:149-162

Rats systemically exposed to either natural or synthetic proteasome
inhibitors develop key features of Parkinson's disease, including
progressive degeneration of the substantia nigra, movement disorders,
and ubiquitin-positive and alpha synuclein-positive intracytoplasmic
inclusions, according to this study.

Rats received either epoxin or PSI over 2 weeks. Epoxin is a
naturally occurring proteasome inhibitor produced by actinomycete
fungi; PSI is a synthetic inhibitor. Results showed:
--Motor dysfunction appeared beginning 1-2 weeks after the final
injection. Compared to untreated controls and as rated by a blinded
investigator, treated animals had slowed movements, which developed
to severe bradykinesia and rigidity over 4 weeks, as well as tremor.
Apomorphine reversed these motor symptoms.
--Treated animals showed a 40% reduction in striatal dopamine
transporter binding at 17-19 weeks after treatment
--Proteasomal function throughout the brain increased 1 week after
treatment, which remained elevated at 2 weeks in cerebral cortex,
striatum, cerebellum, and spinal cord, but was reduced to
approximately 60% normal in ventral midbrain and lower brainstem,
suggesting these areas "have a relatively poor ability to mount or
maintain compensatory proteolytic mechanisms, which could contribute
to their susceptibility to degenerate."
--Immunohistochemistry showed progressive decline in the number of
cell bodies and processes in the SNc and ventral tegmental area, as
well as increased inflammation in the SNc. Marked cell loss also
occurred in the locus coeruleus, dorsal motor nucleus of the vagus,
and nucleus basilis of Meynert, but not in the cerebellum or examined
regions of the cerebral cortex.
--Intracytoplasmic inclusions staining positive for ubiquitin,
parkin, and alpha-synuclein were seen in SNc, locus coeruleus, and
dorsal motor nucleus.

The authors argue that this model resembles idiopathic PD more
closely than other models, in its progressive nature, distribution of
neurodegeneration, and histopathology. "Based on the findings in this
study, it is interesting to speculate on the possibility that
exposure to proteasome inhibitors could underlie some cases of PD,"
they state, since they are produced by bacteria, fungi, and plants.
Actinomycetes are found globally in soil, and can infect root
vegetables and potatoes. "It is thus noteworthy that potent
proteasome inhibitors are found in rural areas and in well water,
both of which have been shown to be associated with an increased risk
of developing PD in epidemiological studies."

July 9, 2004
MovDis 2004)
E-MOVE reports from the Eight International Congress of Parkinson's
Disease and Movement Disorders, Rome June 14-17, 2004. Page (S) and
poster (P) numbers are from Movement Disorders 2004;19 (suppleme

Torsin-mediated neuroprotection against 6-OHDA toxicity in C. elegans
GA Caldwell, C Songsong, CC Gelwix, KA Caldwell
P227, S91

TorsinA and the roundworm analog TOR2 protect against excitotoxicity,
an effect which is not shared by mutant torsinA, according to this
study.

Caenorhabditis elegans overexpressed human torsinA or TOR2 under the
control of a dopaminergic cell-specific promoter. 6-OHDA-induced cell
death was suppressed by 70% in worms overexpressing normal torsins,
versus only 30% in cells expressing mutant torsins.

Combined with a previous study showing that torsinA inhibits
polyglutamine aggregation, these results suggest that "torsins play a
critical role in protection against intracellular stressors,"
according to the authors. A summary of the previous study is archived
at http://www.mdvu.org/emove/article.asp?ID=645
[end]

July 9, 2004

E-MOVE reports from the Eight International Congress of Parkinson's
Disease and Movement Disorders, Rome June 14-17, 2004. Page (S) and
poster (P) numbers are from Movement Disorders 2004;19 (suppleme

Three studies report on the long-term outcome of deep brain
stimulation of the GPi for dystonia in a total of 38 patients. In
agreement with several previous studies, outcome was better in
patients with primary dystonias, and less effective for those with
secondary dystonias.

1. Long-term efficacy of pallidal DBS for treatment of medically
intractable dystonia
M Tagliati, J Miravite, JL Shils, SB Bressman, R Saunders-Pullman, R
Alterman
P935, S321-322

Bilateral GPi stimulators were implanted in 12 patients with primary
dystonia (7 DYT1-positive) and 3 with secondary dystonia. Secondary
dystonias were due to encephalitis or ischemic encephalopathy. All
primary dystonia patients improved, with an average increase in Burke-
Fahn-Marsden Dystonia Rating Scale score of 69% (range 32-97%), and a
50% decrease in disability. Benefits increased over time, with some
evidence of a plateau at 12-18 months. Patients with secondary
dystonias had an average improvement of 33%, with a 20% decrease in
disability.

2. Long-term outcome of chronic GPi stimulation in dystonia: Sixteen
cases
K Boetzel, B Bereznai, JH Mehrkens, U Steude
P264, S102

Two- to three-year follow-up of 16 patients receiving GPi stimulation
for dystonia indicated excellent improvement in 6 patients and fair
improvement in 5. Patients with secondary dystonia tended to do less
well than those with primary dystonia.

3. Deep brain stimulation for dystonia: Outcome at long term follow-
up (3 years or longer)
TJ Loher, A Kaelin-Lang, S Weber, JM Burgunder, JK Krauss
P186, S78

The authors report on 7 patients receiving GPi DBS for dystonia.
Three of 4 patients with complex cervical dystonia continued to have
sustained benefit for at least 4 years, while one returned to
baseline. Benefit was also seen in 1 patient for 7 years with post-
traumatic hemidystonia, in 1 patient for 3 years with generalized
dystonia, and in 1 patient for 8 years with paroxysmal nonkinesogenic
dystonia.

July 19, 2004

E-MOVE reports from the Eight International Congress of Parkinson's
Disease and Movement Disorders, Rome June 14-17, 2004. Page (S) and
poster (P) numbers are from Movement Disorders 2004;19 (suppleme

1. Effectiveness of zonisamide on parkinsonian tremor: A pilot cross-
over study in comparison with trihexyphenidyl
I Nakanishi, Jkohmoto, H Miwa, T Kondo
P402, S147

Thirteen PD patients with tremor were randomized to 100 mg zonisamide
or 1.5 mg trihexyphenidyl as adjunctive therapy for two weeks,
followed by a two-week washout and crossover to the other treatment
arm. Tremor improved significantly and equivalently in both groups.
Trihexyphenidyl, but not zonisamide, caused improvement in UPDRS
motor subscore after excluding tremor improvement. Zonisamide caused
more drowsiness and nausea, while trihexyphenidyl caused more dry
mouth.


2. Randomized, double-blind study of zonisamide with placebo in
advanced Parkinson's disease
M Muratta, K Hasegawa, I Kanazawa, Japan Zonisamide Study Group
P555, S198

One hundred thirty-six patients were randomized to receive zonisamide
(at 50, 100, or 200 mg per day) or placebo as adjunctive therapy for
8 weeks. Low-dose zonisamide significantly improved UPDRS motor score
vs placebo, while improvement from the other two doses just failed to
reach significance. The authors report that zonisamide improved axial
symptoms (neck rigidity, gait disturbance, postural instability) as
well as limb rigidity.

July 19, 2004

E-MOVE reports from the Eight International Congress of Parkinson's
Disease and Movement Disorders, Rome June 14-17, 2004. Page (S) and
poster (P) numbers are from Movement Disorders 2004;19 (suppleme

1. Enteral levodopa infusion as monotherapy is superior to
conventional oral treatment of advanced Parkinson's disease
D Nyholm, N Dizdar, IN Remahl, R Constantinescu, B Holmberg, R
Jansson, SM Aquilonius, H Askmark

Twenty-four patients with motor complications were randomized to
receive either conventional medical treatment (optimized individually
for each patient) or Duodopa by intraduodenal infusion for three
weeks, followed by crossover to the other treatment. Patients were
videotaped every 30 minutes for 8 hours during treatment, and videos
were rated by blinded investigators for "on" vs. "off" with or
without dyskinesias. UPDRS and two quality-of-life scales were also
administered.

Number of ratings in the on state without significant dyskinesias was
82% for conventional treatment vs. 100% for Duodopa (p<0.01). Finger
tapping, hand movements, rising from a chair, gait, and bradykinesia
were also improved. Median UPDRS was 53 on conventional treatment vs.
35 on Duodopa, and both QoL scores were more improved for Duodopa as
well. Adverse events were similar between treatments.


2. Intraduodenal infusion of a gel suspension of levodopa/carbidopa,
Duodopa®, in advanced Parkinson's disease: Safety, tolerability,
efficacy, dosage
D Nyholm, T Lewander, A Johansson, P LeWitt, C Lundqvist, SM
Aquilonius
P496, S177

Fifty-two patients received Duodopa, primarily as monotherapy, for
one year or more (average 4.1 years). Device complications occurred
at a rate of 1.8 times per patient per year. These were primarily
tube occlusions and dislocations. Side effect frequency and severity
was similar to oral levodopa. Eighty-four percent of patients
had "improved" or "much improved" motor fluctuations, and 50% had
improved or much improved dyskinesias. No patients reported worsening
as a result of therapy.

With the help of a fourth grant, a group at Chicago's Northwestern
University led by Dr. Mohan Sapru will use a rat model of
parkinsonism to test the efficacy of a gene therapy technique in
preventing the production of both natural and mutant forms of human
alpha-synuclein. Derangements in alpha-synuclein occur in some rare
forms of Parkinson's disease. If such prevention -- known
as "muting" -- is found to be successful, the experiment could
possibly become the basis for an anti-Parkinson's therapy

In a third project, a team led by Dr. Daniel Lévesque at Laval
University, Ste-Foy, Canada, will explore the relationship among the
brain's dopamine system, levodopa-induced dyskinesias, and a family
of proteins called "retinoid receptors." Using monkeys with
experimental Parkinsonism, researchers will test whether compounds
that act on retinoid receptors can reduce twisting and writhing
movements caused by levodopa. If effective, this approach may offer
hope for patients who

In another funded project, Dr. Philip Thomas from the University of
Texas, in Dallas, will use transgenic mice (that is, animals that are
genetically modified by adding an extra gene or deleting a gene) to
explore the process of brain cell death in PD. Researchers will use
this technique to find out more about the metabolism and chemical
properties of alpha-synuclein -- a protein that has been implicated
in some cases of Parkinson's. Knowledge of the process in transgenic
mice could suggest preventative forms of therapy for human PD patients

One of the successful proposals, from Dr. Gil Levkowitz and
colleagues at the Weizmann Institute of Science in Rehovot, Israel,
will study dopamine cells in zebrafish. The aim of the study is to
identify the genetic signals that control the development and
survival of embryonic dopamine cells. This work has implications for
future cell replacement treatments in PD.

Laurie Barclay, MD
Medscape Medical News 2004. © 2004 Medscape


Aug. 13, 2004 — Repetitive transcranial magnetic stimulation (rTMS)
is as effective as fluoxetine for the treatment of depression in
patients with Parkinson's disease, according to the results of a
placebo-controlled trial published in the August issue of the Journal
of Neurology, Neurosurgery and Psychiatry.


"[rTMS] is a non-invasive, well tolerated technique for stimulating
the brain," write F. Fregni, from Beth Israel Deaconess Medical
Center and Harvard Medical School in Boston, Massachusetts, and
colleagues. "rTMS may have an antidepressant effect by the enhancing
the serotoninergic system and increasing monoamine levels.
Furthermore, previous studies showed that rTMS applied to the
prefrontal area led to an improvement in motor function in patients
with Parkinson's disease."

In this double-blind study, 42 patients with Parkinson's disease and
depression received active rTMS (15 Hz for 10 days) and oral placebo;
or sham rTMS using a specially designed sham coil and 20 mg of
fluoxetine per day.

After two weeks of treatment, the Hamilton Rating Scale for
Depression and Beck Depression Inventory were similarly improved in
both groups (38% and 32% for active rTMS; 41% and 33% for fluoxetine,
respectively). At week 8, activities of daily living were improved
only in the active rTMS group, and there was a nonsignificant trend
for worse scores in the motor function section of the Unified
Parkinson's Disease Rating Scale in the fluoxetine group. Although
scores on the Mini-Mental State Examination improved with both
treatments, it improved faster in the active rTMS group. There were
fewer adverse effects with active rTMS than with fluoxetine.


Study limitations include lack of a placebo group due to ethical
constraints and possible methodological problems involving the sham
coil.

"rTMS has the same antidepressant efficacy as fluoxetine and may have
the additional advantage of some motor improvement and earlier
cognitive improvement, with fewer adverse effects," the authors
write. "The drawbacks of each treatment have to be considered, as
rTMS involves higher costs (TMS equipment, trained people to apply)
and inconveniences (dislocation to treatment centre), and fluoxetine
has some adverse effects, being associated with worsening of the
motor symptoms of Parkinson's disease, although this is still
controversial."

The authors note that more information is needed concerning optimal
stimulation parameters, including number of stimuli per session,
number of sessions per week, and optimum length of a course of
stimulation. They recommend testing a longer period of rTMS treatment
in a similar population.

The authors report no potential financial conflicts of interest.

J Neurol Neurosurg Psychiatry. 2004;75:1171-1174

Reviewed by Gary D. Vogin, MD

NEW YORK (Reuters Health) Aug 26 - Cell biologists are closing in on
the pathogenic processes that underlie the neurodegeneration
associated with familial Parkinson's disease (PD), according to a
report in the August 27th issue of Science.

In familial PD, mutated alpha-synuclein accumulates within the cell,
lead author Dr. Ana Maria Cuervo, of Albert Einstein College of
Medicine in Bronx, New York, told Reuters Health.

"We wanted to know why this protein accumulates and is not removed,"
she said. "We realized that not only is it not removed, it blocks the
removal of other proteins that are normally degraded within the
lysosome, and that is what eventually kills the neuron."

She explained that the lysosome has two pathways for degrading
damaged proteins, one called "chaperone-mediated autophagy" (CMA), in
which a chaperone-substrate complex binds to the lysosomal membrane
receptor. The substrate proteins, including wild-type alpha-
synuclein, are then translocated into the lumen of the lysosome for
enzymatic degradation.

Her group found that aberrant alpha-synuclein binds more tightly to
the lysosome receptors but is then poorly internalized. As a result,
other damaged cytosolic proteins that are normally taken up by the
lysosome and degraded cannot bind to the lysosomal membrane receptor.

Early in this process, another, less selective pathway that degrades
proteins, called macroautophagy, is activated. In this process, large
regions of cytosol are engulfed and degraded. The researchers found
that, although wild-type alpha-synuclein is not subject to
macroautophagy, the mutated forms are. Under these conditions,
however, macroautophagy cannot maintain normal rates of protein
degradation.

"When synuclein blocks one pathway, the other compensates for a
while, but over time it gets overwhelmed," Dr. Cuervo said. That is
one reason why patients "get worse and worse as they age."

"We hope that we can find a way to stimulate the removal system that
the mutant alpha-synuclein blocks," she concluded. "If we can do so
early enough in the disease process and prevent toxic protein
accumulation, hopefully we will ameliorate symptomatology of the
disease."

Science 2004;305:1292-1295.

LONDON (Reuters Health) Aug 12 - In early Parkinson's disease,
selegiline and other monoamine oxidase type B inhibitors are cheap
and effective treatments that reduce disability and the need for
levodopa, according to study findings reported in the August 14th
issue of the British Medical Journal. The study also shows that the
drugs are not associated with increased mortality, as had been
reported in an earlier study.

To further examine the risks and benefits of these drugs, University
of Birmingham researcher Professor Keith Wheatley and colleagues
conducted a meta-analysis of 17 randomized, controlled trials
involving a total of 3525 patients with early Parkinson's disease.

Their analysis showed no significant differences in mortality between
patients on monoamine oxidase type B inhibitors and control patients
(confidence interval 0.94-1.34).

The researchers did find that patients given the drugs had better
total scores, motor scores and activities of daily living scores on
the unified Parkinson's disease rating scale at 3 months, compared to
placebo subjects. Treated patients were also less likely to need
extra levodopa or to develop motor fluctuations.

"Our review provides no evidence that mortality is increased by
selegiline and suggests that this inexpensive drug could be one of
the most clinically effective and cost-effective treatments available
for early Parkinson's disease," the authors write. The evidence for
other drugs in the class is more limited, they add.

The report of increased mortality, which came from a UK study in
1995, was probably a chance finding, they suggest--"although the
confidence interval reported in this review is compatible with a
small increase, or indeed decrease, in mortality."

Given this, further large-scale trials comparing monoamine oxidase
type B inhibitors with other active agents are urgently needed, the
UK investigators conclude. These should include patient-rated quality
of life measures.

BMJ 2004;329.

Three subjects for this week SNC:

Should we destroy babies to make us all well?

Are the obscene profits of the drug companies ok by you?

And will a diet of red meat and coke cola help your constipation issues?



Please buckle up and come on down for this important dialogue.



Regards, GaryC


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Hello, Hope everyone is doing ok.

I would like to know if anyone uses a particular prescription
discount drug card to purchase your medicines?

These days without any medical insurance or prescription drug
coverage, medicines are very expensive, especially for those of us
that are living on "fixed incomes".

Here In our state (mississippi) Medicaid is cutting off 65 thousand
of us from the Medicaid drug coverage. I am one of those that will
be affected as of 15 September 2004.I used to pay $1.00 (one dollar)
per perscription per month and Medicaid would pay the rest. I was
just re-instated to receive medicaid benefits in March 2004, but I
will probably loose this coverage since we are over the limit for a
family of two.

I am on Medicare but now that Jason has been approved for
disability, we are about 100.00 over the limit for our household of
two, so I will not be elliagable for the $600.00 a year Medicare
will give each person to help with their medicine costs. Yes that
bites and it is not fair, but theres nothing I can do about it.

Now that I am faced with having to pay full price on all of my
medicines (not including Jasons medicines), I have to find a good Rx
Drug card that carries the different types of medicines I am taking
and will be taking when I have my second neck surgery in the
future. I have spent hours on the medicare page looking at the
different medicare approved companies that offer these drug discount
cards. There are many different companies and a lot of them do not
carry all of the meds I am taking. I have found 4 companies that
carry all of the meds I am taking. some of these cards charge a
yearly fee to have the card. One does not charge a fee, but the meds
are more expensive.

I have found one company that is based out of Ohio. It is called
Script Solutions Choice D7707. I have found that their annual or
yearly fee for having this card is $14.95 The other two companies
charge $20.00 and $30.00 a year.

Has anyone else tryed useing Script Solutions choice before?

Does anyone have any good Rx drug discount card that carries a wide
variety of generic and non generic medicines that is a good reliable
company with low or no yearly fees you would like to share with us?

Please post your suggestions or comments in reference to useing Rx
discount drug cards. I think we all can really benefit from those
of you that are useing these cards.

Remember some cards are for senior citizens and some cards are for
people with disibilities and for people of all ages (we are not in
the senior citizen category yet).


HUGS
Debbie

IMHO, there is no reason for you to choose between eating and getting your meds.
If I am wrong, please straighten me out. Regards GaryC

sylvia terry <samzco34@...> wrote:First of all, you must meet income
guidelines, then you can just file the pasperwork goto www.needymeds.com, All
pharmecutical companies have plans to supply medications to the truly needy. If
your city or town has a free clinic, they also can provide informationm on thes
programs. I also recommend ScrptSave as a discount program. They don't charge
for the card. Check with your local pharmacy to see if they participate.
----- Original Message -----
From: Gary Coplin

Would you care to share the phone numbers to the free drug programs with us. May
I post that info into all 15 tremor groups? I know everyone would appriciate a
heads up for a source to free drugs. Regards GaryC

sylvia terry <samzco34@...> wrote:
Now that I have founf the free drug programs, it does not concern me. Drug
companies realize that not everyone can afford the prices they must charge in
order to finance R & D





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Tonight on CBS 60 min, they say the drug companies in the USA are making too
much profit on their products. Is this a subject that concerns you?


Prescriptions And Profit
Aug. 22, 2004


There are two recent developments in the continuing battle over the price of
prescription drugs: Illinois announced it will help its residents buy drugs from
Canada, and Vermont announced it's going to sue the Food and Drug Administration
(FDA) for the right of its citizens to buy drugs in Canada.

It may come as no surprise that the pharmaceutical industry is the most
profitable business in the country. American drug prices are the highest in the
world, so more than a million Americans now buy their medications in Canada.

Mayors and governors from North Dakota to Alabama are helping their citizens get
Canadian drugs by mail. Such purchases are technically illegal, but so far, the
federal government has declined to prosecute.

But the FDA has raised the specter of safety and has been waging a campaign
against Canadian importation.
---------------------------------
When correspondent Morley Safer first reported on this story last March, the FDA
commissioner was Dr. Mark McClellan.

The FDA has issued a serious warning that using Canadian drugs could be unsafe.
But how unsafe are these drugs? And how common are the problems for drugs that
people are buying in Canada?

“Well, that's the problem. We don’t know,” says Dr. McClellan. “Because we don't
have the authority to tell where these drugs have come from, or to monitor
closely how they're getting into the United States. And to make sure that the
drugs that come in are safe, it could be a widespread problem.”

“That's a lot of hooey. There is no reason that buying drugs in Canada is any
less safe than buying them in the United States,” says Dr. Marcia Angell, who
was executive editor of The New England Journal of Medicine for 11 years. She’s
just published a book called "The Truth About the Drug Companies."

“The people who say you have to worry about the safety of drugs from Canada are
imagining the way it was in the old days. That there's a moat around the United
States that drugs that are sold in the United States are made by only American
companies. And made in this country,” says Angell.

“It's not that way any more. Pfizer, for example, has 60 manufacturing sites in
32 countries. So the drugs are made all over the world. They're sold all over
the world.”

Most of Pfizer's anti-cholesterol drug Lipitor is made in Ireland. And it's the
same Lipitor that's sold in both U.S. and Canadian pharmacies. Other familiar
drugs like Zocor, Nexium, and Prevacid are the same as the ones sold in Canada.
They're much cheaper there because the drug companies must abide by Canadian
government price controls.

Do the drug companies still make a profit?

“Oh, sure. Why else would they sell them in Canada? They're not charities. Of
course they make a profit,” says Angell.
---------------------------------
The United States is the only industrialized country without some form of
control on the prices of drugs. The U.S. also accounts for more than half of the
industry's profits.

In order to keep those profits up, the drug companies have joined the FDA in
trying to shut down imports from Canada, and Canadian pharmacies are feeling the
pressure. In one pharmacy just over the border, Americans account for 30 percent
of its business. They were nervous about having 60 Minutes mention the actual
name of the pharmacy.

“We've had several letters from the big multi-nationals, certainly threatening
to cut off the drug supply very explicitly if you are supplying medications to
U.S. patients,” says the pharmacist.

This pharmacy supplies drugs to municipal workers in the city of Springfield,
Mass., through a program set up by former Springfield Mayor Michael Albano.

“Major pharmaceutical companies are saying, ‘We're going to limit our supply.’
What does that tell you? It tells you that they want to keep the artificially
high prices in America,” says Albano. “How brazen is that? It just boggles my
mind that they can get away with this.”

When Albano was faced with a budget crunch last year, he had to lay off
firefighters, police officers, and teachers. By arranging for 3,000 city
employees, retirees, and family members to buy Canadian drugs, the city can make
substantial savings.

“We can save anywhere from $4 to $9 million on an annual basis if I get
everybody enrolled and everybody goes to Canada. And that's a huge amount of
money right now,” says Albano. “If I can save $9 million for my city and put it
back, redirect it back into police and fire and to public education, it'll make
a world of difference. So it's a huge savings.”

Does he do it himself?

“I do it for my family's use. My son Mikey is diabetic. And we get his insulin
and related products for diabetes from Canada,” says Albano.

The FDA says importing drugs from Canada or buying drugs from Canada is unsafe.
Does Albano agree?

“The American public is not buying that safety issue. The fact is that it is
getting insulting for the FDA to say that. I view myself as a responsible
father,” says Albano. “And I could tell you that I would not let my son inject
insulin into his body three times a day if I thought there was a safety factor
here.”

Mayor Albano concedes that casually buying drugs on the Internet could be risky,
but says it was quite simple for him to check out his Canadian supplier, and
challenges the FDA to do the same thing.

“The FDA has become a pawn of the pharmaceutical industry, that they are
protecting those high profit margins. If the FDA wanted to put a plan together
similar to what we're doing in Springfield, that would be good for all
Americans, they can do it in 15 minutes, relative to safety,” says Albano.

“We get all our medications from certified, regulated pharmacies in Canada. It's
no different than going to your neighborhood pharmacy. And it's the exact same
medication.”

So why can’t the FDA insure the safety of products from Canadian pharmaceutical
exporters – and make sure that it’s as safe as any product leaving an American
company?

“Under current law, we don't have the authority to insure the safety of foreign
produced, foreign distributed drugs,” says McClellan.
---------------------------------
So what would motivate the FDA, which is not in the business of profiting from
drugs, to put out an alarm about Canadian drugs?

“The influence of the pharmaceutical industry on our government is huge. And the
FDA is a part of the executive branch of the government. And this is just the
propaganda that's put out to do the drug company's bidding, to make sure that
Americans don't have access to cheaper drugs,” says Angell.

“Because then they'll come to know what's going on. And what's going on is that
these drugs, while they're made by global companies all over the world, are sold
in this country for about double what they're sold for everywhere else. And that
they wanna keep secret.”

“Our interest is in protecting and promoting the health of the public,” says
McClellan.

Of course, the whole controversy over Canadian drugs would be moot if Republican
Congressman Dan Burton of Indiana had his way. During the recent debate over the
Medicare bill, he co-sponsored a provision that would have legalized bringing in
Canadian drugs with safeguards.

But Burton says he ran into two brick walls: the drug industry and the U.S.
government: “This is a perfect example, in my opinion, of where a special
interest, the pharmaceutical industry, has been able to manipulate the Congress
and the government of the United States to their benefit, and to the detriment
of the American taxpayer and the American people.”

Since 1999, the drug industry has given more than 45 million dollars in
political contributions, and it's spent hundreds of millions more on an army of
more than 600 lobbyists to work its will on Capitol Hill.

Congressman Burton says the new Medicare act makes it clear the industry got its
money's worth. He says billions of dollars are in it for drug companies in this
new Medicare Prescription Drug Benefit.

“In the new Medicare Act, the federal government is specifically prohibited from
negotiating prices with drug companies,” says Safer.

“That is unconscionable. The government of the United States negotiates prices
in the Defense Department, in every area of government,” says Burton. “And here
we are, going to spend billions and billions and billions and probably trillions
of dollars on pharmaceutical products. And we cannot negotiate the prices with
the pharmaceutical industry. That's just not right.”
---------------------------------
In December, surrounded by members of Congress, President Bush signed the new
Medicare act. Since 1999, these legislators have accepted more than a million
and a half dollars in campaign contributions from people working in the
pharmaceutical industry. President Bush alone has received more than half a
million dollars.

But now, the new Medicare prescription drug benefit is being billed as a big
victory for America’s seniors.

“You gotta be kidding me,” says Burton. “Seniors, when they find out what's in
that bill, are gonna be very angry. The problem is, they're not gonna find out
about it until after this next election.”

The plan doesn’t start until 2006. Does Burton think that will reduce the
attraction of importing drugs from Canada?

“Oh, I don't think so,” says Burton. “Because even when you talk about the
discount cards and the other things, you're gonna find that seniors are gonna be
paying, in many cases, more than they are paying for Canadian imports right
now.”

60 Minutes contacted Bristol-Myers Squibb, Pfizer, Merck, Wyeth, Glaxo
SmithKline, and Eli Lilly. None of them would agree to be interviewed. Safer
asked Dr. Angell about the case the industry invariably makes to justify drug
prices.

“This is a kind of blackmail. What they're saying is, ‘Don't mess with us. Let
us charge whatever we want for our drugs. Otherwise, you won't get the
miracles,’” says Angell. “And the truth is that they spend less in R&D then they
make in profits. And far less then they spend on marketing. And they don't make
that many miracles in the first place … The problem is, is that we're no longer
getting our money's worth.”

Adds Albano: “The pharmaceutical industry is gouging the American consumer.
There's no other conclusion one can draw. And why should we, in this country,
have to pay the highest prices in the world? Why isn't the president doing
something? Why isn't Congress doing something? Someone has to wage this battle.
So we're prepared to do it here.”
---------------------------------
And so are others. Since 60 Minutes first broadcast this story, at least five
more cities and two states are helping people buy drugs from Canada.

As for Dr. Mark McClellan, he's now head of Medicare and Medicaid.



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Unfortunately, I have found most ask the doc's sites not very active or working
very well. I wonder if some one charging $150 per hour to give med opinions
would want to come to a forum and do it for free. If anyone has a link, site,
forum what ever where some very knowledgeable doctors, nurses or practitioners
who are making > $100K per year will dispense free knowledge. Regards GaryC


Cousins family <cousins@...> wrote:Hi Stuart,
One thread you might try is to visit the National parkinsons foundation website
in the USA wher they have an "ask the doctor" ferture. YOu can relay the more
extreme symptoms and ask if they are typical of PD or something else. I hope you
get the answer. Knowing is the first step to coping.
regards
Alf
Adelaide



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Yahoo! Groups Links








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8/14/04 -

It's about time for an update, isn't it?  Between increased needs for Judd's
care, school and technology challenges we have been unable to stay in close
communication with the Parkinson's community and do apologize for a lack of
contact. Correspondence with each of you has been missed and we foresee doing
better in the months ahead.  The really important event - the opening of a
clinic to provide Cord Cell Therapy has not yet occurred - in fact, since Texas
A&M did not take the opportunity for the past 6 months to provide a full faculty
position for Dr. Garg (an essential item before most types of funding can be
secured), he has returned to Pennsylvania to work in the neurosurgical practice
which provided the funds for his research and development to begin with.  So it
may take a longer time schedule than we had hoped for ( it still would only
require six months to clinical trial availability if a private investor was
procured), but things are still developing in a positive direction on our home
care front for getting ready to participate in the pioneering dopamine
replacement implantation when it does become available.



Judd's condition is now reflecting the "unmasked" symptoms 18+ years of
Parkinsons can put on a person.  For the past few months we have successfully
discontinued the Sinimet completely, only re-introducing 5mg of Aricept a day
and still maintaining the stomach acid reducer (Ranitidine) and supplements of
magnesium citrate, essential fatty acids and multi-vitamins. Through this
non-reliance on medications, we have learned first hand a few facts we would
like to share:

   a.. There can be an active, healthy life with Parkinsons - just in different
settings than it used to be.
   b.. The medications that are designed to mask the symptoms don't always
relieve the symptoms, especially if they create others that are actually
detrimental to survival (such as infections or other organ malfunctions that can
lead to hospitalization - a hazard within itself)
   c.. Acceptance of the fact that Parkinsons "marches on", despite whatever the
medical community has to offer, coupled with a true, straightforward awareness
of what can be expected, can lead to much more effective and life-sustaining
ways to cope with the life changes PD presents.
   d..  Fear, denial, misunderstandings and misinformation all can lead to
complications that can shorten a person's life unnecessarily.


These facts have been realized only after years of tough experiences and may not
be known to us yet, except for the specific hope and understanding dopamine
replacement research (such as Dr. Garg has accomplished WITH PEOPLE) has
provided.  It seems that perhaps other research advancements in other areas
(Spheramine, DBS, etc) offer people the hope needed to realize these facts and
make improvements on their lives also.  Have you noticed the article at
http://tinyurl.com/6aps3?  Dr. Okun was Judd's doctor at the time of our
Clozapine trial last August - sure wish he had applied the same reasoning about
his medication plan as he shows to be realizing about the Deep Brain Stimulation
procedure.we all have tended to put our trust in doctors for knowing what we do
need.and research (and our experience) is showing that is no longer the safest
approach to take - unless there is a track record of a good relationship with
good decision making skills evident.



We hope to discuss in more detail what these facts look like day-to-day on the
QC website as well as directly among the many people seeking answers to dealing
with the horrendous effects of neurodegenerative conditions of all kinds.



In this update, we also want to issue a challenge to all who desire to be a part
of finding reachable answers to correct (not just mask) symptoms for themselves
or loved ones. We are asking for help in the direct networking system that can
be effective to reach the individual backer needed to provide the neurosurgical
clinic needed.  We want people who are motivated to start making phone calls,
sending letters and investigating contact sources to find the individual private
funding to make such a clinic available in the short run. There is no reason Dr.
Garg's previously verified research application (though yet unpublished) should
not be made available, published, and verified in the United States along with
all the other many research endeavors going on.  FDA approval is not an issue.  
It may take the work of those in need the most to make a clinic happen - but in
the interest of our own lives, those of our loved ones, and medical advancement
it should be done NOW.  Dr. Garg, as always, is available for direct contact at
drdgarg@....



We can be contacted at the QC hotline (352) 490-6135 anytime night or day to
start pulling ideas together to find that essential support. (If you are
receiving this as a direct mailing please be sure to visit our revised and
informative website at www.questforcure.net).



  May God bless each individual's effort to alleviate the pain neurodegenerative
conditions present.S.F. and Callie Marie Judd






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Special SNC Tue AUG 17 @ special time, 8:30 pm CST USA. This is to allow the
folks on the left coast and in Australia to more easily log in.  Len Casavant
will do a simulcast with Moundsmoo = Marlene Markhardt and Chasmob = Charles
Black and or Rdoppler = Rick Doppler about Marlene’s adventure with DBS and
depression. 3% of folks with DBS installed get depression, but we are not so
sure that doctors properly diagnose this issue. Marlene never lost her sense of
awareness and common sense. She knew that the docs were not helping her
correctly but she was forced into a phyc ward and almost could not get out. She
will describe her adventure on chy radio program. We hope this will help other
folks who might get into a situation like this. Please be sure to test your
yahoo IM with us if you are new to SNC.  We will use the conference window. You
will need to have us set up in your IM friends list.    If you would like to
participate, please add gary_coplin or roadrunner1st1961 or one of
  the above folks to your yahoo IM friend’s list and watch for us to be on line
on this special night and time. SNC is a protected controlled chat. We suggest
folks attend who want to contribute and not do a lot of chit chat. I think that
is more productive. Please turn off invisible setting during this time so we can
easily invite U into the conference window. Regards GaryC



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