Hi! Charles:
I am glad to know that you are working on PD. Obviously it needs more
PhDs than clinicians working in such problems. Not that I am against
Clinicians. (Both of my sons are clinitians, one is a GP and the other is
a Radiation Oncologist.) But, they have so much to do and most often they
don't have even enough time to talk to their patients. I think personally,
especially in the case of PD and related diseases, there must be a good
discussion between the doctor and the patient about the pros and cons of the
disease, effect of medication etc., which I find is currently lacking. It
took me sometime to get to know the disease and its cruel effects on life.
Enough about complaints.
Let us be constructive.
I have been doing some reading on my own. I am working on two concepts.
But, I shall discuss about one of them now:
PHOSPHATIDYL SERINE AND PARKINSON'S DISEASE:
Recent studies have revealed that two drugs Mirapex and Requip have
a beneficial effect in that they both seem to significantly retard the
progression of PD. However, both have some undesirable side effects.
I have some thoughts on the possible etiology of Parkinson's
Disease and a novel approach to find some immediate relief (not cure) for
Parkinsons disease patients.
While I was searching the published literature, I came across the
beneficial effects of a biochemical called phosphatidylserine (PS) on the
nervous system in geneal. In a Tv program, a scientist was telling that PS
reversees the age of the nervous system by about 5-10 years. (However, i
could not find any reference on this in the PUB-MED.) PS, a phospholipid
enriched in the brain, has been validated through double-blind studies for
improving memory, learning, concentration, word recall, and mood in middle
aged and elderly subjects with dementia, or age-related cognitive decline
[Kidd PM, 1999. A review of nutrients and botanicals in the integrative
management of cognitive dysfunction, Altern Med Rev, 4, 144-61].
Several studies have confirmed that PS improves the memory loss due to
age associated memory impairment (AAMI). In fact, PS has been shown to
improve the memory in:
1. AAMI patients [Crook TH et al., 1991, Effects of phosphatidylserine
in age-associated memory impairment. Neurology 41, p. 644-9]
2. Depressive symptoms, memory and behavior in geriatric patients
[Zicchi C. 1990. Effects of phosphatidylserine therapy in geriatric patients
with depressive disorders. Acta Pychiatr Scand 81, 265-70.]
3. Aged rats [Suzuki S et al., 2001. Oral administration of soybean
lecithin trans-phosphatidylated phosphatidylserine improves memory
impairment in aged rats. J Nutr 131, 2951-6]
4. Reversal of memory deficit (amnesia) associated with exposure to
chemicals in rats [Alves CS et al., 2000, Phosphatidylserine reverses
reserpine-induced amnesia. Eur J Pharmacol 404, 161-7]
and in mice [Suzuki et al., 2000. Effect of intracerebroventricular
admnistration of soybean lecithin transphosphatiilated phosphatidylserine on
scopolamine-induced amnesic mice. Japn J Pharmacol. 84, 86-8; Furushiro M et
al., 1997. Effects of oral administration of soybean lecithin
transphosphatidylated phosphatidylserine on impaired learning of passive
avoidance in mice. Jpn J Pharmacol 75, 447-40]
5. Neuronal mechanisms related to learning and memory [Giancoti C et
al., 1993. B-50/GAP-43 phosphorylation in hippocampal slices from aged
rats: effects of phosphatidylserine administration. Neurobiol Aging, 14,
401-6]
6. Improved cognitive abilities in PS exposed otherwise normal mouse
pups when they reached adulthood [Ammassari-Teule M et al., 1990. Chronic
administration of phosphatidylserine during ontogeny enhances
subject-environment interactions and radial maze performance in C57BL/6
mice. Physiol. Behav 47, 755-60]
7. Senile dementia in mice [Sakai, M et al., 1996. Pharmacological
effects of phosphatidylserine synthesized fom soybean lecithin on brain
functions in rodents. J Nutr Sci Vitaminol (Tokyo) 42, 47-54.]
8. Cerebral ischemic damage in gerbils [Suzuki S et al., 1999. Oral
administration of soybean lecithin transphosphatidylated phosphatidylserine
(SB-tPS) reduces ischemic damage in the gerbil hippocampus. Jpn J Pharmacol
81, 237-9].
Thus, all these studies report an overall beneficial effect of
exogenous orally administered phosphatidylserine on the nervous system. The
important thing is that there does not appear to be any undesirable side
effects even in human subjects.
A survey of literature also shows that memory impairment is common to most
of the progresive neurogenerative disordrs like ET, PD, Alzheimer's disese
(AD), Huntington's disease (HD), some types of epilepsy and multiple
sclerosis (MS), as cited below with some sample publications (this is not an
exaustive survey):
A. Memory impairment of different sorts [Howard LA, et al., 2000. The
contribution of apraxic speech to working memory deficits in Parkinson's
disease. Brain Lang 74, 269-88]; Whittington CJ et al., 2000. Recognition
memory impairment in Parkinson's disease: power and meta-analysis.
Neuropsychology 14, 233-46; [Ivory SJ et al. 1999. Verbal memory in
non-demented patients with idiopathic Parkinson's disease. Neuropsychologia
37, 817-28; Mattay VS et al., 2002. Dopaminergic modulation of cortical
function in patients with Parkinson's disease. Ann Neurol 51, 156-64.]
B. Age-associated memory impairment and early Alzheimer's disease share
biochemical similarity [Forstl H et al., 1995. Age-associated memory
impairment and arly Alzheimer's disease. Only time will tell the difference.
Arzneimittelforschung, 45, 394-7]
C. Mild cognitive functional deficit is found in benign Essential
Tremor patients [Lacritz LH et al., 2002. Cognitive functioning in
individual with "benign" essential tremor. J Int Neuropsychol Soc 8, 125-9]
and that
D. depression found in Parkinson's disease patients is primarily related
to memory deficiency [Norman S et al., 2002. Effects of depression and
Parkinson's disease on cognitive functioning. J Neuropsychiatry 14, 31-6].
I rationalized my hypothesis this way. The deficiency in cognitive
functions may have a common physiological steps (signal transdution
pathways) in all these progressive degenerative diseases such as AAMI, AD,
PD, ET, HD and MS. If so, PS should also be able alleviate some of the
symptoms of PD. With that logic and also knowing that PS does not have any
serious side effects, I started taking PS for the past two weeks. [WARNING
DO NOT REPEAT THIS WITHOUT CONSULTING YOUR DOCTOR!] On day 2 after taking
PS, I was signing for my VISA bill at a grocery store and I was pleasantly
surprised to see that I was able to sign my signature almost as good as I
was doing it only last year. (Of late my signature has been just a blerb
and did not resemble my signature a few years ago!) In addition, I see
definite decrease (I do not have any quantitative numbers on this though) in
the degree of amplitude in my tremors. I also see an overall improvement in
my outlook of things. I have not done any dose response studies (I have to
do sme more literature survey on this). I also find a perceivable degree of
decrease in drooling and postural instability, although I do not have any
way to quantitatively study this phenomenon. I am not how long this effect
will last. I am not sure of the appropriate dose, being the first guinea
pig myself.
I am strongly convinced that PS is a compound with high promise in
relieving or ameliorating various symptoms associated with cognitive
functional deficiency, which appears to be related to various symptoms
including tremor, dopamine physiology, speech, depression etc., which may or
may not be common to most of the progressive neurodegenerative diseases
including, PD, ET, HD and MS and AAMI. One can only assume that the common
signal transduction pathway may be affected, albeit at different steps in
different diseases. I am surprised that effect of PS has not been tested on
PD pateints so far. I could think of a major reason why this has not been
tried on PD patients. I suspect that this drug is commonly avaiblable in
stores and, so, cannot be patented, and therefore, the pharmaceutical
companies may not be willing to fund such a study. This study can only be
conducted with government grants to University Professors. I am retired
and I am not a neurologist. I would be willing to collaborate with you if
you are interested in studying this phenomenon in a more formal way to
approach this problem. My gut feeling tells me that PS may be very
effective in very early stages of most of the neurogenerative diseases.
But, we have to conduct proper studies observing all the ethical
considerations, before we can assume anything. The rationale makes sense to
me.
Would like to hear from you.
Raj
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----- Original Message -----
From: "Charles W. Scouten, Ph.D." <[log in to unmask]>
To: <[log in to unmask]>
Sent: Saturday, May 18, 2002 12:48 AM
Subject: Re: Introducing myself
> Our stories run so similar its scary. I am in the propranalol stage
> right now. Except the speech problem is sudden lockup of the face
> muscles so I can't talk when trying to force speech and think at the
> same time. I am a Ph.D. studying PD right now, and working on a grant,
> and just sort of dawned on me that I seem to be in the early stages,
> very much like you have described. Kind of lends an urgency to it all.
> I have had symptoms since about 18 that I would now trace to early
> traces. How common is it to have very early symptoms and warnings?
> Long before diagnosable?
>
> Cordially,
>
> Charles W. Scouten, Ph.D.
> myNeuroLab.com
> 5918 Evergreen Blvd.
> St. Louis, MO 63134
> Ph: 314 522 0300
> FAX 314 522 0277
> [log in to unmask]
> www.myneurolab.com
>
>
> -----Original Message-----
> From: Brightline [mailto:[log in to unmask]]
> Sent: Friday, May 17, 2002 6:45 PM
> To: [log in to unmask]
> Subject: Introducing myself
>
> Dear Friends:
> I am not new, but I have not been very actively involved so far,
> except
> sending a couple of comments once in a while. I am 68, running on 69. I
> am
> an officially retired, but very much active, profesor and my area of
> research was and is cancer. I have been having what everybody thought
> was
> ET (action tremor) since my teen age days. But, come to think of it, I
> had
> a slight facial mask from my twenties or thirties. I recollect in
> 1972-73,
> some of my close friends use to tell me: "You have a nice smile and a
> good
> heart. Why don't you use them to your advantage, instead of putting up
> a
> sorrow face all the time?" I am not sure if I had an early onset PD
> with
> very little true PD symptoms (no resting tremor, posturl instability,
> drooling etc.) As a hind sight, I am sure it might be true.
> In 1998 (at my 65th year), when I was lecturing in my class, I
> noticed a
> slight, occasional slurring of my speech. I did not even dream of PD in
> thse days. Then, I started noticing my right arm did not swing as good
> as
> my left. My action tremor in my right hand became very highly visible
> and I
> began to notice by 2000 my right leg was doing the same in synch with my
> right leg, when I did smething with my right hand fingers. Buttoning my
> shirts takes a lot more time. By the end of 2001, I could not reproduce
> my
> signature; however my handwriting did not become tinies andtiniesas it
> should be for PD; simplyh I cannot right one word without my hand
> running
> crazy all over the place. I was lucky I knew typing. Even that becomes
> very difficult now days, since a couple of my fingers would not want to
> bend
> when I type some letters!
> By the year 2000, I was convinced some thing strange was going on
> There
> fore I saw a neurologist. She told me I ws having ET and not PD. Then
> I
> went and saw the only local Movement Disorder Specialist who thought tht
> I
> was developing PD on top of my ET. I went through the initial phase of
> denial and sought a second opinion from another MDS at Bethesda
> Univesity
> Hospital. She assured me that I did not have PD and prescribed
> Propranalol.
> When my lo al MDS heard this, he refused to see me! Propranalol had
> only
> transient effect on my tremor; soon I started developing high blood
> pressure
> (this is a beta blocker and is not supposed to do this!), increase in
> weight
> and blood sugar, and lethargy and low pulse rate. I stopped taking
> Propranalol; I lost my gained weight, blood sugar became normal, normal
> pulse rate, and my action tremor was getting worse. I have developed
> mild
> postural instability and occasinal drooling, along with sightly
> progressed
> speech slurring.
> I saw another neurologist who prescribed sinemet CR, which I have
> not
> yet started taking. In the meanwhile, the news about mirapex and requip
> delaying the progression of PD. I am wondering if I should see another
> MDS.
> I am waiting to get an appointment with Dr. Tony Lang in Toronto.
> More about me later.
> Raj
> [log in to unmask]
>
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