"This field is in sore need of a success story,"
"Methylene blue has been in use for decades"
Slowing mental ravages of Alzheimer's disease
Well-known drug may combat effects, researchers say
By Jeremy Manier | Chicago Tribune reporter
July 31, 2008
Editor's note: Due to a production error, this story from Wednesday's
newspaper did not run in full. This is the complete text.
Hope is often scarce in research on Alzheimer's disease, but a study
released Tuesday at a Chicago medical conference offered tentative
hope for a new way of slowing elderly patients' mental decline.
The preliminary study of 321 Alzheimer's patients from Singapore and
Britain found that an old drug, previously used for urinary tract
infections and other ailments, reduced the patients' rate of mental
loss by 81 percent, based on a standard measure of cognitive
performance and memory.
The results require further confirmation, but whatever the outcome,
some experts are intrigued by the drug's novel way of attacking the
disease.
Scientists say the medication, which goes by the commercial name
rember, may work by dissolving tangles of a protein that collects in
the brain cells of Alzheimer's patients.
If true, the therapy could be the first to stave off an underlying
cause of Alzheimer's disease, unlike current treatments such as
Aricept, which provide only temporary relief of symptoms through their
effect on brain compounds that are important in cognition.
"The effect size is pretty large for drugs of this class," said Dr.
Raj Shah, an Alzheimer's specialist and medical director of the memory
clinic at Rush University Medical Center.
Researchers presented the findings Tuesday at the 2008 Alzheimer's
Association International Conference on Alzheimer's Disease, being
held this week in Chicago.
Other Alzheimer's treatments have shown early signs of promise but
failed to deliver in clinical trials, making experts cautious about
reading too much into Tuesday's findings.
For example, numerous drugs now in development attempt to take aim at
the plaques of beta-amyloid protein that develop among the brain cells
of many Alzheimer's patients, but some of the outcomes have been
disappointing.
One such drug, tarenflurbil, which had promising results in an early-
phase study, turned out to have no significant effect on the disease
when tested in a larger clinical trial, researchers reported Tuesday.
"This field is in sore need of a success story," said Dr. Marsel
Mesulam, director of the cognitive neurology and Alzheimer's disease
center at Northwestern University.
Unlike drugs aimed at beta-amyloid, rember is meant to dissolve an
abnormal protein called tau, which many experts had thought would be
an elusive target for Alzheimer's treatments.
Some theories suggest the tangles of tau protein that form in
patients' brain cells could cause the symptoms of the disease by
hampering chemical communication in the brain.
It's also possible that the protein tangles are merely byproducts of a
deeper problem that is the real source of cognitive decline.
Study leader Claude Wischik of Aberdeen University's Institute of
Medical Sciences has spent two decades tracing the role of tau protein
tangles in Alzheimer's disease.
He said he agrees that further tests are needed to confirm the
preliminary results, but he's encouraged by the findings so far.
"We've shown you can arrest disease development by targeting the
protein tangle," said Wischik, who is also chairman of TauRx
Therapeutics, which hopes to market the new treatment if it's
successful.
The drug Wischik tested is a purified form of a substance commonly
known as methylene blue, which has been in use for decades as a
treatment for numerous conditions, including urinary tract infections
and carbon monoxide poisoning. Many patients on the drug report that
their urine turns blue, but Wischik said so far the drug appears safe.
Although in principle it would be possible for doctors to use the
common version of the drug in patients before testing is complete,
Wischik and other experts said that would be unwise.
Among other problems, doctors who prescribed the drug on their own
without proof that it works could be open to lawsuits if patients
developed bad side effects, experts said.
Wischik said that if further tests of the compound show promise, the
treatment could be available for general use by 2012 or 2013,
depending on how quickly the drug moves through regulatory hurdles in
the U.S. and in countries overseas.
jman... at (no spam) tribune.com
------------------------------------------
This study showed people began to remember old songs .. with lecithin
a plant oil.
MMW Fortschr Med. 2004 Dec 9;146:99-106. Related Articles, Links
[Improvement in quality of life in the elderly. Results of a
placebo-controlled study on the efficacy and tolerability of lecithin
fluid in patients with impaired cognitive functions]
Volz HP, Hehnke U, Hauke W.
Krankenhaus fur Psychiatrie, Psychotherapie und Psychosomatische
Medizin, Schloss Werneck.
Lecithin, a precursor of the neurotransmitter acetylcholine, has a
positive effect on brain and memory functions.
In a prospective, randomized, double-blind study, the effect of
buerlecithin fluid (BLF) was investigated in comparison with
placebo in patients with mild cognitive disorders.
A total of 96 ambulatory patients (> 55 years) were admitted to the
study.
Treatment duration was 84 days.
In both treatment groups, a clear improvement in all the cognitive
parameters tested was seen.
The main target measure, the overall Sandoz Clinical Assessment
Geriatric (SCAG) score improved by 18.7 (test substance) and 16.4
(placebo) points (p = 0.1620).
A statistically relevant improvement of the secondary target
parameter, response in the SCAG score, was achieved with BLF (85.4%)
in comparison with placebo (62.5%) (p = 0.018).
Furthermore, BLF demonstrated significant superiority in a
number of the other target measures.
The study also confirmed the very good tolerability of BLF.
PMID: 15662899 [PubMed - indexed for MEDLINE]
---------------------------------------------------------------------------------
This compilation of articles .. speaks to phosphatidylcholine ..
lecithin .. simply lecithin ... which is a PREMIERE iron binder /
chelator.
Am J Psychiatry 1979 Nov;136(11):1458-60
Treatment of tardive dyskinesia with lecithin.
Jackson IV, Nuttall EA, Ibe IO, Perez-Cruet J.
Six patients with moderate or severe tardive dyskinesia participated
in a 14-day double-blind crossover comparison of placebo with 50 g/day
of lecithin.
There were no side effects, and Abnormal Involuntary Movement Scale
(AIMS) ratings of videotaped examinations indicated significant
improvement in the dyskinesias of all subjects during the lecithin
trial, even with concomitant administration of a constant dose of
neuroleptic medication to five patients.
----------------------------------
Choline and lecithin in the treatment of tardive dyskinesia:
preliminary results from a pilot study.
Am J Psychiatry 1979 Jun;136(6):772-6
Gelenberg AJ, Doller-Wojcik JC, Growdon JH.
Tardive dyskinesia is thought to reflect increased dopaminergic
activity of the central nervous system.
To compensate for this by increasing CNS cholinergic tone, the
authors administered oral choline and its natural dietary source,
lecithin, to 5 men with mild to severe tardive dyskinesia in a
nonblind trial.
Both choline and lecithin increased serum choline levels and improved
abnormal movements in all patients.
Lecithin had fewer adverse effects.
-----------------------------
Lecithin consumption raises serum-free-choline levels.
Lancet 1977 Jul 9;2(8028):68-9
Wurtman RJ, Hirsch MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations.
In man consumption of choline increases in levels in the serum and
cerebrospinal fluid; its administration is an effective way of
treating tardive dyskinesia.
We found that oral lecithin is considerably more effective
in raising human serum-choline levels than an equivalent quantity of
choline chloride. 30 minutes after ingestion of choline chloride (2-3
g free base), serum-choline levels rose by 86% and returned to normal
values within 4 hours; 1 hour after lecithin ingestion,
these levels rose by 265% and remained significantly raised for 12
hours.
Lecithin may therefore be the method of choice for accelerating
acetylcholine synthesis by increasing the availability of choline, its
precursor in the blood.
---------------------------------
The use of cholinergic precursors in neuropsychiatric diseases. Am J
Clin Nutr 1982 Oct;36(4):709-20
Rosenberg GS, Davis KL.
Preclinical data suggest that cholinergic precursors such as choline
or lecithin, increase levels of acetylcholine in specific brain
structures, and under certain conditions may enhance cholinergic
neurotransmission.
A variety of neuropsychiatric diseases including tardive dyskinesia.
Huntington's chorea, ataxias, Tourette's syndrome, schizophrenia,
affective illness, and senile dementia of the Alzheimer type, has been
implicated with a general underactivity of central cholinergic
mechanisms.
Recent studies have investigated the possibility that cholinergic
precursor loading strategies may provide viable treatments for these
disorders of presumed cholinergic underactivity.
Extensive data demonstrate that the symptoms of tardive dyskinesia can
be reduced by choline or lecithin, whereas investigations in other
disorders have met with mild success, at best, or are still in
preliminary stages.
Further controlled studies with choline or lecithin using broader dose
ranges, longer durations of treatment, and concomitant
administration of agents which may increase the release of
acetylcholine are warranted.
-------------
This article speaks to the oxidation in the brain.
They KNOW the buildup of iron in the brain DUE TO the use of
neuroleptics leads to tardive.
This article pretty much says to TARGET the oxidation in the brain ..
-------------------
Ebselen attenuates reserpine-induced orofacial dyskinesia and
oxidative stress in rat striatum.
Prog Neuropsychopharmacol Biol Psychiatry 2003 Feb;27(1):135-40
Burger ME, Alves A, Callegari L, Athayde FR, Nogueira CW, Zeni G,
Rocha JB
Departamento de Fisiologia, Centro de Ciencias da Saude, Universidade
Federal de Santa Maria, 97105-900, RS, Santa Maria, Brazil
Reserpine-induced orofacial dyskinesia is an alleged animal model of
tardive dyskinesia whose pathophysiology has been related to striatal
oxidative stress.
In the present investigation, the authors examined whether ebselen, an
antioxidant organochalcogen with glutathione peroxidase-like activity,
changes the behavioral and neurochemical effect of acute reserpine
administration.
Reserpine injection for 3 days every other day caused a
significant increase on the tongue protrusion frequency and ebselen
(30 mg/kg ip for 4 days, starting 1 day before reserpine) reversed
partially the effect of reserpine (P<.05).
Reserpine- and reserpine+ebselen-treated groups displayed an increase
in vacuous chewing frequency when compared to control
and ebselen-treated groups (P<.05)
Reserpine increased the duration of facial twitching and ebselen
reversed partially the effect of reserpine
(P<.01).
Reserpine increased significantly the thiobarbituric acid-reactive
species (TBARS) levels, and ebselen reversed the effect of reserpine
on TBARS production in rat striatum.
The results of the present study clearly indicated that ebselen has a
protective role against reserpine-induced orofacial dyskinesia and
reversed the increase in TBARS production caused by
reserpine administration.
Consequently, the use of ebselen as a therapeutic agent for the
treatment of tardive dyskinesia should be considered.
PMID: 12551736, UI: 22440265
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Tom
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