"....
Jan. 7, 2009

Recent animal studies have shown that clioquinol – an 80-year old drug once used to treat diarrhea and other gastrointestinal disorders – can reverse the progression of Alzheimer’s, Parkinson’s and Huntington’s diseases. Scientists, however, had a variety of theories to attempt to explain how a single compound could have such similar effects on three unrelated neurodegenerative disorders.

http://www.mcgill.ca/newsroom/news/item/?item_id=103574

hey -
thank you dear rev,
http://www.answers.com/Clioquinol?af...ookup&nafid=27
it also says it is neurotoxic?

"Scientists, however, had a variety of theories to attempt to explain how a single compound could have such similar effects on three unrelated neurodegenerative disorders."

Because, maybe, just maybe, they are related? That maybe, just maybe, this might be an interesting path for more research and further scientific inquiry? I'm surprised that scientists are so unimaginative.

They just don't get it. They are fixated on "one cause-one disease-one cure" thinking and don't entertain the possibility of something far more complex like "exposure to A sets initial conditions, nothing happens unless B is encountered in which case system is primed, if two or more of C through M impact the system simultaneously then a cascade is triggered with the ultimate disease being determined by the particular combination that initiate the process"

Something along those lines is needed to account for the fact that PD is sporadic yet common but very individualized. Tweak a variable or two and you've got a different condition but it is still messing with your brain and it is still degenerative and it still strikes after mid-life etc.

OK I have rescue my fellow researchers now!! Researchers are not that bad~ most of us get it when you read a paper or when the data is presented. As a patient, I am allowed to speculate and say it out in public any theory I like, its considered ok and encouraged. But as a scientist, I do speculate, dream of out of the box solutions, high profile publications within my lab. But in a publication, my theory has to be strong, be able to stand further testing and most importantly should be based on my own data.
ans mesh wth others work
PubMed has a lot of reports but the quality of the reports is not the same and sometimes, the abstract doesnt even accurately reflect the data presented. Thats the reason, most researchers tend to be cautious which might seem unimaginative or they are not thinking about it.

Even Watson and Crick who discovered the structure of DNA, had just one line at the end of their paper about the potential and impact of their discovery r and it starts "it has not escaped our attention that........
A simple statement about a discovery that formed the basis of modern biology.

thanks, I change my hat now !!!

QUOTE=reverett123;442335]They just don't get it. They are fixated on "one cause-one disease-one cure" thinking and don't entertain the possibility of something far more complex like "exposure to A sets initial conditions, nothing happens unless B is encountered in which case system is primed, if two or more of C through M impact the system simultaneously then a cascade is triggered with the ultimate disease being determined by the particular combination that initiate the process"

Something along those lines is needed to account for the fact that PD is sporadic yet common but very individualized. Tweak a variable or two and you've got a different condition but it is still messing with your brain and it is still degenerative and it still strikes after mid-life etc.[/QUOTE]

Thanks - we need to hear from both of you.

paula

...I apologize to the guy at the bench. [I had my own lab once. Of course, I was twelve years old and it was in my grandmother's shed but with a little sulfur one can turn out some neat stink bombs ]

I see the problem as institutional. There is a pyramid type power structure that demands conformity and preserves itself as well. The result is slow, methodical, and generally correct. Punctuated by moments when some little guy with bad hair and working at the local patent office clears his throat and the pyramid collapses in the proverbial "revolution".

Unfortunately, for us speed is high priority and the current system is not built for speed.

bump bump bump

Has any futher research been done on Clioquinol since 2009 for treatment of PD in conjunction with Vitamin B12? Is it still being used? Is it an over the counter medication in the UK and the US?

I recall being able to buy and use Clioquinol for treatment of gut inections by all manners of pathogens in India. This drug was later withdrawn after reports from Japan that it caused damage to retinal nerves.

See this:

http://www.patentstorm.us/patents/59...scription.html

Thanks

Kenki

There is quite a bit being published, particularly around its role as a chelator. I wonder if it is available through off-shore pharmacies?


1. CNS Neurosci Ther. 2010 Dec 27. doi: 10.1111/j.1755-5949.2010.00231.x. [Epub
ahead of print]

Clioquinol: Review of its Mechanisms of Action and Clinical Uses in
Neurodegenerative Disorders.

Bareggi SR, Cornelli U.

Department of Pharmacology, Chemotherapy and Medical Toxicology, School of
Medicine, University of Milan, Italy Loyola University Medical School, Chicago,
IL, USA.

Clioquinol was produced as a topical antiseptic and marketed as an oral
intestinal amebicide in 1934, being used to treat a wide range of intestinal
diseases. In the early 1970s, it was withdrawn from the market as an oral agent
because of its association with subacute myelo-optic neuropathy (SMON), a
syndrome that involves sensory and motor disturbances in the lower limbs and
visual changes. The first methods for determining plasma and tissue clioquinol
(5-chloro-7-iodo-8-quinolinol) levels were set up in the 1970s and involved HPLC
separation with UV detection, these were followed by a more sensitive GC method
with electron capture detection and a gaschromatographic-massspectrometric
(GC-MS) method. Finally, an HPLC method using electrochemical detection has
proved to be as highly sensitive and specific as the GC-MS. In rats, mice,
rabbits, and hamsters, clioquinol is rapidily absorbed and undergoes first-pass
metabolization to glucuronate and sulfate conjugates; the concentrations of the
metabolites are higher than those of free clioquinol. Bioavailabilty versus
intraperitoneal dosingis about 12%. Dogs and monkeys form fewer conjugates. In
man, single-dose concentrations are dose related, and the drug's half-life is
11-14 h. There is no accumulation, and the drug is much less metabolized to
conjugates. Clioquinol acts as a zinc and copper chelator. Metal chelation is a
potential therapeutic strategy for Alzheimer's disease (AD) because zinc and
copper are involved in the deposition and stabilization of amyloid plaques, and
chelating agents can dissolve amyloid deposits in vitro and in vivo. In general,
the ability of clioquinol to chelate and redistribute metals plays an important
role in diseases characterised by Zn, Cu, Fe dyshomeostasis, such as AD and
Parkinson's disease, as it reduces oxidation and the amyloid burden. Zinc
chelators may also act as anticancer agents. Animal toxicity studies have
revealed species-specific differences in neurotoxic responses that are related to
the serum levels of clioquinol and metabolites. This is also true in humans, who
form fewer conjugates. The results of studies of Alzheimer patients are
conflicting and need further confirmation. The potential therapeutic role of the
two main effects of MPACs (the regulation of the distribution of metals and
antioxidants) has not yet been fully explored.


PMID: 21199452 [PubMed - as supplied by publisher]