I agree there must be a connection, but am clueless beyond that. I have made some observations, though:

1. at diagnosis, our neuro told us that everyone would get PD if we lived long enough (he must subscribe to the "it's a disease of age" theory)...and maybe he is right, yet my grandmother on my dad's side lived to be thirty days shy of 100, and although quite feeble, did not have PD...on my mom's side, grandmother lived to be 96 and although she had "dementia" it did not appear until around year 94, 95. So I am not too sure that it is just a matter of how old you are-look at how many young onsetters there are, including my husband. And look at how many really old folks we have who do NOT have it, including the black fellow in the news during the last election, he was, I think it was, 102 and voting!

2. on the environmental theory, I see that, but did read something recently that made me pause: in India they have been using mucuna to treat PD symptoms for over 4,000 years (6,000 according to one thing I read), all of this was way before we had the chemicals, stress, lifestyle we have now...makes me wonder about how strong the connection between PD and those things is (not that I am discounting that, and we personally live as stress free as one can with two young kids, and grow some of our food, buy organic when we can)...

3. my husband's father, I am pretty sure, also has PD, it is hard to be 100% sure because he will not discuss it and is being treated for more serious heart and lung issues. But I think he does. He is close to 80 but my husband was dx'd at 43. It seems young onsetters have more than a coincidental link with someone in their immediate family with PD. So personally, I believe there is a genetic propensity for this in the first place, but have no idea what the trigger is, or if there even is a trigger.

4. connection between these diseases? They do all affect our brain, but with PD who knows what really happens first? We really are not even sure PD is a "neurological" disease...just now they are making noises that maybe, just maybe, there may be more systems involved, but the neuros don't like that for obvious reasons.

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]

I'm sure that problems cropping up and patent expirations are totally unrelated and I'm just a grumpy old cynic....

Clioquinol's use as an antiprotozoal drug has been restricted or discontinued in some countries due to an event in Japan where over 10,000 people developed SMON (subacute myelo-optic neuropathy) between 1957 and 1970. The drug was used widely in many countries before and after the SMON event without similar reports.[6] As yet, no explanation exists as to why it produced this reaction, and some researchers have questioned whether clioquinol was the causative agent in the disease, noting that the drug had been used for 20 years prior to the epidemic without incident, and that the SMON cases began to reduce in number prior to the discontinuation of the drug.[7] Theories suggested have included improper dosing, the permitted use of the drug for extended periods of time, [8] and dosing which did not consider the smaller average stature of Japanese; however a dose dependant relationship between SMON development and clioquinol use was never found, suggesting the interaction of another compound. Researchers have also suggested the SMON epidemic could have been due to a viral infection with a Inoue-Melnick virus.[9]

1: Mol Nutr Food Res. 2006 Feb;50(2):229-34.

Green tea catechins as brain-permeable, natural iron chelators-antioxidants for
the treatment of neurodegenerative disorders.

Mandel S, Amit T, Reznichenko L, Weinreb O, Youdim MB.

Eve Topf, Haifa, Israel. mandel@tx.technion.ac.il

Neurodegeneration in Parkinson's, Alzheimer's, or other neurodegenerative
diseases appears to be multifactorial, where a complex set of toxic reactions,
including oxidative stress (OS), inflammation, reduced expression of trophic
factors, and accumulation of protein aggregates, lead to the demise of neurons.
One of the prominent pathological features is the abnormal accumulation of iron
on top of the dying neurons and in the surrounding microglia. The capacity of
free iron to enhance and promote the generation of toxic reactive oxygen
radicals has been discussed numerous times. The observations that iron induces
aggregation of inert alpha-synuclein and beta-amyloid peptides to toxic
aggregates have reinforced the critical role of iron in OS-induced pathogenesis
of neurodegeneration, supporting the notion that a combination of iron chelation
and antioxidant therapy may be one significant approach for neuroprotection. Tea
flavonoids (catechins) have been reported to possess divalent metal chelating,
antioxidant, and anti-inflammatory activities, to penetrate the brain barrier
and to protect neuronal death in a wide array of cellular and animal models of
neurological diseases. This review aims to shed light on the
multipharmacological neuroprotective activities of green tea catechins with
special emphasis on their brain-permeable, nontoxic, transitional metal (iron
and copper)-chelatable/radical scavenger properties.

Publication Types:
Review

PMID: 16470637 [PubMed - indexed for MEDLINE]