View Full Version : Experimental evidence that Fungi causes Parkinsons; Fungal Transposons
Experimental evidence that Fungi causes Parkinsons; Fungal Transposons
Tonight on the evening news out of Sioux City came the
report that Well Water on farms which contains bacteria and
fungi causes rats to come down with Parkinsons.
A report in the Annals of Neurology.
I would be interested to know whether ** Transposons** are
involved??
I would guess also that in England alot of well water is
prevalent for Prion disease and whether it is a particular
species of fungus.
Yes, indeed, tonight we celebrate on this news that the
idea of Fungus Transposons is moving ahead as the
probable cause of not only Parkinsons but also Alzheimers
and Prion diseases.
Now I wonder if Parkinsons, Alzheimers and Prion are rare
for people who live all their life in dry desert climates??
Yes, indeed, toast the champagne for I believe the correct
path to understanding Alzheimers, Parkinsons and Prion
diseases is Transposons and especially of fungus and perhaps
some bacteria and viruses.
Anyone know if the report in Annals Neurology mentions what
fungus and whether they mention Transposons?
Archimedes Plutonium www.archimedesplutonium.com
www.iw.net/~a_plutonium whole entire Universe is just one
big atom where dots of the electron-dot-cloud are galaxies
Archimedes Plutonium wrote:
> Tonight on the evening news out of Sioux City came the
> report that Well Water on farms which contains bacteria
> and fungi causes rats to come down with Parkinsons.
>
> A report in the Annals of Neurology.
>
> I would be interested to know whether ** Transposons** are
> involved??
>
> I would guess also that in England alot of well water is
> prevalent for Prion disease and whether it is a particular
> species of fungus.
>
> Yes, indeed, tonight we celebrate on this news that the
> idea of Fungus Transposons is moving ahead as the probable
> cause of not only Parkinsons but also Alzheimers and Prion
> diseases.
>
> Now I wonder if Parkinsons, Alzheimers and Prion are rare
> for people who live all their life in dry desert
> climates??
>
> Yes, indeed, toast the champagne for I believe the correct
> path to understanding Alzheimers, Parkinsons and Prion
> diseases is Transposons and especially of fungus and
> perhaps some bacteria and viruses.
>
> Anyone know if the report in Annals Neurology mentions
> what fungus and whether they mention Transposons?
>
Article: "Systemic Exposure to Proteasome Inhibitors Causes
a Progressive Model of Parkinson's Disease," McNaught,
Pearl, Brownell, Olanow, Annals of Neurology June 21, 2004
I saw no mention of specific fungus. I did see mention of
epoxomicin saying it was one of the most potent proteasome
inhibitors produced by actinomycetes bacteria found in soil.
I wonder if the fungus involved is yeast species or genus
of fungus.
No mention of Transposons, but since my theory says that all
three diseases of Alzheimers Parkinsons and Prion are family
related since all 3 are in the majority Hereditary diseases
that all 3 thus would have an environmental component. And
since fungus are implicated in Parkinsons would suggest that
fungus causes Prion and causes Alzheimers.
It maybe that fungus proteasome inhibitors is all that is
needed to create Parkinsons in humans and from drinking well-
water. No wonder the highest Parkinsons rate is Midwest USA
with all those wells.
But for Alzheimers and Prion, it may involve fungus more
than proteasome inhibitors. It may involve fungus of fungus
transposons or bacterial transposons or even virus
transposons. And in the end, Parkinsons may involve not just
proteasome inhibitors but actually transposons.
I am happy to say that this long road of finding out and
understanding of how Alzheimers and Parkinsons and Prion are
coming to its "truthful end road". And that the Prusiner
Model of the last century was a muddled, misguided detour of
falsehoods. That the correct path to understanding starting
in the 20th century was to group these 3 diseases as one and
to Cross Reference each amoung themselves. So that if
"protein only vector" is implausible in Parkinsons or
Alzheimers then it is implausible and a laughable fake model
in Prion disease. And if fungus are found to cause
Parkinsons as recently reported then by cross reference
implies that fungus are the cause of Prion and also
Alzheimers.
The entire century of the 20th was a poor science operation
as far as understanding these diseases of the brain. It had
lone-wolf models as separate from the other 2 diseases. And
even today of 3 July, many stupid science journals print as
to how the Prusiner Model causes variants in PrP which is
laughable because the entire Prusiner Model is a folly with
its epicycle building up of more folly.
Ironic that real science data comes in and tells us that
Fungus creates Parkinsons and yet science journals print the
folly of how Prusiner Model can jive with PrP variants.
No virus has ever been found in connection with Prion
disease. There have been Nucleic Acids found. Now that
Parkinsons is found to be caused (can caused) by Proteasome
Inhibitors of Fungus or bacteria. We can go back to Prion
disease in the environment and look for Fungus proteasome
inhibitors. We can look for Fungus Transposons and other
Transposons.
In Alzheimers we have the curious protein of Tau. We do not
know how tau is related to the overall disease. We can apply
Transposon Hypothesis and ask whether a Transposon causes
the APP scissors to become rogue scissors and creates
betaamyloid. Would a Transposon cause the APP scissors to
become rogue and would it also cause tau to be created??
Archimedes Plutonium www.archimedesplutonium.com
www.iw.net/~a_plutonium whole entire Universe is just one
big atom where dots of the electron-dot-cloud are galaxies
Sat, 03 Jul 2004 14:30:18 -0500 Archimedes Plutonium
wrote: (snipped)
>
> Article: "Systemic Exposure to Proteasome Inhibitors
> Causes a Progressive Model of Parkinson's Disease,"
> McNaught, Pearl, Brownell, Olanow, Annals of Neurology
> June 21, 2004
>
> I saw no mention of specific fungus. I did see mention of
> epoxomicin saying it was one of the most potent
> proteasome inhibitors produced by actinomycetes bacteria
> found in soil.
>
> I wonder if the fungus involved is yeast species or genus
> of fungus.
>
> No mention of Transposons, but since my theory says that
> all three diseases of Alzheimers Parkinsons and Prion are
> family related since all 3 are in the majority Hereditary
> diseases that all 3 thus would have an environmental
> component. And since fungus are implicated in Parkinsons
> would suggest that fungus causes Prion and causes
> Alzheimers.
>
> It maybe that fungus proteasome inhibitors is all that is
> needed to create Parkinsons in humans and from drinking
> well-water. No wonder the highest Parkinsons rate is
> Midwest USA with all those wells.
>
> But for Alzheimers and Prion, it may involve fungus more
> than proteasome inhibitors. It may involve fungus of
> fungus transposons or bacterial transposons or even virus
> transposons. And in the end, Parkinsons may involve not
> just proteasome inhibitors but actually transposons.
>
I think that Protease Inhibitors alone as the cause of
Parkinsons (if not inherited) is enough of an explanation.
Because in Parkinsons it is the accumulation of unwanted
alphasynuclein that kills the neuron cells. So in
Parkinsons, a proteasome inhibitor can be the sole cause.
But in Prion disease, I believe a proteasome inhibitor would
not alone cause the disease. An inhibitor that accumulates
unwanted PrP proteins. I think in Prion disease, more than
just a proteasome inhibitor is needed to drive the disease.
Here we need some Nucleic Acid to drive the Prion disease
and since fungus proteasome inhibitors cause Parkinsons, I
am guessing that fungus transposons would be required to
drive Prion disease.
In Alzheimers, again, more is needed than just a proteasome
inhibitor because the APP scissors is creating the unwanted
betaamyloid.
It may turn out the case where both a Nucleic Acid and
proteasome inhibitor work in conjunction with one another in
driving the disease. Such as in Alzheimers where a
Transposon or viruslike particle corrupts the APP scissors
and then later, proteasome inhibitors allow for betaamyloid
to continue to aggregate.
In Prion disease, a likely model is that some Transposon or
viruslike particle corrupts the manufacturing of PrP
proteins and then some proteasome inhibitors allow for the
accumulation of PrP proteins.
Archimedes Plutonium www.archimedesplutonium.com
www.iw.net/~a_plutonium whole entire Universe is just one
big atom where dots of the electron-dot-cloud are galaxies
Sat, 03 Jul 2004 14:30:18 -0500 Archimedes Plutonium
wrote: (snipped)
>
> Article: "Systemic Exposure to Proteasome Inhibitors
> Causes a Progressive Model of Parkinson's Disease,"
> McNaught, Pearl, Brownell, Olanow, Annals of Neurology
> June 21, 2004
>
> I saw no mention of specific fungus. I did see mention of
> epoxomicin saying it was one of the most potent
> proteasome inhibitors produced by actinomycetes bacteria
> found in soil.
>
> I wonder if the fungus involved is yeast species or genus
> of fungus.
>
Tonight I made a search for Cordyceps fungus that attacks
ant brains and protease inhibitors and got a curious hit for
Tropolone.
I found that tropolone can be produced by
actinomycetes also.
So perhaps Cordyceps fungus is involved with Parkinsons
disease. And if so there is the possibility that Cordyceps
is involved with Prion disease also.
I wonder if any scientist has researched in detail how
Cordyceps destroys the brains of ants? As to what chemicals
Cordyceps destroys ant brains. Ant brains are far different
from mammal brains of sheep, cow and humans but perhaps
several of the chemicals that Cordyceps produces can create
not only Parkinsons but also Prion disease. Perhaps even
Alzheimers. If that be the case then one fungus can create
either Parkinsons, or Prion or Alzheimers depending on
whether the Cordyceps releases a toxin of protease
inhibitors or Transposons that produce unwanted proteins.
Perhaps yeast fungus produces Transposons that creates Prion
disease. Which would be a huge shame for some people would
shun eating breads or other yeast products.
Apparently this Tropolone can cause cancer tumours so it
must be potent.
And one website described Tropolone as an antifungal. How
could that be if Tropolone in produced by a fungus of
Cordyceps? Unless there are many variants of Tropolone. So I
wonder if people who spray and apply the antifungal of
Tropolone have been known to be more susceptible to
Parkinsons or to CJD diseases, and perhaps even Alzheimers.
Anyone have statistics as to whether people who spray
antifungals come down with either Alzheimers, CJD or
Parkinsons more so than other people???
Archimedes Plutonium www.archimedesplutonium.com
www.iw.net/~a_plutonium whole entire Universe is just one
big atom where dots of the electron-dot-cloud are galaxies
Sun, 04 Jul 2004 04:43:17 -0500 Archimedes Plutonium
wrote: (snipped)
> Sat, 03 Jul 2004 14:30:18 -0500 Archimedes Plutonium
> wrote: (snipped)
>
> >
> > Article: "Systemic Exposure to Proteasome Inhibitors
> > Causes a Progressive Model of Parkinson's Disease,"
> > McNaught, Pearl, Brownell, Olanow, Annals of Neurology
> > June 21, 2004
> >
> > I saw no mention of specific fungus. I did see mention
> > of epoxomicin saying it was one of the most potent
> > proteasome inhibitors produced by actinomycetes bacteria
> > found in soil.
> >
> > I wonder if the fungus involved is yeast species or
> > genus of fungus.
> >
>
> Tonight I made a search for Cordyceps fungus that attacks
> ant brains and protease inhibitors and got a curious hit
> for Tropolone.
>
> I found that tropolone can be produced by
> actinomycetes also.
>
Now I wonder if in Alzheimers the corruption of the APP
scissors that creates the betaamyloid is due to the
prescence of some protease inhibitor because of the
prescence of a fungus or bacteria?? So that the protease
inhibitors present due to the fungus present force the
APP scissors to cut wrongly and then betaamyloid is
created. And normally the betaamyloid would be removed if
not for the prescence of other protease inhibitors by
fungus and bacteria.
In Alzheimers there could be several protease inhibitors in
action simultaneously to create the disease. In Parkinsons
it maybe the prescence of one protease inhibitor.
Searching on the web for Transposons, it appears that yeast
fungus are notorious for transposons. So I wonder if
Cordyceps has transposons that are disease bearing. I wonder
if ants affected by Cordyceps are also given a dose of
Cordyceps Transposons? I wonder if it is common for a
Cordyceps infection that transposons are routinely emitted.
Archimedes Plutonium www.archimedesplutonium.com
www.iw.net/~a_plutonium whole entire Universe is just one
big atom where dots of the electron-dot-cloud are galaxies
>Subject: AnnalsNeurology Proteasome Inhibitors causes...Parkinsons Re:
>From: Archimedes Plutonium a_plutonium@iw.net
>Date: 7/3/2004 1:30 PM Mountain Daylight Time
>Message-id: <40E70949.6CD235D7@iw.net>
<<snip>> iron may be the factor that triggers vascular
amyloidosis <<snip>>
Brain Res. 2004 Mar 26;1002(1-2):67-75. Related
Articles, Links
Lysosomal deposition of Abeta in cultures of brain vascular
smooth muscle cells is enhanced by iron.
Frackowiak J, Sukontasup T, Potempska A, Mazur-Kolecka B.
Department of Developmental Neurobiology, New York State
Institute for Basic Research in Developmental Disabilities,
1050 Forest Hill Rd., Staten Island, NY 10314, USA.
Janusz.Frackowiak@omr.state.ny.us
Recently, we found that brain vascular smooth muscle cells
from Tg2576 mice over-expressed the APP transgene in
culture, secreted amyloid-beta peptide (Abeta) and
accumulated Abeta intracellularly. Now we detected this
intracellular Abeta inside lysosomes, which were also rich
in C-terminal domain of APP, but not in endoplasmic
reticulum, Golgi apparatus, or trans-Golgi network.
Treatment of cultures with ferrous ions (50-150 microM)
increased the proportion of muscle cells with Abeta
immunoreactive granules and the amounts of intracellular Abeta1-
40 and Abeta1-42 in a dose-dependent manner. This increase
of intracellular Abeta1-40 by iron was inhibited by alpha-
tocopherol, but not by a water-soluble antioxidant
melatonin. The increase of intracellular Abeta1-42 by iron
was not inhibited by alpha-tocopherol or melatonin. Cell
treatment with iron did not alter the lysosomal localization
of Abeta immunoreactivity. Cell treatment with iron (II and
III), copper (II), zinc (II) and aluminum (III) increased
cellular levels of carbonyls. However, the effect of zinc on
Abeta accumulation in cultures was weak, and there were no
effects of copper and aluminum. The data suggest that iron
may be the factor that triggers vascular amyloidosis.
Lysosomal accumulation of APP and Abeta initiates deposition
of amyloid in blood vessels in Tg2576 mice.
PMID: 14988035 [PubMed - indexed for MEDLINE]
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03 Jul 2004 20:10:23 GMT doe wrote:
> >Subject: AnnalsNeurology Proteasome Inhibitors
> >causes...Parkinsons Re: From: Archimedes Plutonium
> >a_plutonium@iw.net Date: 7/3/2004 1:30 PM Mountain
> >Daylight Time Message-id: <40E70949.6CD235D7@iw.net>
>
> <<snip>> iron may be the factor that triggers vascular
> amyloidosis <<snip>>
>
> Brain Res. 2004 Mar 26;1002(1-2):67-75. Related
> Articles, Links
>
> Lysosomal deposition of Abeta in cultures of brain
> vascular smooth muscle cells is enhanced by iron.
>
> Frackowiak J, Sukontasup T, Potempska A, Mazur-Kolecka B.
>
> Department of Developmental Neurobiology, New York State
> Institute for Basic Research in Developmental
> Disabilities, 1050 Forest Hill Rd., Staten Island, NY
> 10314, USA. Janusz.Frackowiak@omr.state.ny.us
>
> Recently, we found that brain vascular smooth muscle cells
> from Tg2576 mice over-expressed the APP transgene in
> culture, secreted amyloid-beta peptide (Abeta) and
> accumulated Abeta intracellularly. Now we detected this
> intracellular Abeta inside lysosomes, which were also rich
> in C-terminal domain of APP, but not in endoplasmic
> reticulum, Golgi apparatus, or trans-Golgi network.
> Treatment of cultures with ferrous ions (50-150 microM)
> increased the proportion of muscle cells with Abeta
> immunoreactive granules and the amounts of intracellular
> Abeta1-40 and Abeta1-42 in a dose-dependent manner. This
> increase of intracellular Abeta1-40 by iron was inhibited
> by alpha-tocopherol, but not by a water-soluble
> antioxidant melatonin. The increase of intracellular Abeta1-
> 42 by iron was not inhibited by alpha-tocopherol or
> melatonin. Cell treatment with iron did not alter the
> lysosomal localization of Abeta immunoreactivity. Cell
> treatment with iron (II and III), copper (II), zinc (II)
> and aluminum (III) increased cellular levels of carbonyls.
> However, the effect of zinc on Abeta accumulation in
> cultures was weak, and there were no effects of copper and
> aluminum. The data suggest that iron may be the factor
> that triggers vascular amyloidosis. Lysosomal accumulation
> of APP and Abeta initiates deposition of amyloid in blood
> vessels in Tg2576 mice.
>
> PMID: 14988035 [PubMed - indexed for MEDLINE]
Thanks for the reference.
My logic would reply that since the Transposon Principle
that every Hereditary disease is created or creatable by a
foreign particle whether Transposon or some viruslike
particle. That principle dismisses all other things in the
environment that is not *Nucleic Acid*
So, in other words, iron or even my spell of magnetic
manganese for many months and my spell on aluminum are all
dismissed as causes of Alzheimers, Prion or Parkinsons.
Metals my influence the disease progression but according to
the Transposon Principle, only Nucleic Acids can recreate
the Hereditary disease, not some metal.
So the metals may influence but not cause the disease.
Alzheimers, Prion, and Parkinsons collectively are caused
75% in all cases by the body's own genetics of
inheritance. The other 25% of cases are caused by the
environment and the only thing according to the Transposon
Principle that can recreate these hereditary diseases is
some form of Nucleic Acid. Whether a transposon or
bacteria or viruslike particle.
I can sympathize with those authors desire to implicate
metals in the environment for I spent some considerable time
myself on the issue of whether metals can cause Alzheimers
Prion or Parkinsons and with the Transposon Principle, the
logic says that since it is fact that these 3 are Hereditary
diseases would dismiss metals as causative agents. They
maybe influencing agents in speeding up the disease but not
causative agents. The complement of Hereditary disease is a
Nucleic Acid in the environment such as Transposons or
viruslike particles or bacteria etc--- some form of nucleic
acid is the compliment to hereditary disease.
Archimedes Plutonium www.archimedesplutonium.com
www.iw.net/~a_plutonium whole entire Universe is just one
big atom where dots of the electron-dot-cloud are galaxies
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