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would david rind or jim chinnis comment on the following?
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eml
medicine forum Guru Wannabe


Joined: 12 Jun 2005
Posts: 135

PostPosted: Tue Jul 18, 2006 2:12 pm    Post subject: would david rind or jim chinnis comment on the following? Reply with quote

Northwestern University


Posted: July 6, 2006


Variations In Detoxifying Genes Linked To Lou Gehrig's Disease
Genetic variations in three enzymes that detoxify insecticides and
nerve gas agents as well as metabolize cholesterol-lowering statin
drugs may be a risk factor for developing sporadic amyotrophic lateral
sclerosis (ALS, or Lou Gehrig's disease), and possibly responsible for
a reported twofold increased risk of ALS in Gulf War veterans.


These findings, from a study led Teepu Siddique, M.D., and colleagues
at Northwestern University, open the door to investigating
gene-environment interactions as a cause of ALS and other illnesses and



to the development of molecular targets for specific treatments. The
study was published in the August 22 online issue (available now) of
the journal Neurology.


Siddique is Les Turner ALS Foundation/Herbert C. Wenske Professor,
Davee Department of Neurology and Clinical Neurosciences, professor of
cell and molecular biology and director of the Neuromuscular Disorders
Program at Northwestern University Feinberg School of Medicine.


ALS is a complex neurodegenerative disorder of the motor neurons that
results in muscle weakness, difficulty speaking, swallowing and
breathing and eventual total paralysis and death generally within five
years.


In 1993 Siddique and collaborators determined that mutations in a gene
known as SOD1 account for 20 percent of familial, or inherited, ALS (2
percent of all cases of ALS). However, the cause of sporadic ALS is
still unknown.


In earlier research Siddique and other researchers hypothesized that
sporadic ALS is modulated by variations in multiple genes interacting
with each other and environmental exposures.


The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are
located on chromosome 7q21.3, code for the production of detoxifying
enzymes involved in the metabolism of a variety of drugs,
organophosphate insecticides, such as parathion, diazinon and
chlorpyrifos, and nerve gas agents such as sarin.


Previous research described a possible twofold increased risk for
developing ALS in veterans of the Gulf War, indicating a war-related
environmental exposure to organophosphates and sarin in genetically
susceptible individuals as a possible cause.


PON gene cluster variants have previously been associated with other
neurodegenerative and vascular disorders, including Alzheimer's
disease, Parkinson's disease, coronary artery disease and stroke.


Although the Northwestern DNA study samples were not analyzed for
inclusion of Gulf War veterans, Siddique and co-researchers found
significant evidence that gene variations (polymorphisms) on the
chromosome region encompassing PON2-PON3 were strongly associated with
sporadic ALS.


"Thus, single nucleotide polymorphism genotyping in the intergenic
regions of the PON gene cluster, and replication, gene expression,
gene-gene interaction and PON serum/enzymatic studies may help
elucidate the complexity of PON cluster association with ALS,"
Siddique said.


Siddique hopes to study DNA samples from Gulf War veterans with
increased incidence of sporadic ALS and has applied for their DNA from
the Veterans Administration collection.


Collaborating with Siddique on this research were Mohammad Saeed, M.D.;



Nailah Siddique; Wu-Yen Hung; Elena Usacheva; Erdong Liu, M.D.; Robert
L. Sufit, M.D.; Scott L. Heller, M.D., Northwestern University Feinberg



School of Medicine; Jonathan L. Haines, Vanderbilt University Medical
Center; and Margaret Pericak-Vance, Duke University Medical Center.


This study was supported by grants from the National Institute of
Neurological Disorders and Stroke; Les Turner ALS Foundation; V. E.
Schaff ALS Research Trust; Wenske Foundation; Harold Post
Professorship; Les Turner ALS Foundation/Herbert C. Wenske Foundation
Professorship; Falk Foundation Fund; and The David C. Asselin M.D.,
Memorial Fund.
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Jim Chinnis
medicine forum Guru


Joined: 30 Apr 2005
Posts: 1030

PostPosted: Thu Jul 20, 2006 1:37 am    Post subject: Re: would david rind or jim chinnis comment on the following? Reply with quote

I found this very interesting and I read it carefully. Unfortunately, I have
no expertise in this area. I'll only say that it looks promising for more
research.

Thanks for the post.

Jim

"eml" <mmlevy46@hotmail.com> wrote in part:

Quote:
Northwestern University


Posted: July 6, 2006


Variations In Detoxifying Genes Linked To Lou Gehrig's Disease
Genetic variations in three enzymes that detoxify insecticides and
nerve gas agents as well as metabolize cholesterol-lowering statin
drugs may be a risk factor for developing sporadic amyotrophic lateral
sclerosis (ALS, or Lou Gehrig's disease), and possibly responsible for
a reported twofold increased risk of ALS in Gulf War veterans.


These findings, from a study led Teepu Siddique, M.D., and colleagues
at Northwestern University, open the door to investigating
gene-environment interactions as a cause of ALS and other illnesses and



to the development of molecular targets for specific treatments. The
study was published in the August 22 online issue (available now) of
the journal Neurology.


Siddique is Les Turner ALS Foundation/Herbert C. Wenske Professor,
Davee Department of Neurology and Clinical Neurosciences, professor of
cell and molecular biology and director of the Neuromuscular Disorders
Program at Northwestern University Feinberg School of Medicine.


ALS is a complex neurodegenerative disorder of the motor neurons that
results in muscle weakness, difficulty speaking, swallowing and
breathing and eventual total paralysis and death generally within five
years.


In 1993 Siddique and collaborators determined that mutations in a gene
known as SOD1 account for 20 percent of familial, or inherited, ALS (2
percent of all cases of ALS). However, the cause of sporadic ALS is
still unknown.


In earlier research Siddique and other researchers hypothesized that
sporadic ALS is modulated by variations in multiple genes interacting
with each other and environmental exposures.


The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are
located on chromosome 7q21.3, code for the production of detoxifying
enzymes involved in the metabolism of a variety of drugs,
organophosphate insecticides, such as parathion, diazinon and
chlorpyrifos, and nerve gas agents such as sarin.


Previous research described a possible twofold increased risk for
developing ALS in veterans of the Gulf War, indicating a war-related
environmental exposure to organophosphates and sarin in genetically
susceptible individuals as a possible cause.


PON gene cluster variants have previously been associated with other
neurodegenerative and vascular disorders, including Alzheimer's
disease, Parkinson's disease, coronary artery disease and stroke.


Although the Northwestern DNA study samples were not analyzed for
inclusion of Gulf War veterans, Siddique and co-researchers found
significant evidence that gene variations (polymorphisms) on the
chromosome region encompassing PON2-PON3 were strongly associated with
sporadic ALS.


"Thus, single nucleotide polymorphism genotyping in the intergenic
regions of the PON gene cluster, and replication, gene expression,
gene-gene interaction and PON serum/enzymatic studies may help
elucidate the complexity of PON cluster association with ALS,"
Siddique said.


Siddique hopes to study DNA samples from Gulf War veterans with
increased incidence of sporadic ALS and has applied for their DNA from
the Veterans Administration collection.


Collaborating with Siddique on this research were Mohammad Saeed, M.D.;



Nailah Siddique; Wu-Yen Hung; Elena Usacheva; Erdong Liu, M.D.; Robert
L. Sufit, M.D.; Scott L. Heller, M.D., Northwestern University Feinberg



School of Medicine; Jonathan L. Haines, Vanderbilt University Medical
Center; and Margaret Pericak-Vance, Duke University Medical Center.


This study was supported by grants from the National Institute of
Neurological Disorders and Stroke; Les Turner ALS Foundation; V. E.
Schaff ALS Research Trust; Wenske Foundation; Harold Post
Professorship; Les Turner ALS Foundation/Herbert C. Wenske Foundation
Professorship; Falk Foundation Fund; and The David C. Asselin M.D.,
Memorial Fund.
--

Jim Chinnis Warrenton, Virginia, USA
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David Rind
medicine forum Guru Wannabe


Joined: 02 May 2005
Posts: 205

PostPosted: Thu Jul 20, 2006 3:59 pm    Post subject: Re: would david rind or jim chinnis comment on the following? Reply with quote

Jim Chinnis wrote:
Quote:
I found this very interesting and I read it carefully. Unfortunately, I have
no expertise in this area. I'll only say that it looks promising for more
research.

Thanks for the post.

Jim

For some reason I didn't see the original post in this thread, only Jim
Chinnis' reply.

The article is really preliminary. People are finding gene linkages all
the time that don't really turn out to mean anything.

I can't claim any particular knowledge or expertise in this specific
area (genes associated with sporadic ALS), but I would not make much of
this report until there is future research.

Once you find an association, you can often come up with some theory to
show why that association might explain some observed fact. I just don't
find this article very convincing.

--
David Rind
drind@caregroup.harvard.edu
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Susan
medicine forum Guru


Joined: 05 May 2005
Posts: 932

PostPosted: Thu Jul 20, 2006 9:27 pm    Post subject: Re: would david rind or jim chinnis comment on the following? Reply with quote

x-no-archive: yes


David Rind wrote:

Quote:
For some reason I didn't see the original post in this thread, only Jim
Chinnis' reply.

The article is really preliminary. People are finding gene linkages all
the time that don't really turn out to mean anything.

I can't claim any particular knowledge or expertise in this specific
area (genes associated with sporadic ALS), but I would not make much of
this report until there is future research.

Once you find an association, you can often come up with some theory to
show why that association might explain some observed fact. I just don't
find this article very convincing.


So, here's a possibly rilly, rilly dumb question from a lay person: is
it possible that allegedly genetically linked illnesses are really the
result of similar environmental exposures to pathogens or other
environmental disruptors of some sort?

I think of neuroborreliosis, as a model, for example. Fallon has
described bipolar disorder as the single presenting manifestation.
Families live and have tick exposure together. Or asymptomatic mothers
may carry their children and pass along congenital infections, which is
known to happen with Lyme and ehrlichiosis, for example.

Why not other CNS infections, viral, parasitic and/or bacterial that we
haven't connected to the outcomes?

Since borrelia are known to modulate host immunity, can some of these
changes alter host genetics in any way?

Susan
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Jim Chinnis
medicine forum Guru


Joined: 30 Apr 2005
Posts: 1030

PostPosted: Fri Jul 21, 2006 12:55 am    Post subject: Re: would david rind or jim chinnis comment on the following? Reply with quote

Susan <nevermind@nomail.com> wrote in part:

Quote:
x-no-archive: yes


David Rind wrote:

For some reason I didn't see the original post in this thread, only Jim
Chinnis' reply.

The article is really preliminary. People are finding gene linkages all
the time that don't really turn out to mean anything.

I can't claim any particular knowledge or expertise in this specific
area (genes associated with sporadic ALS), but I would not make much of
this report until there is future research.

Once you find an association, you can often come up with some theory to
show why that association might explain some observed fact. I just don't
find this article very convincing.


So, here's a possibly rilly, rilly dumb question from a lay person: is
it possible that allegedly genetically linked illnesses are really the
result of similar environmental exposures to pathogens or other
environmental disruptors of some sort?

Here's a rilly, rilly dumb answer from a lay person: Sure. I assume you mean
that a genetic phenotype makes one capable of developing multiple diseases
if one is exposed to a pathogen, toxin, or such.

Quote:
I think of neuroborreliosis, as a model, for example. Fallon has
described bipolar disorder as the single presenting manifestation.
Families live and have tick exposure together. Or asymptomatic mothers
may carry their children and pass along congenital infections, which is
known to happen with Lyme and ehrlichiosis, for example.

It would be hard to demostrate any genetic susceptibilty working within a
family.

Quote:
Why not other CNS infections, viral, parasitic and/or bacterial that we
haven't connected to the outcomes?

Why not?

Quote:
Since borrelia are known to modulate host immunity, can some of these
changes alter host genetics in any way?

I doubt it.

(It's quiet here, so I thought I'd play geneticist and infectious disease
expert.)
--
Jim Chinnis Warrenton, Virginia, USA
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Susan
medicine forum Guru


Joined: 05 May 2005
Posts: 932

PostPosted: Fri Jul 21, 2006 2:05 pm    Post subject: Re: would david rind or jim chinnis comment on the following? Reply with quote

x-no-archive: yes

Jim Chinnis wrote:

Quote:
Here's a rilly, rilly dumb answer from a lay person: Sure. I assume you mean
that a genetic phenotype makes one capable of developing multiple diseases
if one is exposed to a pathogen, toxin, or such.

No, actually. I meant is the interpretation of the reason for the
incidence incorrect. That shared exposures are the cause, rather than
genetics.

Quote:
(It's quiet here, so I thought I'd play geneticist and infectious disease
expert.)
--

Yeah, I thought I'd play rilly, rilly dumb. ;-)

Susan
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