Thursday, February 27, 2014

Alzheimer's puzzle: Is the mitochondria damaged by herpes or diacetyl and does this cause amyloid plagues? in the lungs or the brain?

This post specific is not focused on an autoimmune disease but Alzheimer's.  I am looking at the  notion of amyloid plaques and the mitochondria.  A continuation of the the Alzheimer's and parkinson's posts. Where it is the destruction of the mitochondria that is key to the development of the diseases.

amyloidosis and the mitochondria (genetic)
http://www.ncbi.nlm.nih.gov/pubmed/19018796
http://www.nature.com/ejhg/journal/v18/n8/full/ejhg201036a.html

amyloidosis and mycobacteria
http://www.deepdyve.com/lp/elsevier/reactive-amyloidosis-in-a-patient-with-mycobacterium-simiae-pulmonary-XcACtyHSzn
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC459761/

type 2 diabetes and mycobacteria
http://www.sciencedirect.com/science/article/pii/S0306987705002045

amyloidosis, Karposi's, and herpes (non genetic)
http://www.ncbi.nlm.nih.gov/pubmed/10842716
http://www.ncbi.nlm.nih.gov/pubmed/498024 
herpes virus 8 with karposi? Alzheimer's is connected to herpes virus 1

Herpes destroys host's mitochondrial DNA
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1796774/
the herpes virus drives the mitochondria down the nerve root to other nerves!
http://www.sciencedirect.com/science/article/pii/S1931312812001047 
herpes causes amyloid
http://www.ncbi.nlm.nih.gov/pubmed/17980964
http://www.ncbi.nlm.nih.gov/pubmed/16109164
 
 Herpes and Alzheimer's Patients
http://www.ncbi.nlm.nih.gov/pubmed/18973185
http://www.ncbi.nlm.nih.gov/pubmed/22216291
http://www.ncbi.nlm.nih.gov/pubmed/18982063
http://www.ncbi.nlm.nih.gov/pubmed/23261465


in Cardiac tissue? similar to nerves?
http://www.ncbi.nlm.nih.gov/pubmed/24182678 

Popcorn diacetyl and bronchiolitits obliterans....are amyloids there?
http://www.ncbi.nlm.nih.gov/pubmed/12151470
http://www.ncbi.nlm.nih.gov/pubmed/17541015
http://www.ncbi.nlm.nih.gov/pubmed/17464280
http://www.ncbi.nlm.nih.gov/pubmed/18772104
 http://www.livescience.com/22308-new-microwave-popcorn-chemical-linked-to-lung-damage.html

http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17541015&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVLinkOut 

Renal amyloid after bronchioltitis ?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004490/

At this point  I am looking at or for evidence that herpes or diacetyl destroys the mitochondria causing amyloid plaques in similar ways.

Here is the link to an older post looking at the overlap of Alzheimer's & Parkinson's
http://angelabiggs.blogspot.com/2013/09/alzheimers-parkinsonstourettes-how-do.html 

Genetic forms of Alzheimer's and mitochondria damage (not herpes or diacetyl but mitochondria is key)
http://www.ncbi.nlm.nih.gov/pubmed/24569455 

Mother's of Downsyndrome children have increased risk of Alzheimer's (more evidence of faulty mitochondrias)
http://www.ncbi.nlm.nih.gov/pubmed/7914304
http://www.ncbi.nlm.nih.gov/pubmed/11571320
http://www.ncbi.nlm.nih.gov/pubmed/10402505

Monday, February 24, 2014

Is scleroderma an autoimmune disease caused by cross-targeting?

Cross-targeting of the immune system triggers autoimmunity by layering immune system attacks onto one target.  One viral marking the inside of the target and one visible marking the outside of the target...like a fungus or bacteria.

Epstein barr virus and scleroderma
http://www.ncbi.nlm.nih.gov/pubmed/24164500
http://www.ncbi.nlm.nih.gov/pubmed/24129067

Cryptococcus neoformans and scleroderma
http://www.ncbi.nlm.nih.gov/pubmed/23496879
http://www.ncbi.nlm.nih.gov/pubmed/22381693
this is the fungus found in the droppings of wild birds

Crest syndrome (connective tissue is the target?)
http://en.wikipedia.org/wiki/CREST_syndrome
http://www.ncbi.nlm.nih.gov/pubmed/21956352

What would cause the hardened skin? cryptococcus secretes Mucopolysaccharidoses

https://books.google.com/books?id=eLHQAgAAQBAJ&pg=PA807&lpg=PA807&dq=Cryptococcus+secretes&source=bl&ots=LTAfTTSaQg&sig=5199n_brNSVOVS0e66h6Q_PM7Bs&hl=en&sa=X&ved=0ahUKEwiax62J24TNAhVVO1IKHZ4sDOcQ6AEITjAG#v=onepage&q=Cryptococcus%20secretes&f=false

Mucopolysaccharides are also called glucosaminoglycans and are also found in the fluids that lubricate joints. Glucosaminoglycans are major components of connective tissue like tendons.  Glucosaminoglycans: dermatan sulfate and chondroitin sulfate associate with the collagen of the tendon.

Glucosaminoglycans are increased in scleroderma
http://www.sciencedirect.com/science/article/pii/S0022202X15481126

I had previously connected sjogern's to candida infections and Hashimoto's thyroid.
Here is a personal post from someone who has hashimoto's with scleroderma. Do they have cryptococcus?
http://www.inspire.com/groups/autoimmune-diseases/discussion/hashimotos-rheumatoid-arthritis-scleroderma-i/

I am also looking at nickel allergy and it's relationship to crytococcosis:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697809/
allergy and scleroderma
http://www.inspire.com/groups/scleroderma-foundation/discussion/nickle-exposure-and-scleroderma/

note that cyrptococcus gatti infects the lungs, the skin, the lymph nodes, bones, and joints
while the epstein barr virus (mono) infects primarily lymphatic cells....this could the the area of overlap.

here are posts of people with scleroderma and swollen lymph nodes
http://treato.com/Scleroderma,Swollen+Lymph+Nodes/?a=s 

the lymphatic system and scleroderma
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829123/

Epstein barr can infect any cell with an estrogen receptor so it could be infecting the connective tissue directly too

Tendons and estrogen receptors
http://www.ncbi.nlm.nih.gov/pubmed/20073985

Does this make sense to anyone else out there? Can anyone see what i see?





Friday, February 14, 2014

Myasthenia Gravis Autoimmune disease starts in the thymus

This is an autoimmunity hypothesis for Myasthenia gravis:

Cross-targeting of the immune system triggers autoimmunity by layering immune system attacks on one target. In this case an infection of the thymus overlaps a viral infection of the thymus.  Raising the level of tlr-4 too high?

Possible viral triggers are:

West nile virus and MG
http://www.ncbi.nlm.nih.gov/pubmed/23559196
http://cdn.f1000.com/posters/docs/250566628

epstein-barr and MG
http://www.ncbi.nlm.nih.gov/pubmed/21961056 
http://www.ncbi.nlm.nih.gov/pubmed/20517934

coxsackie and MG?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC514990/

Note these viral infections must infect the target or generate antibodies toward the target.

MG has been associated with RA, lupus and type 1 diabetes so I am looking into mycoplasmas as the infection which may have taken up residence in the thymus (non viral)

specifically M.fermentans
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC415086/

and C. pneumoniae (detected in thymus)
http://www.ncbi.nlm.nih.gov/pubmed/9593019

Tlr-4 and MG
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1603452/

note that this is slightly different then Graves.

Sunday, February 9, 2014

Could naltrexone uncouple the autoimmunity caused by cross-targeting by blocking tlr-4? is tlr-4 the issue?

Cross-targeting is when 2 infections in the same place triggers autoimmune disease. A virus marking the inside of the target and an infection like a bacteria, mycobacteria, fungus, or mycoplasma marking the outside of the target. This is my hypothesis and I am looking into how this would involve tlr-4. ( this may not be the only overlap )

tlr-4 increased and involved with MG
http://www.ncbi.nlm.nih.gov/pubmed/24397961

murine diabetes blocked by tlr-4 suppression
http://www.ncbi.nlm.nih.gov/pubmed/23340441

Dendritic cells sample environment using tlr then talk to both t and b cells (antigen presenting)
http://en.wikipedia.org/wiki/Dendritic_cell

tlr-4 is involved in early steps of pathogen recognition
http://www.ncbi.nlm.nih.gov/pubmed/22240038

tlr-4 & gram negative bacteria
http://en.wikipedia.org/wiki/TLR_4
gram negative bacterias
sutterella
e.coli

strep is gram positive...but strep pyogenes involves tlr-4  (the autoimmune triggering strep)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3067360/

tlr-4 and viruses
http://www.ncbi.nlm.nih.gov/pubmed/23997950
(specifically the flu)
http://www.jimmunol.org/content/178/4/2448.full 

tlr-4 and inflammation/autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/21664961
www.ncbi.nlm.nih.gov/pubmed/17763416
http://link.springer.com/article/10.1007/s12016-013-8402-y

Naltrexone is an antagonist of tlr-4
http://www.ncbi.nlm.nih.gov/pubmed/23062774


Naltrexone is now being used to suppress autoimmune disease
References to be posted. This page is still under construction.
http://www.ncbi.nlm.nih.gov/pubmed/21918649
http://www.ncbi.nlm.nih.gov/pubmed/21256121

http://www.ncbi.nlm.nih.gov/pubmed/21174518
ms
http://www.ncbi.nlm.nih.gov/pubmed/20695007
http://www.ncbi.nlm.nih.gov/pubmed/19041189

cytokine storm and autoimmune? does the overlap of infections cause some degree of this?

cytokine storm and flu
http://www.birdfluhealth.com/taxonomy/term/38


TLR-4 activates 2 pathways the myD88 which leads to inflammation cytokines and the TRIF-dependent side.
The TRIF-dependent side is involved with E.coli infections. 
Note that the Bird (avian) flu involves the myD88 pathway. 

If they are both going though the same TLR-4 the response could be amplified.  At what point does the immune system lose control? here?

Wednesday, February 5, 2014

Can Autism's sutterella cross the blood brain barrier?

If autism is caused by autoimmune cross-targeting and the target is the brain, how do the antibodies get past the blood brain barrier? note that this is not always the case because antibodies against the brain have been found in pregnant mothers crossing the blood brain barrier. I am just trying to figure out if it is just antibody driven as an autoimmune disease or if the infection can move there.

Strep and E.coli infections are able to get past the blood brain barrier and the intestinal barrier.

Invasion of the brain by strep by receptor-ligand
http://www.ncbi.nlm.nih.gov/pubmed/9393798

Invasion of brain by e.coli by receptor-ligand
http://www.ncbi.nlm.nih.gov/pubmed/10496943

Mycobacteria can also break the blood-brain barrier causing a hole by cytoskeleton alterations but it does not use a receptor to get into the host cell. (this reference is a review paper by Kim)
http://www.ncbi.nlm.nih.gov/pubmed/16542662

Here is just Kim's table of what can transverse the blood brain barrier:
http://www.nature.com/nrmicro/journal/v6/n8/fig_tab/nrmicro1952_T1.html

Does sutterella have the ability to cross in the same way?  by receptor- ligands?  It has been found in brain abcesses.....does it know how to cross the barriers?

I am looking for this "ligand" in the genetic code but it doesn't even appear to be elucidated in Strep. They think it is choline related because with out choline virulence is lost.
http://www.ncbi.nlm.nih.gov/pubmed/19433549
Choline immediately makes me think of neurons.....how foreboding.

Once sutterella is infecting the neurons would a measles shot cause them to be targeted?  The cross-targeting would cause the brain cells to be attacked by the immune system seeing not just the infections as the issue but the brain's neurons?

This is based on a ton of assumptions.  First that sutterella is a culprit because it is found in half of autistic kids indicating it's involvement.

This page is still under construction.

I am wondering if:
Classic autism is the maternal antibody driven kind
Childhood disintegrative disorder is the sutterella driven kind.