Newer posts have decided that morphology does not connect to gluten and casein. Rather what all these infections have in common is the ability to cross barriers: the intestine and the Blood brain barrier.
http://angelabiggs.blogspot.com/2015/03/infections-that-break-tight-junction.html
Several autoimmune diseases have gluten and casein sensitivities. This could be due to morphology shifting. For fungus that means yeast to mold. For bacteria: rod to string like lengths.
Schizophrenia and t.gondii
http://www.ncbi.nlm.nih.gov/pubmed/24413543
T. gondi has the LON enzyme http://www.uniprot.org/uniprot/B6K9X1
I didn't find t. gondi to have morphology switching so I do not know what we are looking at.
Schizophrenia has the gluten sensitivity: http://www.ncbi.nlm.nih.gov/pubmed/22446142
So something is happening:
T. gondii morphology may not be altered by LON rather the ability of it and other parasites to invade cells. Here is a paper talking about serine proteases and cystene proteases inhibition preventing cell invasion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1797762
http://aac.asm.org/content/43/6/1358.full
What I am considering is the PVM, parasitiophorous vauole membrane, is a threadlike extension that T.gondii creates during infection. Could this thread like system be sensitive to gluten and casein like the mold form of a fungus? Is the LON enzyme involved here?
The PVM appears to be the specialized invasion tool
http://www.ncbi.nlm.nih.gov/pubmed/18512349
LON is casein sensitive (and I believe with the similar amino acid sequence gluten sensitive too). This could explain the gluten sensitive of schizophrenia. The parasite is inhibited by gluten...and may react.
T.gondii appears to cross the blood brain barrier.
http://www.ncbi.nlm.nih.gov/pubmed/13678858
Lets consider that maybe it doesn't cross the BBB. what if it is only when the antibodies get across the BBB when a mycobacteria or strep creates a hole? but then...if you read on...i had previously found that gluten sensitive occur after mice were infected with t. gondi. If only t.gondi was dimorphic...then this would make sense to me.
By antibodies i am referring to my earlier post of pan/apple domains and receptors. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030169
THE OTHER POSSIBILITY:
There exists more then one type of schizophernia. The Ovarian teratoma tumor form generates NMDA receptor antibodies just like t.gondii but the tumor's antibodies can't cross the BBB (blood brain barrier) unless another infection which is gluten and casein sensitive does.
So autoimmune schizophrenia has these possibilities:
t.gondii followed by a virus like herpes virus 8
or
tumor with BBB crossing-infection then the herpes virus
This could be why all cases are not gluten casein sensitive. The most likely infection would be mycobacterias because some schizophrenia has been associated with MS and psoriasis...which i have linked to mycobacterias!
http://asdresearchinitiative.wordpress.com/2014/02/22/schizophrenia-greater-risk-of-other-autoimmune-diseases/
Mycobacterias are gluten and casein sensitive. Changing morphology with them.
Previous thoughts on Schizophrenia:
Here are the references and thoughts I have on Schizophrenia.
First schizophrenia can be autoimmune in that antibodies generated against the NMDA receptor of the brain can cause Hallucinations
ref: Antibody mediated encephalitis: a treatable cause of schizophrenia
British Journal of Psychiatry 2012
200:92-94
The bacteria infection T. gondii can be linked to the NMDA receptor through pan/apple domains.
T. gonii has pan/apple on it.
ref: A novel pan/apple domain containing protein for Toxoplasma gondii: characterization and receptor indentification
PLoS
Schizophrenia has T. gondi antibodies
ref: Antibodies to Toxoplasma gondii in patients with Schizophrenia.
schizophrenia bulletin vol 33 no 3 pp 729-736
In our body when blood clots are degraded, plasminogen which has the PAN sequence in it, is activated by tPA (tissue plasminogen activator)
t-PA binds not just plasminogen but the NMDA receptor. Does this mean the NMDA receptor has a PAN/apple domain?
ref: t-PA is a new ligand of NMDA receptor
JBC papers Sept 23. 2004
If antibodies develop against T.gondii included the pan/apple domain does this mean the antibodies might also bind the NMDA receptor?
Now I can apply my autoimmune hypothesis to it. A dimorphic infection triggers an autoantibody precursor stage which then progresses into the the disease following a viral infection cross targeting event.
The strain ME49 of T.gondi contains more then one morphology. Both spherical vesicles and tubular elements are found.
The change in morphology might be just like e.coli using LON. T.gondii appears to trigger a gluten response....but perhaps in this case gluten is inhibiting the "root like" PVM?
ref: Anti-gluten immune response following toxoplasma gondii infection in mice.
PLo S Nov 29 2012 , 7 (11)e50991
Schizophrenia has been associated with gluten and casein
ref. The gluten connection: the association between schizophrenia and celiac disease.
Acta Psychiatr Scand 2006 Feb: 113(2): 82-90
ref: Specific IgA antibody increases in Schizophrenia
1995 society of biological psychiatry
So we have the bacteria creating the antibodies where the immune system is looking at the neuron's receptor but then we need the cross-targeting virus. The virus would infect the inside of the neurons bearing these receptors thus causing the immune system to have verification of the neuron as a target. Cross targeting would push one into attacking one's self....making schizophrenia an autoimmune disease.
Retroviruses were linked to schizophrenia patients in 2001in Germany. An example of a retroviruses is the Borna virus...a virus which infects the central nervous system.
OR a herpes which infects nerves could be involved. Herpes virus 8 and 2 are suspects. Could the this virus trigger the cross targeting? The t.gondii antibodies marking the outside of the neuron and the herpesvirus 8 marking the inside of the neurons?
herpes 2
http://www.ncbi.nlm.nih.gov/pubmed/15319094
herpes 8
http://www.ncbi.nlm.nih.gov/pubmed/24560611
Only after cross-targeting would the autoimmune form of schizophrenia develop...but this is a hypothesis and this is just something to consider. It is not proven.
Schizophrenia, infections, and autoimmune disease genetic predisposition (evidence schizophrenia is autoimmune like celiac disease and autism?)
http://www.ncbi.nlm.nih.gov/pubmed/24557043
http://www.ncbi.nlm.nih.gov/pubmed/22193673
http://www.ncbi.nlm.nih.gov/pubmed/16513876
http://angelabiggs.blogspot.com/2015/03/infections-that-break-tight-junction.html
Several autoimmune diseases have gluten and casein sensitivities. This could be due to morphology shifting. For fungus that means yeast to mold. For bacteria: rod to string like lengths.
Schizophrenia and t.gondii
http://www.ncbi.nlm.nih.gov/pubmed/24413543
T. gondi has the LON enzyme http://www.uniprot.org/uniprot/B6K9X1
I didn't find t. gondi to have morphology switching so I do not know what we are looking at.
Schizophrenia has the gluten sensitivity: http://www.ncbi.nlm.nih.gov/pubmed/22446142
So something is happening:
T. gondii morphology may not be altered by LON rather the ability of it and other parasites to invade cells. Here is a paper talking about serine proteases and cystene proteases inhibition preventing cell invasion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1797762
http://aac.asm.org/content/43/6/1358.full
What I am considering is the PVM, parasitiophorous vauole membrane, is a threadlike extension that T.gondii creates during infection. Could this thread like system be sensitive to gluten and casein like the mold form of a fungus? Is the LON enzyme involved here?
The PVM appears to be the specialized invasion tool
http://www.ncbi.nlm.nih.gov/pubmed/18512349
LON is casein sensitive (and I believe with the similar amino acid sequence gluten sensitive too). This could explain the gluten sensitive of schizophrenia. The parasite is inhibited by gluten...and may react.
T.gondii appears to cross the blood brain barrier.
http://www.ncbi.nlm.nih.gov/pubmed/13678858
Lets consider that maybe it doesn't cross the BBB. what if it is only when the antibodies get across the BBB when a mycobacteria or strep creates a hole? but then...if you read on...i had previously found that gluten sensitive occur after mice were infected with t. gondi. If only t.gondi was dimorphic...then this would make sense to me.
By antibodies i am referring to my earlier post of pan/apple domains and receptors. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030169
THE OTHER POSSIBILITY:
There exists more then one type of schizophernia. The Ovarian teratoma tumor form generates NMDA receptor antibodies just like t.gondii but the tumor's antibodies can't cross the BBB (blood brain barrier) unless another infection which is gluten and casein sensitive does.
So autoimmune schizophrenia has these possibilities:
t.gondii followed by a virus like herpes virus 8
or
tumor with BBB crossing-infection then the herpes virus
This could be why all cases are not gluten casein sensitive. The most likely infection would be mycobacterias because some schizophrenia has been associated with MS and psoriasis...which i have linked to mycobacterias!
http://asdresearchinitiative.wordpress.com/2014/02/22/schizophrenia-greater-risk-of-other-autoimmune-diseases/
Mycobacterias are gluten and casein sensitive. Changing morphology with them.
Previous thoughts on Schizophrenia:
Here are the references and thoughts I have on Schizophrenia.
First schizophrenia can be autoimmune in that antibodies generated against the NMDA receptor of the brain can cause Hallucinations
ref: Antibody mediated encephalitis: a treatable cause of schizophrenia
British Journal of Psychiatry 2012
200:92-94
The bacteria infection T. gondii can be linked to the NMDA receptor through pan/apple domains.
T. gonii has pan/apple on it.
ref: A novel pan/apple domain containing protein for Toxoplasma gondii: characterization and receptor indentification
PLoS
Schizophrenia has T. gondi antibodies
ref: Antibodies to Toxoplasma gondii in patients with Schizophrenia.
schizophrenia bulletin vol 33 no 3 pp 729-736
In our body when blood clots are degraded, plasminogen which has the PAN sequence in it, is activated by tPA (tissue plasminogen activator)
t-PA binds not just plasminogen but the NMDA receptor. Does this mean the NMDA receptor has a PAN/apple domain?
ref: t-PA is a new ligand of NMDA receptor
JBC papers Sept 23. 2004
If antibodies develop against T.gondii included the pan/apple domain does this mean the antibodies might also bind the NMDA receptor?
Now I can apply my autoimmune hypothesis to it. A dimorphic infection triggers an autoantibody precursor stage which then progresses into the the disease following a viral infection cross targeting event.
The strain ME49 of T.gondi contains more then one morphology. Both spherical vesicles and tubular elements are found.
The change in morphology might be just like e.coli using LON. T.gondii appears to trigger a gluten response....but perhaps in this case gluten is inhibiting the "root like" PVM?
ref: Anti-gluten immune response following toxoplasma gondii infection in mice.
PLo S Nov 29 2012 , 7 (11)e50991
Schizophrenia has been associated with gluten and casein
ref. The gluten connection: the association between schizophrenia and celiac disease.
Acta Psychiatr Scand 2006 Feb: 113(2): 82-90
ref: Specific IgA antibody increases in Schizophrenia
1995 society of biological psychiatry
So we have the bacteria creating the antibodies where the immune system is looking at the neuron's receptor but then we need the cross-targeting virus. The virus would infect the inside of the neurons bearing these receptors thus causing the immune system to have verification of the neuron as a target. Cross targeting would push one into attacking one's self....making schizophrenia an autoimmune disease.
Retroviruses were linked to schizophrenia patients in 2001in Germany. An example of a retroviruses is the Borna virus...a virus which infects the central nervous system.
OR a herpes which infects nerves could be involved. Herpes virus 8 and 2 are suspects. Could the this virus trigger the cross targeting? The t.gondii antibodies marking the outside of the neuron and the herpesvirus 8 marking the inside of the neurons?
herpes 2
http://www.ncbi.nlm.nih.gov/pubmed/15319094
herpes 8
http://www.ncbi.nlm.nih.gov/pubmed/24560611
Only after cross-targeting would the autoimmune form of schizophrenia develop...but this is a hypothesis and this is just something to consider. It is not proven.
Schizophrenia, infections, and autoimmune disease genetic predisposition (evidence schizophrenia is autoimmune like celiac disease and autism?)
http://www.ncbi.nlm.nih.gov/pubmed/24557043
http://www.ncbi.nlm.nih.gov/pubmed/22193673
http://www.ncbi.nlm.nih.gov/pubmed/16513876
