Could colored letters help dyslexia?

This is not really an autoimmune topic...I just stumbled upon the idea reading up on Asperger's. 

I read an article in the new scientist where an Asperger's patient dealt with the sensory overload of emotion by projecting a color aura.  His mind simplified what he was seeing using color which is probably one of the first neural networks laid down in our minds.

I have heard of minds projecting color before: color-graphemic synesthesia.  Where children who learned their numbers using colored frig magnets had the colors forever automatically projected even on to black type numbers by their minds.  Imagine rainbow phone numbers...much easier to remember.

If one's brain can learn to use colors to overcome sensory overload could this be use this for Dyslexia?  If the shapes of letters are overwhelming could we assign colors to letters when they are learning and overcome the issue? Could their minds eventually project the color and aid them in reading?

It would be a simple program to write on the computer...each letter getting it's own color.  Could someone out there try it? Maybe it could help Dyslexia?

Hopeful
Angela Biggs

NOTE: I am considering that dyslexia maybe connected to ulcerative colitis which has daisy allergies (sometimes including latex which was made from dandelions)

Autoimmune Schizophrenia

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 apears to trigger a gluten response.

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 receptor but then we need the cross-targeting virus. The virus would infect the nerves bearing these receptors thus causing the immune system to have verification of the neuron, brain cell, as an issue...cross targeting would push one into attacking one's self. 

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. 

Only then would the autoimmune form of schizophrenia develop...but this is a hypothesis and this is just something to consider. It is not proven.

Multiple sclerosis and cross-targeting autoimmunity

Autoimmune hypothesis:

Stage one
A bacterial or mycobacterial infection creates  a hyper state of auto-antibodies through morphology changes or pigment changes. The infection appears to disappear and reappear to our immune system.

Stage two
A virus infection causes cross-targeting by infecting or creating antibodies that overlap the existing ones from stage one.

Multiple sclerosis

Stage one
Multiple sclerosis is associated with eczema. A meningitis type of bacteria like the staphylcoccus aureus has been associated with eczema.  (Staph produces yellow pigment when exposed to milk or egg which explains the eczema allergies)  It is possible this bacteria produces antibodies against the nervous system but not does not succeed in causing meningitis.  These antibodies are the first to target nerves.

Reference: Varicella, ephemeral breastfeeding and eczema as risk factors for multiple sclerosis in Mexicans.  Acta Neurol Scand 2002 105, 88-94 http://www.ncbi.nlm.nih.gov/pubmed/11903117

Donald Leung of National jewish has isolated staph from some eczema but has not claimed that it is the cause.

Staph and MS (specific type of staph is involved)
http://www.ncbi.nlm.nih.gov/pubmed/21212089


Bacterial toxins and MS
http://www.direct-ms.org/pdf/InfectiousMS/Bacterial%20toxins%20MS%2007.pdf

C. pneumoniae  is another possible culprit
http://www.medscape.com/viewarticle/574944_3

It can infect the CNS
http://www.medscape.com/viewarticle/574944_3 
http://www.ncbi.nlm.nih.gov/pubmed/10401775

NOTE: it is not the exact infection so much as the location of the infection marking the outside of the target nerve that is significant.

Mycobacteria and MS
 http://www.ncbi.nlm.nih.gov/pubmed/21409957
http://www.ncbi.nlm.nih.gov/pubmed/14616302
also
http://www.ncbi.nlm.nih.gov/pubmed/15150306 and http://rheumatology.oxfordjournals.org/content/39/8/930.full (which I think psoriatic athritis and psoriasis are mycobacterias)

note that the mycobacteria bind to the nerves : http://www.pnas.org/content/96/17/9857 
using the laminin which the myelin forms on http://www.ncbi.nlm.nih.gov/pubmed/10576890

Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack. A virus as infecting the inside of a cell marks the inside for immune system attack.

Stage 2
 A virus that infects the nerves such as Herpes Zoster, shingles, causes the immune system to cross target the nerves.

References:
 Increased risk of multiple sclerosis following herpers zoster: A nationwide, population based study.
http://www.ncbi.nlm.nih.gov/pubmed/21653524

Herpes Zoster and Multiple sclerosis
JID 2011:204, 177-178
http://www.ncbi.nlm.nih.gov/pubmed/23035074


I have also been considering that fact that HERVs could act as the virus causing cross-targeting but i do not have enough information. Cross-targeting or something else...i am not sure.
  http://www.ncbi.nlm.nih.gov/pubmed/15782388

Again this is not proven it is a hypothesis. Does anyone see the pattern I see?

Lupus: mycoplasmas were linked to RA in 1974. Could lupus be cross-targeting autoimmunity with mycoplasmas andepstein barr virus? (mono)

Lupus

30% have photo sensitivity
We know from genetic Heme disorders that excess porphyrins cause photosensitivity. So is something happening to the red blood cells?
 
81 % have fatigue with anemia
This would support the notion that somehow Lupus is a blood autoimmune disease. 

Epstein barr virus, aka mono, has been associated with Lupus. EBV infects the B cells of the immune system.  If you consider my cross targeting theory of autoimmunity we need to find the culprit that created the antibodies that started the immune system looking at the B cells.

B cells are not red blood cells but both of these are in the bloodstream.  I would think that we are looking at some kind of bacterial blood infection which is consuming the cells of the blood stream indiscriminately, red and white cells.

Lupus with antibodies against red blood cells
http://www.ncbi.nlm.nih.gov/pubmed/10723973

Could blood infections in Lupus be the initial instigator?  Which is then triggered by mono compromising the immune system by making it attack itself to a degree? Going everywhere blood goes.

Looking at mycoplasmas.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1006269/

Fibromyalgia tends to be nightshade sensitvie or triggered.  I have no evidence to substantiate this notion but I hope people look and make sure this is not what is happening. 

Xanthomonas is a bacteria that infects nightshade plants.  They use butyrolactones as signalling molecules between them.

In our bodies butyrolactones is converted to GHB which is then converted to GABA.  GABA is the neurotransmitter. How our nerves talk to each other. 

A form of Xanthomonas has been found to infect the respiratory tract of people and is considered a new bacterial genus: named Stenotrophomonas. 

My notion is actualLy a question: does the Stentorophomonas still make these signalling molecules when exposed to nightshades like a bell pepper when it infects us? Could this explain the painful reactions to nightshades that Fibromyalgia patients have? Are antibodies directed at the butyrolactones causing antibodies to GABA thus causing one's own immune system to attack our nerves?

Just a thought. Has anyone looked at this?

cross targeting causes autoimmunity

Hypothesis:

Cross targeting is when 2 different infections cause antibodies to target the same self protein.  Often times the first infection, a bacterial or fungal infection causes a build up of antibodies including the molecular mimicry type antibodies, the auto-antibodies.   For example,  E.coli breaking down red blood cells makes bilirubin like the liver. It is easy to imagine antibodies would start flagging the liver for attack but the body's immune system holds back.   Then a second infection creates a similar antibody by infecting the organ itself, like hepatitis C.  It is this cross targeting that I believe causes the development of autoimmune disease.  When the immune system now has another reason to attack one's own body, in this example the liver resulting in autoimmune liver disease.

Sutterella the bacterial culprit of autism has an omega fat coat much like our nerves, antibodies against nerves develop, then the measles vaccine which is known to cause antibodies against nerves...would cause cross targeting of the immune system.

Schizophrenia hallucinations could be T.gondi  induced through PAN/apple domains toward the NMDA receptor and i believe that the Bona virus or herpes virus would have to infect the brain cell to trigger the autoimmune disease. That the immune system itself causes the schizophrenia by attacking the receptor.  (the ME49 strain of T. gondi is dimorphic) 

Hypothesis: it is not one infection that induces autoimmune disease but the cross targeting of 2.  A bacterial/fungal followed by a secondary viral one...or vaccine.

Added thoughts on March 6:  After a flu epidemic cases of Type 1 diabetes increases. The flu virus incubates and divides in the pancreas (according to Italian turkeys).
 http://www.ncbi.nlm.nih.gov/pubmed/?term=Ilaria+Capua+pancreas 
Swine flu H3n2 is one of the viruses that would infect the pancreas and cause diabetes.

autoimmune mechanism

The conundrum of how autoimmune diseases develop can be solved if we have a decent mechanism to work with.  Focusing on celiac disease which is now the most common autoimmune disease effecting 1.5 million Americans and then by looking at the areas of overlap that exists with other autoimmune diseases we can illuminate and then validate a basic core autoimmune mechanism.  The right mechanism will be applicable to all autoimmune diseases.  

The mechanism needs to explain the 2 stages of autoimmunity: the antibody precursor stage and then the viral induced attack stage where self-organs are damaged.

 In the case of celiac disease the proteins gluten and casein have been shown to induce several antibodies. Induced antibodies are against these polypeptides and to various self-proteins, autoantibodies.  Why are antibodies developing?   Removal of said proteins calms the immune system and removes the risk of autoimmune disease development but how could these proteins cause this? The proteins must be acting on something which then elicits an immune response. Our immune system is geared to respond to infection.  Can we reasonable place an infection between these proteins and our immune system?

There is a considerably high association between urinary tract infections and patients with celiac disease. Most urinary tract infections, 80%, are caused by E.coli.   The strain B of e.coli has a filamentous form and a rod form.  The filamentous form of this e.coli can be triggered by casein hydrolysate. In other words, casein induces a morphological change in e.coli.   The enzyme in E.coli responsible for the morphology change was named LONG or LON for short. It is a serine protease which has been shown to interact with casein. Is it not feasible that our immune system could be reacting to the morphology change of e.coli? Could gluten which has such a similar protein structure to casein act on LON and also cause a morphology change?

With an infection changing morphology it seems possible that some people’s immune system might become confused. Their immune system could have the genetic predisposition to grab too quickly the triggers gluten and casein while the infection evades detection disappearing only then later to reappear on their immune system radar.   The HLA of genetic predisposition is the t-cell mailbox which has been shown to have a high affinity for gluten and casein.  Their immune systems are acting too quickly and missing the real culprit E.coli.  The resulting situation is an infection in hiding and a hyper looking immune system. 

The second stage is the viral provoker.  It has long been a mystery, why some people develop an autoimmune disease after a viral infection while others do not. George Eisenbarth showed that before the virus the vulnerable patients already had autoantibodies. In the case of type one diabetes antibodies existed against insulin long before the development of the disease. Insulin is normally made by our pancreas.  

If e.coli has something that could cause the molecular mimicry of insulin this could make sense. Celiac patients often progress to type one diabetes.

Then the virus, like the flu virus which inflames and incubates in the pancreas itself could cause a crosstalk target. In other words the immune system which is already looking for a hidden infection is given a second reason to attack the pancreas by the virus.  Cross targeting of the viral and bacterial settings of the immune system could be the key to the development of autoimmune disease. Pandemics of flu are often followed by new cases of type one diabetes. Coxsackie virus also causes severe pancreatitis which could also cause the cross targeting. 

Let us consider autoimmune liver disease which also overlaps celiac disease.  E.coli when it gets into the blood stream and breaks down red blood cells produces bilirubin much like our liver.  If antibodies exist against bilirubin and then hepatitis C infects the liver the immune system would have cross targeting or 2 reasons to attack the liver.   Not everyone who has celiac disease has autoimmune liver disease and not everyone has autoimmune liver disease after Hepatitis but some do.  The cross targeting could be reason. 

Perhaps we should consider something similar to celiac disease but drastically different, autism.  Autism has been associated with gluten and casein proteins and the MMR vaccine.  Very recently autism has also been associated with the sutterella bacteria.  If you put sutterella in the middle you find that sutterella is dimorphic which means it could change morphology much like E.coli. Sutterella was distinguished from Campylobacter by a distinctive cell wall. Sutterella has long chain fatty acids in it’s cell wall much like our nerves myelin sheath.  I phrase it in this way because it is well documented that the measles vaccine produces antibodies against myelin sheath protein.  Cross targeting could be occurring. The herpes simplex virus has been shown to produce similar nerve antibodies and could also cause the same reaction.  

Neither autism nor psoriasis which have the gluten and casein sensitivity seem to be associated with type one diabetes. These infections must not drop or have something that could be confused with insulin. Candida albicans has been associate with type one and must have something that would induce antibodies toward the pancreas.  Candida does have more than one morphology: a mold and a yeast form.

 ......any thoughts? anyone out there understand me?