If...and that is a huge if...parkinson's has mycobacterias as part of the causation then how do we end up with alpha-synuclein plaques?
(Parkinson's could be cross-targeting of mycobaterias and avian flu)
http://angelabiggs.blogspot.com/2013/06/autoimmune-basal-ganglia-from-2.html
We know that Mycobacterias use/eat glutamate and it is routinely used as a component of growth plates.
What if....syn which is involved with the vesicles and secretions of Glutamate by neurons is precipitating in parkinson's disease thus forming the signature synuclein plaques because the demand for glutamate has increased? more transport vesicles moving the glutamate....extra synuclein proteins...neurons stuck in secretion mode.
Alpha-synuclein is increased in Parkinson's verse Alzheimer's
http://www.ncbi.nlm.nih.gov/pubmed/23362176
Over expression of synuclein in mice looks like Parkinson's
http://www.sciencedaily.com/releases/2013/06/130607160329.htm
The amount of glutamate does appear to be increased in Parkinson's disease patients.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030918
They say that Rifampicin which is a antibiotic against mycobacterias interferes with synuclein expression by interfering with the synthesis of RNA.....it could be helping parkinson's patients more then we realize.....if mycobacterias are instigators of the disease itself.
This could be too far fetched to be real.....but if mycobacterias are in the brain are they attached to the neurons? is it the immune system attacking the nerves?
Alcoholics have increased synuclein and they do not have parkinson's but can have parkinson's like symptoms. Alcohol causes an increase in GABA release and a decrease of glutamate. which means the issue is not so much glutamate but synuclein...which is part of the release vesicle.
http://www.ncbi.nlm.nih.gov/pubmed/15897720
(glutamate is the green light stimulation transmitter while the GABA is the red light calming nerves)
Not all alcoholics have parkinson's features. Not all mycobacteria infected people have parkinson's....so it still comes down to our own immune system cross-targeting.
The avian flu under suspicion as a Parkinson's trigger increases the expression of synuclein. Proving that the virus was in the neurons involved. http://www.ncbi.nlm.nih.gov/pubmed/23851655
Imagine the outside of the brain cell clutched by a mycobacteria and the inside infected by the flu...even after the infections are gone the immune system has cross-targeted the nerves..the ones with extra synuclein.
Is parkinson's a state where the immune system does not stop with the infection but continues because of the autoimmune cross-targeting...stuck in a state of inflammation?
(Parkinson's could be cross-targeting of mycobaterias and avian flu)
http://angelabiggs.blogspot.com/2013/06/autoimmune-basal-ganglia-from-2.html
We know that Mycobacterias use/eat glutamate and it is routinely used as a component of growth plates.
What if....syn which is involved with the vesicles and secretions of Glutamate by neurons is precipitating in parkinson's disease thus forming the signature synuclein plaques because the demand for glutamate has increased? more transport vesicles moving the glutamate....extra synuclein proteins...neurons stuck in secretion mode.
Alpha-synuclein is increased in Parkinson's verse Alzheimer's
http://www.ncbi.nlm.nih.gov/pubmed/23362176
Over expression of synuclein in mice looks like Parkinson's
http://www.sciencedaily.com/releases/2013/06/130607160329.htm
The amount of glutamate does appear to be increased in Parkinson's disease patients.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030918
They say that Rifampicin which is a antibiotic against mycobacterias interferes with synuclein expression by interfering with the synthesis of RNA.....it could be helping parkinson's patients more then we realize.....if mycobacterias are instigators of the disease itself.
This could be too far fetched to be real.....but if mycobacterias are in the brain are they attached to the neurons? is it the immune system attacking the nerves?
Alcoholics have increased synuclein and they do not have parkinson's but can have parkinson's like symptoms. Alcohol causes an increase in GABA release and a decrease of glutamate. which means the issue is not so much glutamate but synuclein...which is part of the release vesicle.
http://www.ncbi.nlm.nih.gov/pubmed/15897720
(glutamate is the green light stimulation transmitter while the GABA is the red light calming nerves)
Not all alcoholics have parkinson's features. Not all mycobacteria infected people have parkinson's....so it still comes down to our own immune system cross-targeting.
The avian flu under suspicion as a Parkinson's trigger increases the expression of synuclein. Proving that the virus was in the neurons involved. http://www.ncbi.nlm.nih.gov/pubmed/23851655
Imagine the outside of the brain cell clutched by a mycobacteria and the inside infected by the flu...even after the infections are gone the immune system has cross-targeted the nerves..the ones with extra synuclein.
Is parkinson's a state where the immune system does not stop with the infection but continues because of the autoimmune cross-targeting...stuck in a state of inflammation?
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