This post concerns AMYOTROPHIC LATERAL SCLEROSIS (ALS) and various greedy ass-clowns, google, that are attempting to patent procedures that could lead to a cure or at least a treatment for ALS. While doing a search I came across a patent by google.
There is currently no effective pharmacological treatment for amyotrophic lateral sclerosis (ALS). Since there is growing evidence that multiple molecular pathways underlie ALS pathogenesis, it was tested in a mouse model of ALS a combination therapy composed of three generic drugs for distinct targets in the complex pathway to neuronal death. The ALS mice used for drug testing are derived from a well established mouse line, the SODIG37R line 29 with an average life span of above 48 weeks. The cocktail administered in the mouse diet at late stage of disease consisted of minocycline—an antimicrobial agent that inhibits microglial activation, riluzole—a glutamate antagonist, and nimodipine—a voltage gated calcium channel blocker. This combination therapy, called miripine, ….
Here’s the thing. Screw anybody that tries to patent a cure for ALS.
In the reading I have done I have found the following.
In research date February 6, 2014, the researchers found that a toxin that “triggered a biochemical cascade in the motor neurons that essentially causes them to undergo a controlled cellular explosion”. As of yet the researchers have not identified the toxin.
Glutamic Acid, a transmitter for the human body. Glutamic acid usually is wiped clear after each transmission. With ALS it is surmised that the Glutimic Acid is not cleared. It is surmised the presence of Glutamic Acid creates and environment where the neural transmitter continues to transmit or fire.
Now the hypothesis I would put forth is the toxin is the Glutamic Acid that is not wiped from the Neural Transmitter. This causes the cascade effect found by the original researchers. There appear to be multiple contributing factors for this. One is the Thyroid not producing enough Taurine an inhibitory amino acid for Glutamic Acid.
The patent I am not requesting, I am just making this public knowledge prior to any corporation trying to patent the idea.
If you increase the volume of Iodine to between 100 mcg and 700 mcg and Selenium to between 100 mcg and 300 mcg with say Taurine or any other inhibitory amino acid for Glutamic Acid. This may have a positive result in retarding the progress of ALS. Google for Iodine Deficiency Disorder, UNICEF, Cretinism and you will see the thyroid is pretty important.
The thyroid governs your body with hormones. This includes physical and mental needs for your body. The brain and the chemicals to run it properly are governed by your thyroid.
I am just putting this out there in case it does work, nobody can patent or trademark it.
Some links for reading:
This is from 2011, Specifically 5. Schwann Cells
5. Schwann Cells
Schwann cells—peripheral myelin generating cells—are closely associated
with motor neuron axons and aid the axonal development and regeneration.
So far, very little is known about Schwann cell involvement in ALS
pathology. Studies of human ALS show peripheral myelin changes along the
motor neuron axons which are most likely due to axonal degeneration .
Recent studies show limited or unexpected Schwann cell involvement in the
disease progression. One study expressed mutant SOD1G93A transgene only in
protein zero (P0) positive Schwann cells and these mice were identical to
control animals with no changes to locomotion, neuronal loss, or axonal
degeneration . The study demonstrates the lack of specific causal
involvement of myelinating P0 Schwann cells in the ALS disease onset or
progression. A second study used a different approach, and, instead of
inducing higher synthesis of SOD1, they removed mutant SOD1G37R from
Schwann cells using Cre-mediated gene excision. Surprisingly, the authors
discovered that even though disease onset was not altered, the disease
progression was dramatically accelerated suggesting a connection between
disease progression in ALS and a protective effect of mutant SOD1G37R in
Schwann cells. Finally, they observed that reduced mutant SOD1 expression
was associated with diminished levels of insulin-like growth factor 1
. A close relationship between Schwann cells and motor neuron axons
warrants more studies to help us better understand the pathology of ALS.
There were some articles about CU65, copper, but I will have to see if
they are just more BS trying to make a buck. It does make sense to a point
about the copper.
Prolonged excitation is toxic to nerve cells. Neurobiologists recognize
that the nerve cell messenger, glutamate, can cause harm when its messages
are overwhelming. Normally glutamate is swiftly cleared from the nerve
cell junctions to keep the messages brief. Molecules called transporters
aid in keeping glutamate in proper concentrations around nerve cells.
Abundant evidence points to glutamate as a destructive factor in ALS and
investigators are working to find out how this can be changed. Gene
therapy approaches are under investigation to deliver glutamate
transporters to cells affected by ALS. Other avenues towards control of
glutamate in ALS are also under active investigation.
Glutamate Research Could Lead to ALS Treatment
Decades of research on the neurotransmitter glutamate have produced
promising results that could lead to treatment for Amyotrophic Lateral
Sclerosis (ALS). Scientists believe excessive exposure to glutamate may be
one of the reasons that nerve cells (motor neurons) die in ALS. Preventing
the rise of glutamate levels could be the key to protecting motor neurons
and impeding the progress of the disease.
markf @ July 17, 2014