seems a little fishy to me that the "animal" problem with the fda just about coincided with Barnham's findings. I once thought it was quite possible that the grubbers with power needed a piece without sending up alarms/pps. One thing is for sure a fact- the board is once again flooded with brainless parasites- A very positive sign. Either you believe in MPAC's (prana is world leader) or you don't.
The harmful effect of glutamate upon the CNS were first observed in 1954 by T. Hayashi, a Japanese scientist who noted that direct application of glutamate to the CNS caused seizure activity, though this report went unnoticed for several years. The toxicity of glutamate was then observed by D. R. Lucas and J. P. Newhouse in 1957, when the subcutaneous injection of monosodium glutamate to newborn mice destroyed the neurons in the inner layers of the retina. Later, in 1969, John Olney discovered the phenomenon was not restricted to the retina, but occurred throughout the brain, and coined the term excitotoxicity. He also assessed that cell death was restricted to postsynaptic neurons, that glutamate agonists were as neurotoxic as their efficiency to activate glutamate receptors, and that glutamate antagonists could stop the neurotoxicity. Subsequent research by Mark Mattson provided evidence for the involvement of excitotoxicity in Alzheimer's disease, and other age-related neurodegenerative conditions that involve oxidative stress and cellular energy deficits.
The NMDA receptor is an ionotropic receptor that allows for the transfer of electrical signals between neurons in the brain and in the spinal column. For electrical signals to pass, the NMDA receptor must be open. To remain open, glutamate and glycine must bind to the NMDA receptor. An NMDA receptor that has glycine and glutamate bound to it and has an open ion channel is called "activated."
Chemicals that deactivate the NMDA receptor are called antagonists. NMDAR antagonists fall into four categories: Competitive antagonists, which bind to and block the binding site of the neurotransmitter glutamate; glycine antagonists, which bind to and block the glycine site; noncompetitive antagonists, which inhibit NMDARs by binding to allosteric sites; and uncompetitive antagonists, which block the ion channel by binding to a site within it.
Most clinical trials involving NMDA receptor antagonists have failed due to unwanted side effects of the drugs; since the receptors also play an important role in normal glutamatergic neurotransmission, blocking them causes side-effects. These results have not yet been reproduced in humans, however. This interference with normal function could be responsible for neuronal death that results from NMDA receptor antagonist use. Mild NMDA receptor antagonist's like Amitriptyline have been found to be helpful in Benzodiazepine withdrawal.
Low Ca2+ buffering and excitotoxicity under physiological stress and pathophysiological conditions in motor neuron (MNs). Low Ca2+ buffering in amyotrophic lateral sclerosis (ALS) vulnerable hypoglossal MNs exposes mitochondria to higher Ca2+ loads compared to highly buffered cells. Under normal physiological conditions, the neurotransmitter opens glutamate, NMDA and AMPA receptor channels, and voltage dependent Ca2+ channels (VDCC) with high glutamate release, which is taken up again by EAAT1 and EAAT2. This results in a small rise in intracellular calcium that can be buffered in the cell. In ALS, a disorder in the glutamate receptor channels leads to high calcium conductivity, resulting in high Ca2+ loads and increased risk for mitochondrial damage. This triggers the mitochondrial production of reactive oxygen species (ROS), which then inhibit glial EAAT2 function. This leads to further increases in the glutamate concentration at the synapse and further rises in postsynaptic calcium levels, contributing to the selective vulnerability of MNs in ALS. Jaiswal et al., 2009.
Excitotoxicity is the pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate (glutamate receptors) such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic storm. Excitotoxins like NMDA and kainic acid which bind to these receptors, as well as pathologically high levels of glutamate, can cause excitotoxicity by allowing high levels of calcium ions (Ca2+) to enter the cell. Ca2+ influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.
These findings also suggest that other microRNAs may also be important markers of severity for other neurological diseases such as Parkinson’s disease and Alzheimer’s disease. Further research is already being conducted in Parkinson’s Disease by Myers and his colleagues.
(Boston)–A new genetic discovery in the field of Huntington’s disease (HD) could mean a more effective way in determining severity of this neurological disease when using specific treatments. This study may provide insight for treatments that would be effective in slowing down or postponing the death of neurons for people who carry the HD gene mutation, but who do not yet show symptoms of the disease.
The work was led by researchers at Boston University School of Medicine (BUSM) and currently appears in BMC Medical Genomics.
HD is a fatal, inherited neurological disease that usually manifests between 30 and 50 years of age. The disease is caused by a genetic defect that is passed from parent to child in the huntingtin gene. Having too many repeated elements in the gene sequence causes the disease and an increasing number of repeats leads to earlier onset and increased severity of the disease.
The researchers studied the brains of people who died from HD and those who died of other, non-neurological diseases and identified a very specific genetic signal that strongly correlates disease severity and extent of neuronal, or brain cell death. The genetic signal, also called a microRNA, silences certain genes in the DNA. Genes that lead to the toxic effects of the huntingtin gene may be silenced by these microRNAs, in particular the miR-10b-5p microRNA.
well put kad, thanks for posting. I had no problem averaging down especially with the excitotoxicity results finally revealed.
A molecule containing copper that binds specifically with DNA and prevents the spread of cancer has been developed by scientists. First results show that it kills the cancer cells more quickly than cisplatin -- a widely used anti-cancer drug that is frequently administered in chemotherapy.