Dr. Rajnish Kumar

Best Neurologist In Delhi

Five years ago, the world woke up to the news of the first cases of rare neurological disorders linked to traumatic brain injury.

Now, a research team led by University of Maryland neurologist James V. Kastner says we may have just discovered one of the causes: the breakdown of certain proteins found in the brain.

The proteins, called glutamate, are released when neurons become damaged or injured.

“There’s no question that this is a critical element of neurodegeneration,” said Dr. James V., chief of the neurology department at the University of Baltimore.

“We don’t know exactly how it happens, but we think that it is the precursor to the onset of symptoms, and we think it is a precursor to many of the other neurodegeners that we’re seeing.”

Dr. Kestner and his colleagues are the first to link the release of glutamate to the progression of rare and disabling neurological disorders.

The researchers report in the journal Neurology that the proteins release in the brains of patients who have suffered brain trauma, but the release also occurs in patients who don’t have severe brain injuries.

The findings, reported at the annual meeting of the American Academy of Neurology, could lead to new treatments for patients who develop these neurological disorders after they have suffered significant brain trauma.

The scientists were able to study the release in a group of healthy volunteers, including a group who had suffered multiple brain injuries, including head trauma, and in a subset of patients with a form of severe traumatic brain injuries that is associated with long-term loss of neurons in the hippocampus.

The group who hadn’t suffered brain injuries also didn’t show significant glutamate release in their brains.

“This study shows that glutamate is an important element of brain pathology,” said V. Michael Kastne, a neurologist at the Johns Hopkins University School of Medicine in Baltimore and lead author of the study.

“It’s something that we haven’t really studied yet.”

“We have a lot of questions about what is going on in the neuronal cell that’s responsible for these glutamate release processes, but there’s no reason why glutamate would be a cause for that,” said Kastney.

“But if we can identify some of these glutamate-related proteins in the neurons that are releasing them, we could possibly find some mechanisms that would explain the pathway of these brain injuries.”

Dr Kastna said the study shows a critical role for the glutamate pathway in the pathogenesis of neuropathology.

“You have to think about it as a pathway that we can understand from the inside,” said Gabor Sánchez, a professor of neurology at the Hospital Universitario, in Madrid.

“Glutamate is the one molecule that causes the neuronal damage that we see in neurodegenesis.”

The findings are important because they have important implications for the development of new treatments and treatments for neurological disorders such as depression and Parkinson’s disease, he added.

“A lot of research is being done on glutamate, and there’s still a lot that we don’t understand,” Sáncyz said.

“And there’s also the possibility that this could be something that could be targeted in the treatment of neuroinflammation and other brain disorders.”

Researchers have been studying the release mechanism of glutamate for several years, but now they are seeing some evidence that glutamate releases in the presence of neuronal damage in the human brain.

It’s also clear that the release occurs in the absence of inflammation, a key factor in many neurological disorders and which is associated in some cases with neurodegening.

The protein is produced in the synapse, a part of the brain that connects the brain’s nerve cells.

When cells communicate, they form a network of nerve cells that connect to other nerve cells, and when those cells die, the neurons themselves die, too.

The presence of inflammation is known to cause the loss of some of the cells in these networks.

This process is known as apoptosis.

The release of this protein in neurons is thought to cause damage to those cells, but other mechanisms are also thought to play a role.

In addition to the glutamate protein, the researchers identified proteins that are produced in cells that have been damaged or damaged in the same way as neurons.

These proteins are also released by the synapses, and the release is thought of as an indirect pathway for glutamate release.

“The release of these proteins is known from previous studies to occur in the context of inflammation,” Kastnor said.

When a protein is released in a particular location, such as in the synaptic cleft, it acts as a trigger for the cell to release more glutamate.

The cell can then continue to release glutamate, but if the protein isn’t released at the right time, it can damage other cells, which triggers the death of those cells.

“In this case, we found that these proteins were released in the very area that had a high concentration of neuronal cells,” Kestney said.

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