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Researchers Find an Amino Acid That May Reduce Epilepsy


Researchers at Florida State University School of Medicine found that amino acids in the brain can help prevent epilepsy.

A certain type of seizure called a temporal lobe. epilepsy It can cause permanent damage, including death and loss of function of neurons. Researchers believe that amino acids could play a vital role in preventing this type of seizure.

Temporal lobe epilepsy, the most common form of focal (partial) epilepsy, involves seizures that begin in one or both temporal lobes. Seizures usually last one to two minutes and can lead to a total loss of consciousness or a deterioration of consciousness.

Symptoms of these types of seizures include:

One may feel an unusual sensation (aura) before the seizure occurs, which serves as a warning. However, not all people with temporal lobe seizures will have auras or will remember them after regaining consciousness.

The aura marks the beginning of a temporal lobe seizure.

Symptoms or feelings may include:

  • A sudden feeling of unprovoked fear or joy
  • A deja vu experience: a feeling that what is happening has already happened before
  • A sudden or strange smell or taste
  • A rising sensation in the abdomen, similar to being on a roller coaster.

Of course, you may not be able to respond to others after having a seizure. This type of seizure can last from 30 seconds to two minutes.

Signs and symptoms include:

  • Loss of awareness of the environment.
  • Curious
  • Lip smacking
  • Swallowing or chewing repeatedly.
  • Unusual movements of the fingers, such as pinching movements

After a temporal lobe seizure, you may have:

  • A period of confusion and trouble speaking.
  • Inability to remember what happened during the seizure.
  • Unawareness of having had a seizure.
  • Extreme drowsiness

Sanjay Kumar, an associate professor in the Department of Biomedical Sciences at the School of Medicine, hopes to find a cure for this debilitating disease. The team discovered a particular mechanism in the brain that triggers these types of seizures. They also found that a certain amino acid called D-serine can prevent this mechanism from causing seizures. The findings have been published in the journal Communications from nature.

The temporal lobe helps decode sensory input, creates memories, understands conversations, and processes emotions. Temporal lobe epilepsy (TLE) occurs in about 6 out of 10 adults with partial epilepsy. Unfortunately, current antiepileptic drugs do not help prevent symptoms.

“A hallmark of TLE is the loss of a vulnerable population of neurons in a particular brain region called the entorhinal area,” Kumar said. “We are trying to understand why neurons in this region of the brain die in the first place. From there, is there anything we can do to prevent these neurons from dying? It’s a very fundamental question. “

The study of temporal lobe epilepsy

Kumar and his team study underlying receptors in the brain to better understand how TLE occurs. Receptors, proteins in the spaces between two or more communicating neurons, help convert signals between them. Through their research, the team found a new type of receptor in the entorhinal cortex of the brain. They have informally called it the “FSU receptor,” which may become the new approach to TLE therapy.

“The surprising thing about this receptor is that it is highly permeable to calcium, which is what we believe underlies the hyperexcitability and damage to neurons in this region,” said Kumar.

When too much calcium enters the neurons of the FSU receptors, patients with TLE experience seizures when the neurons become overstimulated. This overstimulation by the influx of calcium causes neurons to die, a process known as excitotoxicity. Additionally, the team found that D-serine blocks these receptors, preventing excess calcium from entering neurons. This results in the prevention of seizures and neuronal death.

“What is unique about D-serine, unlike any other drug out there, is that D-serine is produced in the brain itself, so it is well tolerated by the brain,” Kumar said. “Many medications that treat TLE are not well tolerated, but because this occurs in the brain, it works very well.”

The team found reduced levels of D-serine in animals with epilepsy, which suggests that the brains of patients with TLE may not produce much D-serine.

“The loss of D-serine essentially removes the brakes on these neurons, making them hyper-excitable,” Kumar said. “So calcium comes in and causes excitotoxicity, which is why neurons die. So if we provide the brakes, if we provide D-serine, then that loss of neurons is not lost. “

What Causes Lower D-Serine Levels in Epilepsy Patients?

Kumar’s team believes that neuroinflammation causes reduced levels of D-serine in the entorhinal cortex of the brain. Glial cells normally produce D-serine, but the neuroinflammation caused by TLE leads to cellular and molecular brain changes that inhibit its production. So since the team identified D-serine as a usable therapy, they want to focus on viable delivery options.

“We have to find creative ways to deliver D-serine to that particular region of the human brain,” Kumar said. “Getting to the right place is the challenge. We have to see what effect it has when administered locally in that region of the brain compared to systemically through an IV, for example. “

TLE is often the result of a serious brain injury such as a concussion. However, D-serine can block the side effects of this type of injury when administered correctly.

“A cake-in-the-sky kind of idea is a hypothetical scenario where you would have to have a nebulizer or have people inhale D-serine, go play soccer, and if they experience a concussion, they wouldn’t lose neurons because the D- serine would provide a kind of cushion in case there is a traumatic brain injury that can cause the loss of neurons in the temporal lobe, “said Kumar.

“There are some very interesting questions to ask and solve,” he added. “The important thing is that we have described the basic mechanisms of why D-serine works. What we have established is the discovery of the receptors, the discovery of the antagonist of these receptors (D-serine), how it works and how to prevent the appearance of TLE. Mechanisms and pathophysiology are as relevant to the animal model as they are to humans, and that’s where the emotion lies. “





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