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Health News from Ben-Gurion University of the Negev

January 15, 2020

We begin the New Year with resolutions often reflecting our desire to be healthier – quit smoking, lose weight, exercise more and decrease stress. But for some people health problems are far more serious and harder to relieve and control. At Ben-Gurion University research is ongoing in a wide variety of areas and the pressure is on to achieve results that will help people everywhere.

Here are two stories that point to a better future for so many people, and a recorded webinar about treating and curing Type 1 Diabetes.

BGU's Prof. Varda Shoshan-Barmatz in collaboration with NIH's Dr. Jay Chung have succeeded in showing that the mitochondrial protein VDAC1 is critical for the release of mitochondrial DNA (mtDNA) associated with the pathology of Lupus disease.

BGU, The National Institute for Biotechnology in the Negev (NIBN) and US National Institutes of Health researchers have identified the path mitochondrial DNA use to exit cells in order to trigger autoimmune diseases and how to block that escape route.

Prof. Varda Shoshan-Barmatz (pictured above) of BGU’s Department of Life Sciences and the founding Director of The National Institute for Biotechnology in the Negev (NIBN), discovered a unique mechanism involving the mitochondrial protein voltage-dependent anion channel (VDAC1) in the exit of mitochondrial factors such as pro-cell death proteins and mitochondrial DNA (mtDNA) that trigger some autoimmune diseases.

When VDAC1 is over-expressed, as found in several diseases, a large pore composed of several VDAC1 units is formed, allowing the release of pro-cell death factors and mtDNA.

Prof. Shoshan-Barmatz has developed a molecule that inhibits cell death and restores mitochondrial functions associated with several diseases. That novel molecule prevents the formation of the large pore caused by VDAC1 overexpression and thereby prevents the exit of these factors from the mitochondria. Without the release of these factors, cell death in diseases such as Alzheimer's and Parkinson's diseases, or mtDNA release like in Lupus is avoided.

“Our breakthrough is identifying a new pathway for the exit of mitochondrial DNA that we can either trigger under controlled conditions or inhibit using our novel molecule that we specifically developed to prevent the formation of this pathway,” says Prof. Shoshan-Barmatz.

“Since the results thus far with lupus have been so promising, we believe that the molecule will be beneficial with regards to other diseases such as Alzheimer’s, Crohn’s and ulcerative colitis - as our preliminary results already support,” she adds.

Lupus is a chronic autoimmune disease that can attack various parts of the body. According to the Lupus Foundation, there are five million cases around the world. Prof. Varda Shoshan-Barmatz in collaboration with a group from NIH, headed by Dr. Jay Chung, have had remarkable success in lupus mouse models so far and are beginning to take the next steps towards other diseases.

mtDNA has also been found in the plasma of patients of other autoimmune diseases such as Colitis and Crohn's diseases. This gives rise to new hope that this VDAC1-modulating molecule will lead to more therapies in an expanding list of other diseases that are associated with cell death or release of DNA from the mitochondria.

A large percentage of children with autism have a hard time falling asleep, wake up frequently in the middle of the night, and wake up early in the morning. A new research study from Ben-Gurion University of the Negev's National Autism Research Center of Israel shows that their brain waves are shallower particularly during the first part of the night, indicating difficulty falling into a deep, rejuvenating sleep.

Previous studies have shown that forty to eighty percent of children on the autism spectrum have some form of sleep disturbance, which creates severe challenges for the children and their families. Determining the causes that create these sleep disturbances is a first critical step in finding out how to mitigate them.

A team led by Prof. Ilan Dinstein, head of the National Autism Research Center of Israel and a member of BGU's Department of Psychology, examined the brain activity of 29 children with autism and compared them to 23 children without autism. The children’s brain activity was recorded as they slept during an entire night in the Sleep Lab at Soroka University Medical Center, managed by Prof. Ariel Tarasiuk. Normal sleep starts with periods of deep sleep that are characterized by high amplitude slow brain waves. The recordings revealed that the brain waves of children with autism are, on average, 25% weaker (shallower) than those of typically developing children, indicating that they have trouble entering deep sleep, which is the most critical aspect of achieving a restful and rejuvenating sleep experience.

"It appears that children with autism, and especially those whose parents reported serious sleep issues, do not tire themselves out enough during the day, do not develop enough pressure to sleep, and do not sleep as deeply," says Prof. Dinstein. "We also found a clear relationship between the severity of sleep disturbances as reported by the parents and the reduction in sleep depth. Children with more serious sleep issues showed brain activity that indicated more shallow and superficial sleep."

Now that the team has identified the potential physiology underlying these sleep difficulties, they are planning several follow-up studies to discover ways to generate deeper sleep and larger brain waves, from increasing physical activities during the day to behavioral therapies, and pharmacological alternatives such as medical cannabis.

Watch this fascinating video about new developments in treating and curing Type 1 Diabetes:
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