“Wherever the art of Medicine is loved, there is also a love of Humanity”

- Hippocrates

On Friday October 18, 2013, The Blue Bird Circle will honor Mark W. Kline, M.D., recognized worldwide for his selfless dedication to children’s health.

Dr. Kline’s reach has gone beyond our borders to the sickest of children across the globe. For more than 17 years he has led the Baylor International Pediatric Aids Initiative, part of Texas Children Hospital’s Global Health Initiative. What began as a small program in Romania has grown into a network of children’s health centers that provide medical and preventative services not only for HIV/AIDS but other medical conditions including malaria, tuberculosis, and cancer.  More than 160,000 children are treated each year in these centers, more than any other program worldwide.  In 2010 Dr. Kline was selected for The Jefferson Award, also known as the Nobel Prize for public service, which honors an individual for outstanding, unique, and heroic personal acts that have made a positive impact on a community, and in his case, helping thousands of others in the spirit of public service.

As Physician–in–Chief of Texas Children’s Hospital and Chair of the Department of Pediatrics at Baylor College of Medicine, Dr. Kline is also firmly committed to American children and his role in ensuring that they have access to healthcare second to none.

“This year’s Gala honoree, Dr. Mark Kline, has been a visionary leader enabling remarkable growth in research, in excellent patient care, and in outstanding teaching at Texas Children’s Hospital and Baylor College of Medicine. His enthusiastic support of neurology has been unwavering and has allowed us to double the number of outstanding physicians, to more than double the number of patients seen in The Blue Bird Clinic, and to increase the number of research protocols and grants by fivefold. It has been on his watch that we have completed the Jan and Dan Duncan Neurologic Research Institute and initiated The Blue Bird Circle Clinical Research Center.”

Dr. Gary Clark, Chief of Neurology, Texas Children’s Hospital

 As we honor Dr. Kline, the Circle graciously requests your financial support for the Gala, our principal annual fundraiser.  As a Sponsor, you will have a direct impact on the lives of children affected by neurological disorders. Please join us on Friday, October 18, 2013 at River Oaks Country Club as a Blue Bird Circle Gala Sponsor.

Sponsor online today!

A growing understanding of the link between epilepsy and some forms of inherited Alzheimer’s disease led to the finding that could point the way toward new drugs for seizure disorders said Dr. Jeffrey Noebels, professor of neurology at BCM, and director of the Blue Bird Circle Developmental Neurogenetics Laboratory.

In her research, Jerrah Holth, a graduate student in molecular and human genetics at BCM who was working with mice with the severe form of epilepsy in Noebel’s laboratory, deleted the gene for tau. She found that reducing or eliminating tau also prevented the seizures in a severe form of epilepsy that has been associated with sudden death and educed deaths in the animals.

In an earlier experiment, Noebels, in collaboration with Dr. Lennart Mucke at the Gladstone Research Laboratory at the University of California San Francisco, found that mice who carried a human gene that leads to accumulation of the beta amyloid protein and the amyloid plaques that accumulate in the brains of people with Alzheimer’s disease, also had epileptic seizures arising in the hippocampus, the region of the brain associated with memory storage and retrieval.

“This led to the paradigm-shifting hypothesis that excessive neuronal network activity, rather than too little, may contribute to lower cognitive performance and dementia in some forms of Alzheimer’s disease. When this happens, the progression of memory loss may accelerate,” said
Noebels.

The finding also demonstrated the two disorders may share defects in signaling within brain memory circuits.

The two labs went on to show that deleting the second gene for tau ameliorated both cognitive losses and seizures in the mice whose inherited disorder mimicked Alzheimer’s disease found in humans.

Holth’s finding demonstrates that tau is involved in a far broader range of epilepsy than previously suspected, said Noebels. The type of epilepsy she studied resulted from an inherited potassium ion channel defect that affects the flow of the potassium in and out of nerve cells. She found that removing the gene encoding Tau not only dramatically reduced seizures, but prevented the mice from dying early, which typically happens in these animals.

“Even a partial reduction of the amount of tau protein by 50 percent was highly effective,” said Holth. Her finding suggests developing new drugs that lower the normal interactions of the tau protein may reduce seizures and sudden unexpected death for persons with intractable epilepsies, a problem in nearly one-third of the 5 million Americans with this disorder.

Currently, Noebels and his colleagues in the Blue Bird Laboratory are studying whether the loss of tau can correct a seizure disorder once it is already established. If these studies prove fruitful, “the pharmacological discovery programs under development for treatment of Alzheimer’s disease may one day find their way to the epilepsy clinic,” said Noebels.

Others who took part in this work include: Valerie C. Bomben, J. Graham Reed, Taeko Inoue, Robia G. Pautler and Juan Botas, all of BCM; and Linda Younkin and Steven G. Younkin, both of the Mayo Clinic. Dr. Noebels also holds The Cullen Trust for Health Care Endowed Chair.

The work was funded by the National Institutes of Health (R01NS29709,P01 AG022074, NS042179, R01AG029977, P30DK079638), the Epilepsy Foundation and the Blue Bird Circle Foundation.

HOUSTON — (January 5, 2011) — Zinc ions released at the junction between two neurons (called a synapse) are important signals, but when too much zinc accumulates, cells become dysfunctional or die.

Researchers in the Blue Bird Circle Developmental Neurogenetics Laboratory in the department of neurology at Baylor College of Medicine have discovered that zinc enters cells through specialized protein gates known as ZIP transporters, and removing these ZIP proteins from cells in the hippocampus (an area of the brain that facilitates storing and retrieving memory) significantly protects them from injury. The results are published in the latest issue of Journal of Neuroscience.

New type of neuroprotective medicine

“These findings pave the way for the development of a new type of neuroprotective medicine for conditions such as seizures, stroke, brain trauma and other neurodegenerative disorders,” said Dr. Jeffrey L. Noebels, professor of neurology, neuroscience and molecular and human genetics at BCM as well as director of the Blue Bird Circle Developmental Neurogenetics Laboratory. Many laboratories are looking for such drugs, and this provides an important clue.

Large amounts of synaptic zinc are found in the hippocampus. However, this brain circuit is a common site for epileptic seizures, and hippocampal cells are extremely vulnerable to damage during a prolonged brain “storm,” as seizures are sometimes called. Since seizures activate many other molecules that may potentially injure cells and also are accompanied by a cutoff off of oxygen and glucose to nerves, the contribution of excessive zinc released during the seizure has not been clear.

Zinc finds its way into brain cells through multiple entry sites: ion channels, glutamate receptors, and a family of special uptake transporters known as ZIP proteins. Dr. Jing Qian, assistant professor of neurology at BCM, used optical imaging techniques in brain slices to demonstrate that most zinc enters neurons through two ZIP proteins, ZIP1 and ZIP3. Qian also found that the entry is accelerated by neuronal firing.

When he analyzed cellular damage following prolonged seizures in mice that were genetically engineered to be missing the two ZIP genes, he found that a crucial group of hippocampal neurons are remarkably undamaged following even severe seizures lasting six hours or longer.

ZIP proteins

“This study is exciting, because for the first time we have shown that reducing zinc entry alone, without removing it from the diet or interfering with its other important functions, is an effective way to protect brain cells from damage due to seizures, and probably a variety of other insults to the brain,” said Noebels. “We now believe these ZIP proteins represent new and important molecular targets for the development of drugs that can specifically reduce zinc entry and protect memory circuits in the brain from damage.”

Others who took part in the research include Kaiping Xu, Jong Yoo, and Tim T. Chen, all of BCM and Glen Andrews of the University of Kansas Medical Center in Kansas City, Kansas.

Funding for this research came from the National Institutes of Neurological Disorders and Stroke and the Blue Bird Circle Pediatric Neurology Research Foundation.

Noebels holds the Cullen Trust for Health Care Endowed Chair.

See the feature on ABC 13.

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