Indian-origin scientist paves way for improved epilepsy treatments

Researchers at the University of Toronto, including one of Indian-origin, have now discovered a complex network of proteins that could help in the treatment of neurological disorders such as epilepsy, autism spectrum disorder and schizophrenia.

“Our study pertains to the discovery of the ying-yang for neuronal cross-talk that is essential for normal healthy brain function,” Chennai born Vivek Mahadevan, a Ph.D student at the University of Toronto in Canada, was quoted as saying to IANS.

Neurons in the brain communicate with other neurons through synapses, communication that can either excite or inhibit other neuron.

According to lead investigator of the study, professor Melanie Woodin, “an imbalance among the levels of excitation and inhibition - a tip towards excitation, for example, causes improper brain function and can produce seizures.”

This complex brings together three key proteins - KCC2, Neto2 and GluK2 - required for inhibitory and excitatory synaptic communication.

KCC2 is required for inhibitory impulses, GluK2 is a receptor for the main excitatory transmitter glutamate, and Neto2 is an auxiliary protein that interacts with both KCC2 and GluK2.

The discovery of the complex of three proteins is path breaking as it was previously believed that KCC2 and GluK2 were in separate compartments of the cell and acted independently of each other.
“Finding that they are all directly interacting and can co-regulate each other's function reveals for the first time a system that can mediate excitation-inhibition balance among neurons themselves,” Mahadevan added.

As there is no cure for epilepsy and the treatments which are available can only curb its effects such as convulsions and seizures, the main focus should be on its prevention.

Mahadevan, along with other biologists carried out the study on mice brain via biochemistry, fluorescence imaging and electrophysiology experiments.

The findings appeared in the journal Cell Reports.

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Brain may play key role in development of diabetes

A new study has shown that the brain plays a key role in glucose regulation and the development of type 2 diabetes.

Lead author of the Diabetes and Obesity Center of Excellence  and his colleagues , suggested that normal glucose regulation depends on a partnership between the insulin-producing cells of the pancreas, the pancreatic islet cells, and neuronal circuits in the hypothalamus and other brain areas that are intimately involved in maintaining normal glucose levels.

The development of diabetes type 2, the authors argued, requires a failure of both the islet-cell system and this brain-centred system for regulating blood sugar levels.

The researchers review both animal and human studies that indicate the powerful effect this brain-centered regulatory system has on blood glucose levels independent of the action of insulin.

One such mechanism by which the system promotes glucose uptake by tissues is by stimulating what is called “glucose effectiveness.” As this process accounts for almost 50 percent of normal glucose uptake, it rivals the impact of insulin-dependent mechanisms driven by the islet cells in the pancreas.

The findings lead the researchers to propose a two-system model of regulating blood sugar levels composed of the islet-cell system, which responds to a rise in glucose levels by primarily by releasing insulin, and the brain-centred system that enhances insulin-mediated glucose metabolism while also stimulating glucose effectiveness.

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Bipolar Disorder Drugs May 'Tweak' Genes Affecting Brain

Medications taken by people with bipolar disorder may actually be nudging hundreds of genes that direct the brain to behave more normally, according to new research.

The study suggests that anti-psychotic drugs activate a wide range of genes, changing their function. 

"A gene's activity in any given cell will vary depending on what it's exposed to.

It's not often that scientists stumble upon something in research that they totally weren't expecting to see. "It was a major surprise to us that people treated with an antipsychotic [medication] had changes in the gene expression pattern.

The findings could help point the way to new gene-targeted and stem cell therapies, and provide valuable insight into what causes manic-depressive mood swings.

However, a genetics expert not connected to the study was more cautious about drawing implications from its findings.

Bipolar disorder, also known as manic-depressive illness, affects about 5.7 million American adults, or about 2.6 percent of the U.S. population aged 18 and older, according to the U.S. National Institute of Mental Health (NIMH). The brain disorder causes severe and unusual shifts in mood, energy, activity levels, and the ability to carry out routine daily tasks.

The new research, published in a recent issue of the journal Bipolar Disorders, involved examining 26 brains donated to a nonprofit brain bank. Fourteen of the brains were from people who had bipolar disorder. Of those, seven were from people who had been taking one or more antipsychotic medications -- such as clozapine, risperidone and haloperidol -- when they died. Twelve brains were from those with no mental health condition.

In comparing the brains, the scientists observed that the genes of those that had been exposed to anti-psychotics at the time of death or during their lifetime were similar to those from people who did not have bipolar disorder. This suggests that the drugs may normalize or suppress the kinds of brain pathology one would expect in bipolar disorder, according to the researchers.

The study also supports the idea that the ability of brain cells to effectively communicate with each other may be impaired in people with bipolar disorder. The researchers found that the brains of people who were taking anti-psychotics and those who did not have bipolar disorder showed striking similarities in how their brains relayed signals between cell gaps, or synapses, and on high-speed neuronal "freeways" called the nodes of Ranvier.

While anti-psychotic medications can often be effective in moderating the effects of bipolar disorder, the side effects are often difficult for people to deal with. These include metabolic syndrome -- a combination of symptoms that increase the risk of developing cardiovascular disease and diabetes -- as well as weight gain, increased blood sugar levels, and tremors.

"It's still not known if these changes just happen to occur or play a key role in the therapeutic effect," said a Dr. 

The researchers don't have data on what medications the brains were exposed to during their lifetimes. Patients [with bipolar disorder] are exposed to antidepressants, drugs of abuse, and other medications, and we don't have medication exposure data on the brains [of the people without bipolar disorder].

According to the study, the research represents a step toward a radical evolution in the design of drugs for psychiatric conditions by the pharmaceutical industry.

"A lot of these psychiatric illnesses fluctuate, but now we give medications at a constant rate, almost as if we were giving a diabetic the same amount of insulin no matter what the person's blood sugar is," a  researcher said. "Medications as we know them will change based on our understanding of the biological mechanisms behind disease."