“Flicker” treatment is a striking non-pharmaceutical approach aimed at slowing or reversing Alzheimer’s disease. It represents a reversal of EEG: not only recording brain waves, but reaching into the brain and cajoling cells to dance. One neuroscientist commentator called the process "almost too fantastic to believe."
With flashing lights and buzzing sounds, researchers think they can get immune cells in the brain to gobble up more amyloid plaques, the characteristic clumps of protein seen in Read more
Young, who is world-renowned for his work on the role of neuropeptides in regulating social behavior, uses voles to investigate the neurobiological and genetic mechanisms underlying social behavior. Using the monogamous prairie vole (vs. the promiscuous meadow vole) as a model organism, Young and his research team identified the oxytocin and vasopressin receptors as key mediators of social bonding and attachment. In addition, they are examining the consequences of social bond disruption as a model of social loss-induced depression.
This work has important implications for developing novel treatment strategies for psychiatric disorders associated with social cognitive deficits, including autism spectrum disorders and schizophrenia.
You may have already heard that last month Emory held its fifth annual predictive health symposium â€œHuman Health: Molecules to Mankind.â€ Researchers, physicians, health care workers and members of the community from throughout the country met to learn about intriguing research and provocative commentary by health care experts.
One of those experts, Paul Wolpe,Â director of the Emory Center for Ethics,Â says health care has changed as more and more aspects of ordinary life or behaviors are being redefined as medical. For example, being drunk and disorderly has become alcoholism. Now, virtually all of life is being redefined in biological terms, he says. And that, says Wolpe, has led to an increase in health care costs. We have an enormous amount of new things that we are calling illness, and we expect our health care system to treat them, he says. â€œWe are creating a new category of disease called pre-symptomatic.â€
Geshe Lobsang Tenzin Negi, PhD, senior lecturer in the Department of Religion at Emory, and Charles Raison, MD, in the Department of Psychiatry and Behavioral Sciences, Emory School of Medicine, have been associates, colleagues and friends whose relationship has grown as a result of their participation in the Tibetan Studies Program at Emory. Together they have served for the last several years as co-directors of the Emory Collaborative for Contemplative Studies.
Geshe Lobsang Tenzin Negi, PhD
Charles Raison, MD
Negi and Raison recently collaborated on a study at Emory looking at the practice of compassion meditation and its effect of on inflammatory responses when people are stressed. The study required one group of college students to attend compassion meditation class sessions, while a control group attended classes on topics relevant to the mental and physical health of college students.
Negi developed and taught the compassion meditation program that was used in the study based on a thousand-year-old Tibetan Buddhist mind-training practice called â€œlojongâ€ in Tibetan. Raison and his team of researchers tested the participants and analyzed the data.
The study, which has been published in two articles in the medical journal Psychoneuroendocrinology in 2009, succeeded in showing a strong relationship between time spent practicing meditation and reductions in inflammation and emotional distress in response to psychological stress.
The success of this initial study has led the pair to embark on an expanded protocol for adults called the Compassion and Attention Longitudinal Meditation study (CALM). The CALM study will compare compassion meditation with two other interventions â€“ mindfulness training and a series of health-related lectures.
The outcome of the CALM study, combined with the data from the initial meditation study, will help neuroscientists to further expand the awareness of how mind and body are connected, and the power of the mind to effect both illness and health.
Raison is clinical director of the Emory Mind-Body Program, and director of the Behavioral Immunology Clinic at Emory’s Department of Psychiatry and Behavioral Sciences. He specializes in scientific studies that show how stress can have a negative impact on the bodyâ€™s immune system.
Negi earned the highest degree of learning in Tibetan Buddhism, the degree of Geshe Lharampa, from Drepung Loseling Monastery, and received his PhD from Emory’s Graduate Institute for the Liberal Arts in 1999. In addition to teaching at Emory, he serves as spiritual director of Drepung Loseling Monastery, Inc., which has been affiliated with Emory since 1998 and which serves as the North American seat for Drepung Loseling Monastery, one of the largest Tibetan Buddhist monastic centers in exile in India.
An Emory project studying schizophrenia genetics is a good example of how geneticists are shifting from examining small, common mutations to “rare variants” when studying complex diseases.
From studies of twins, doctors have known for a long time that heredity plays a big role in causing schizophrenia. But dissecting out which genes are the most important has been a challenge.
Threelandmarkstudies on schizophrenia genetics published this summer illustrate the limitations of “genome wide association” studies. New York Times science reporter Nicholas Wade summarized the results in this way:
“The principal news from the three studies is that schizophrenia is caused by a very large number of errant genes, not a manageable and meaningful handful.”
The limitations from this type of study comes from the type of markers geneticists are looking at, says Steve Warren, chair of the human genetics department at Emory.
Genome wide association studies usually follow SNPs — single nucleotide polymorphisms. This is a one-letter change somewhere in the genetic code that is found in a fraction of the population. It’s not a big change in the genome, and in many cases, it will have a small effect on disease risk.
Researchers looking for the genes behind complex diseases such as schizophrenia and autism are starting to shift their efforts away from genome wide association studies, Warren says.
Think of a SNP like a misspelling of a word in a certain place in a book, he says. In contrast, the “rare variants” geneticists are starting to study more intensively are more like printers’ errors or missing pages. The rapid sequencing technology that allows scientists to investigate these changes easily is just now coming on line, he says.
One example of these rare variants is DiGeorge syndrome, a deletion that gets rid of dozens of genes on one copy of chromosome 22. Children who have this chromosomal alteration often have anatomical changes to their heart and palate. But it also substantially increases the risk of schizophrenia – to about 25% lifetime risk. That’s a lot more than any of the SNPs identified this summer.
Working with several Emory colleagues, researcher Brad Pearce is planning to examine the genes missing in DiGeorge syndrome in several groups of patients: people with DiGeorge, patients with “typical” schizophrenia and people at high risk of developing schizophrenia.
An article in this spring’s Emory Health describes genetic research on autism. Several of the researchers mentioned there, such as geneticist Joe Cubells and psychiatrist Opal Ousley, are involved in this schizophrenia project as well, because deletions on chromosome 22 also lead to an increased risk of autism.