UAB Magazine Weekly - Features on Research
How Human Interaction Impacts Evolution
By Tara Hulen
Literature tells us that no man—or woman—is an island. Over millennia, humans have formed an interconnected web that spans the planet.
In fact, that interaction may play a key role in human survival. Eduardo Neiva, Ph.D., professor in the UAB Department of Communication Studies, and James Lull, Ph.D., emeritus professor at San Jose State University, have written The Language of Life: How Communication Drives Human Evolution (2012: Prometheus Books), which revolves around “the idea that communication is central to all biological development,” Neiva explains. In other words, survival goes to the most communicative as well as to the fittest. And since communication involves cooperation, the one who offers the helping hand usually has the advantage over the backstabber.
UAB Magazine: As a humanities professor, what brought you to write about what is usually a topic for biologists?
Neiva: The humanities have operated with the strict notion that what matters are differences: of cultures, of the sexes, in everything. The idea in this book is that everything is unified. Life is actually a great chain of interaction; all living forms interact with one another, and that creates change.
UAB Magazine: People usually think of that interaction in evolution in a negative way—survival of the fittest—but you don’t seem to see it like that.
Neiva: One reason we wrote the book is that we were very frustrated with some general notions that were attached to evolution—one of them is it’s all about survival of the fittest. Evolutionary theory has always favored that phrase, which has, in the popular mind, been considered the dominant factor. But that notion forgets many other things that are absolutely key to evolution, such as cooperation.
The idea is not a new one. Prince [Pyotr Alexeyevich] Kropotkin wrote a brilliant book, Mutual Aid: A Factor of Evolution, in 1902 about how mutual aid drives evolution. Oral traditions, passing on skills, the existence of societies—all of these advance evolution and require mutual aid.
Communication and social life are not just human traits, either, despite what people often think of as the rule. Social life is everywhere. Bees, for instance, are a marvel of elaborate social division.
What Glutamate Can Teach Us About Depression, Schizophrenia, Cancer, and More
By Kathleen Yount
Glutamate is the incredible, edible neurotransmitter. This amino acid is found in chips, yogurt, and ice cream, as well as the much-maligned MSG. It is also the key ingredient that helps neurons communicate, learn, make memories, and perform other essential functions.
For years, scientists have kept an eye on glutamate, suspecting that it plays a role in several debilitating diseases. But only recently have they discovered how to do anything about it. UAB researchers are leading the way in studies that could bring new treatments and new hope for people suffering from depression, schizophrenia, and even brain cancer.
All Hail the King
Glutamate is the most abundant excitatory neurotransmitter, which means its job is to stimulate neurons. It works in tandem with GABA, the main inhibitory neurotransmitter, to maintain balance in the brain.
Glutamate and GABA are the king and queen of neurotransmitters. All others—including the more-famous serotonin, norepinephrine, and dopamine—have important functions of their own, but ultimately they serve to modulate the glutamate and GABA systems.
The brain’s glutamate balancing act revolves around a highly evolved system of molecules called receptors to which glutamate binds to produce actions in the brain’s cells. Another family of molecules called transporters mops up unused glutamate after it has been released. Much of the current research on glutamate dysfunction centers on these processes of give, take, and transport, to see if understanding the exchange can shed light on what happens when the glutamate system goes wrong, and how we might make it right again.
Taking Sleep Science into the Bedroom
By Matt Windsor
You may think you're getting enough sleep, but your wrist might tell a different story.
Using a motion-sensing chip built into a wristwatch-shaped device, sleep scientists can create a highly accurate map of a person’s daily cycle of sleep and wakefulness. The method is called actigraphy, and UAB investigators are using it to take the university’s sleep research program to a new place: patients’ own bedrooms.
“An overnight sleep study is the gold standard” in order to get a precise understanding of a person’s sleep issues, says Kristin Avis, Ph.D., associate director of the Pediatric Sleep Disorders Center at Children’s of Alabama and associate professor of pediatrics at UAB. Overnight sleep studies are routinely conducted for adults at UAB Highlands Sleep Wake Disorders Center and for children at the Pediatric Sleep Disorders Center at Children’s of Alabama. “But in many cases, we would like to establish what a patient’s sleep pattern is over time, and how they sleep in their everyday environment," says Avis. "And we can’t do that in the clinic.”
Aging-related diseases are not the only causes of learning and memory problems, as anyone who has suffered from depression can tell you. Women are diagnosed with depression twice as often as men and tend to be more susceptible to depression during hormonal changes like puberty, postpartum, and menopause, says Lori McMahon, Ph.D., Jarman F. Lowder Professor of Neuroscience at UAB, director of the UAB Comprehensive Neuroscience Center, and associate director of the Center for Aging. But “estrogen doesn’t cause the depression—it’s due to the misregulation of hormones,” she explains.
Moreover, McMahon’s research in animal models indicates that estrogen can alleviate some of the cognitive problems associated with depression. By looking at neurons in the hippocampus directly, McMahon’s lab found that estrogen has a neuroplastic effect, increasing the number of synapses (sites of neuronal connections).
By looking at neurons in the hippocampus directly, McMahon’s lab found that estrogen has a neuroplastic effect, increasing the number of synapses (sites of neuronal connections).
At first glance, McMahon’s findings appear to contradict the results from the Women’s Health Initiative study, which reported that hormone replacement therapy did not provide any benefits to women experiencing memory problems after menopause. However, McMahon points out that the benefits may have been missed because most of the women went without estrogen for 10–15 years before treatment. In a study published in Proceedings of the National Academy of Sciences in 2010, McMahon found that even very old animals benefitted from estrogen replacement after ovary removal (a mimic of menopause)—but only if the period between removal and the start of estrogen therapy was short. “So, it’s really not chronological age, but the period of hormone deprivation that’s the problem,” she notes. If hormone replacement therapy is started too late, “age-related mechanisms are probably already in motion.”
McMahon’s lab continues to investigate the impact of estrogen loss in aging and the value of estrogen replacement, as well as estrogen’s role in depression. The researchers are particularly interested in NR2B, a subunit of the NMDA glutamate receptor implicated in learning and memory. A new paper by the scientists in the journal Hippocampus shows that estrogen increases NR2B function, which in turn increases novel object recognition. This follows a landmark 2006 finding by the McMahon lab that increased activation of NR2B is also responsible for a rise in synaptic plasticity in the hippocampus, “suggesting that the increase in plasticity underlies increases in learning and memory,” McMahon says.
UAB neurologist Erik Roberson, M.D., Ph.D., uses clinical observations to guide his laboratory research, focusing on the ways that disease interferes with the brain’s ability to store and retrieve memories. In particular, he is interested in cognitive deficits related to Alzheimer’s. Initially, researchers assumed that the memory loss in Alzheimer’s was a result of neuronal death, but Roberson says that the process actually begins earlier.
Most research related to the cause of Alzheimer’s disease has focused on two proteins: amyloid beta and tau. But changes in amyloid beta occur in the pre-symptomatic stages of the disease. By the time patients are diagnosed with Alzheimer’s, the levels of amyloid beta in their brains are so high that drugs to target the protein may not have an effect, Roberson notes. This could explain why clinical trials of such drugs have not been very successful.
Since the changes in tau happen closer to the onset of symptoms, Roberson suggests that it may be a more relevant target for treating patients showing the clinical signs of Alzheimer’s. Supporting this idea, he found that eliminating tau in animal models prevents the cognitive deficits caused by amyloid beta. “We think that tau is modifying what the amyloid beta does,” he says. “There’s something about the presence of tau that is permissive for amyloid beta to exert its adverse effects.”
Since turning off all of the tau in the human brain would be very difficult, Roberson is looking for other ways to block specific functions. His research suggests that another protein, Fyn—also involved in learning and memory—interacts with tau to exert pathologic effects. Roberson’s lab is now collaborating with researchers at Southern Research Institute to find and study drugs that block the interaction between the proteins.