UAB Researcher Dr. Kristen Triebel Awarded Multiyear Grant for Research on Cancer and Decision-Making
Published on December 12, 2014
CCTS KL2 Awardee Granted American Cancer Society Mentored Research Scholars Grant
Kristen Triebel, PsyD, will start her new year off right by beginning a five-year, $728,000 American Cancer Society Mentored Research Scholars grant on January 1, 2015.
Triebel’s research is on “Decisional Capacity Evaluation in Metastatic Brain Cancer,” looking at long-term decision-making abilities in patients with advanced cancers, including lung and breast cancer that has metastasized to the brain, and pancreatic cancer. It also examines issues in these patients’ treatment, cognitive function and quality of life.
“These patients are seriously ill and have to make a lot of important medical decisions,” Triebel says. “We are looking to see if our initial findings from metastatic cancer patients can generalize to other cancer populations who have comparable levels of illness—even those who don’t get tumors that spread to the brain.” The goal, she says, is to be able to improve decision-making capacity. “We hope this research leads to better understanding of patients at risk, so we can advise on best practices for assessment and interventions to support patients in this capacity, ultimately improving their quality of life.”
Triebel, who received a KL2 award from the CCTS in 2012, leveraged that research into this five-year grant from the American Cancer Society (ACS). She is an assistant professor of Neurology and Director, Neuropsychology Fellowship Training Program in the Department of Neurology. The award provides opportunities to conduct grow a research program by fostering collaboration with other cancer investigators in the Comprehensive Cancer Center, she says. It also allows her to pursue career development opportunities in coursework, plus participate in research conferences.
Triebel’s primary mentor on the award is Karen Meneses, PhD, RN, FAAN, Professor and Associate Dean for Research, UAB School of Nursing. Her primary mentor on the KL2 award is Burt Nabors, MD, Department of Neurology, UAB School of Medicine. She learned of the award through her affiliation with UAB’s Comprehensive Cancer Center, she says.
"Kristen’s research is an extremely important area of study for which we have little data, specifically decision-making and quality of life among a seriously ill population," says Meneses. "She is a remarkable young scientist with the requisite strength, tenacity, and clinical experience to conduct and complete this vital work. I consider it a great honor to serve as her mentor along with Dr. Burt Nabors and our interdisciplinary mentoring team."
An article on Triebel’s research entitled, “Cognition in patients with newly diagnosed brain metastasis: profiles and implications,” was published in 2014 in the Journal of Neuro-Oncology. (Gerstenecker, A., Nabors, L. B., Meneses, K., Fiveash, J., Marson, D. C., Cutter, G., Martin, R., Meyers, C. A., & Triebel, K. L. Cognition in patients with newly diagnosed brain metastasis: profiles and implications. Journal of Neuro-Oncology 2014; 120(1): 179-185.[PMCID in process]) Two other UAB researchers are currently conducting research funded by an ACS Mentored Research Scholars grant: Dori Peckmezi, PhD, assistant professor in the Department of Health Behavior, School of Public Health; and Elizabeth Kvale, MD, associate professor, School of Medicine and director of the UAB Supportive Care and Survivorship outpatient clinic.
In her research career, Triebel says, “the CCTS has been and continues to be critical, providing research support in terms of my time and effort, and a lot of resources. The resources of the Training Academy have been wonderful in helping me come up with a road map for what would be competitive for the KL2.”
Triebel emphasizes the protected time and money to conduct the research that the KL2 allowed, as well as “access to successful researchers who taught me how to conduct research and write grants,” she says. “That grant was great, providing two years of support that allowed me to do the research, which in turn helped me secure this larger grant.”
Triebel says she also benefited from CCTS activities such as the Training Interdisciplinary and Emerging Research Scholars (TIERS) program. She attended the Association for Clinical and Translational Science annual Translational Science conference in Spring 2014 where she presented this research. “It was an excellent opportunity to see people advocating for NIH funding and getting to present the research.”
“I’m a huge advocate of the CCTS, I couldn’t have done this work without it,” Triebel says. “For people starting out there’s really nothing else like it, for mentoring, for networking.” In addition to the CCTS, she acknowledges “incredible support” received from the UAB Department of Neurology, including Dr. David Standaert and Dr. Daniel Marson, UAB President Dr. Ray Watts, the Comprehensive Cancer Center, and her research team, including Amanda Eakin, program coordinator.
Brain Inflammation a Hallmark of Autism, Study ShowsCompliments of US News & World Report - Health News - By Robert Preidt, HealthDay Reporter
WEDNESDAY, Dec. 10, 2014 (HealthDay News) -- Brain inflammation, triggered by an overactive immune system, is common among people with autism, a new study finds.
However, this inflammation does not cause the developmental disorder. Rather, it's a response to the different factors that can trigger autism, the researchers stressed.
Their findings are based on autopsies performed on 72 brains of people with and without autism. In the brains of those who had autism when they were alive, a certain type of cell had its genes for inflammation permanently turned on.
"There are many different ways of getting autism, but we found that they all have the same downstream effect," study author Dan Arking, an associate professor at the Institute for Genetic Medicine at Johns Hopkins University School of Medicine in Baltimore, said in a university news release.
"What we don't know is whether this immune response is making things better in the short term and worse in the long term," he added.
The next step is to find out whether treating this inflammation would reduce symptoms of autism, Arking said.
The study was published online Dec. 10 in the journal Nature Communications.
"This type of inflammation is not well understood, but it highlights the lack of current understanding about how innate immunity controls neural circuits," study co-author Andrew West, an associate professor of neurology at the University of Alabama at Birmingham, said in the news release.
The U.S. National Institute of Neurological Disorders and Stroke has more about autism.
Copyright © 2014 HealthDay. All rights reserved.
Study suggests potential therapy for second most common form of dementiaA new UAB study reports on a potential new treatment for frontotemporal dementia, the second most common type after Alzheimer’s disease.
Written by Bob Shepard
Drugs that boost the function of a specific type of neurotransmitter receptor may provide benefit to patients with the second most common type of dementia, according to research by scientists at the University of Alabama at Birmingham published today in the Journal of Neuroscience.
Frontotemporal dementia, known as FTD, is a devastating disease in which patients have rapid and dramatic changes in behavior, personality and social skills. The age of onset for FTD is relatively young, usually striking patients in their mid- to late 50s. The prognosis is grim; patients quickly deteriorate and usually die within 10 years after onset. Currently, there is no effective treatment for FTD.
The UAB research team’s effort focused on mutations in certain genes, primarily in the Microtubule Associated Protein Tau gene. An accumulation of tau protein is associated with Alzheimer’s disease, the most common form of dementia; but little is known how tau mutations affect specific brain regions and cause FTD.
The UAB researchers used a new mouse model expressing human tau with an FTD-associated mutation. These mice demonstrate physical behaviors similar to those seen in humans with FTD — compulsive, excessively repetitive actions such as grooming, for example. The mice also had impaired synaptic and network function in certain brain network regions.
“We found that mutant tau impairs synapses — the connections between neurons — by reducing the size of the anchoring sites of an essential glutamate receptor called NMDA,” said Erik Roberson, M.D., Ph.D., associate professor in the Department of Neurology and primary investigator for the study. “Reduction of the anchoring sites left fewer NMDA receptors available at the synapse to receive excitatory signals, thus limiting synaptic firing and network activity.”
The team then employed cycloserine, a drug already approved for use by the FDA, which is known to assist NMDA receptor function. This boost of NMDA receptor function was able to restore synaptic firing and thereby restore network activity in the animal model. The restoration of normal network activity reversed the behavioral abnormalities seen in the mice.
“This study provides mechanistic insight into how a tau mutation affects specific brain regions to impair a network,” said Roberson. “It also provides a potential therapeutic target, the NMDA receptor, which appears to correct the network and behavioral abnormalities.”
Roberson’s team hypothesizes that increasing NMDA receptor function may benefit human FTD patients. With further preclinical validation, this hypothesis could be tested in clinical trials using the already available drug cycloserine.
Dr. Marissa Natelson Love Awarded ACA Grant
Dr. Marissa Natelson Love, a UAB Memory Disorders Fellow, was awarded a grant November 14, 2014, from Alzheimer’s of Central Alabama (ACA) at their Annual Meeting to assist in funding research at UAB on Clinical Correlates of Family Quality of Life in Dementia. Dr. Natelson is pictured here accepting the award from Alacare President John Beard, ACA Executive Director Miller Piggott, and ACA Vice President for Research Dr. Lindy Harrell.