Research Resources

Office of the Vice President for Research & Economic Development (OVPRED)

Leadership for all administrative research units serving the research enterprise at UAB. OVPRED oversees Core Facilities, Institutional Animal Care and Use Committee, and Institutional Review Board.

Integrated Research Administration Portal (IRAP)

Electronic submission of funding applications and compliance forms for future research initiatives.

UAB Institute for Innovation and Entrepreneurship

The nexus for UAB innovation, entrepreneurial educational models, applied research, and management of intellectual property.

Funding Sources and Grant Opportunities

Presentations and general information related to effective grant writing.

Office of Postdoctoral Education

UAB is committed to the development and success of outstanding postdoctoral scientists.

Conflict of Interest Review Board (CIRB)

Charged with the ongoing development of policies and procedures related to conflicts of interest in sponsored research, review of disclosures of financial interests submitted by investigators, and the development of conflict of interest management plans.

Research News

UAB researcher wins early-stage investigator award for epigenetics of substance abuse research
UAB researcher wins early-stage investigator award for epigenetics of substance abuse research
A UAB researcher focusing on the epigenetics of drug abuse wins a significant funding award from the National Institutes of Health.

jeremy dayJeremy DayJeremy J. Day, Ph.D., assistant professor in the Department of Neurobiology at the University of Alabama at Birmingham, has been named one of six inaugural recipients of new research awards from the National Institute on Drug Abuse. The Avenir Award programs in HIV/AIDS and epigenetics are newly developed programs that reward early-stage investigators who propose highly innovative studies. Avenir means ‘future’ in French.

The Avenir Award Program for Genetics or Epigenetics of Substance Abuse supports early-stage investigators who show promise of being tomorrow’s leaders in the field of genetics or epigenetics of substance abuse. Epigenetics is an emerging field that studies how environmental factors influence changes in gene expression without altering the DNA sequence.

Day says his proposal examines exposure to drugs of abuse, which produce long-lasting changes in neuronal circuits that control learning and decision-making.

“This project will investigate the role of epigenetic mechanisms in these changes, providing insight into the molecular basis by which these mechanisms contribute to drug addiction,” said Day. “We will use these insights to develop new tools that target specific epigenetic processes in the brain, which will lead to more effective epigenetics-based treatment and prevention strategies for drug addiction and improve quality of life for addicted individuals.”

“The innovative proposals by these young scientists in the fields of HIV/AIDS and epigenetics are very exciting,” said NIDA Director Nora D. Volkow, M.D. “We’re pleased to support these creative approaches and are looking forward to seeing the results of their research.”

Research finds males and females process chronic pain differently
Research finds males and females process chronic pain differently
Male and female mice use different immune cells to process chronic pain, indicating that different therapies for different genders could better target the problem.

robert sorgeNew research by University of Alabama at Birmingham researcher Robert Sorge, Ph.D., and team published today in Nature Neuroscience online challenges the common belief that males and females process pain in the same way.

The majority of existing research shows that men and women have different sensitivity to pain — women are more sensitive to pain overall — but the assumption has always been that a common pain circuit exists in both sexes that is altered by circulating hormones like estrogen.

Sorge and colleagues from three laboratories in the United States and Canada found that this assumption may be false, and that males and females may use very different biological systems to process pain. The key sex difference appears to be in the immune system, and under control of the male hormone, testosterone.

“Realizing that females likely process pain differently than males will allow us to focus on creating alternate pain therapies for each sex,” said Sorge, an assistant professor in the Department of Psychology in UAB’s College of Arts and Sciences. “Females could respond better to a treatment that is different from what is prescribed for males — that’s something we as researchers were not looking at before, and this study has helped us uncover that need.”

For years, researchers who study the brain did not think the immune system had much to do with brain functions such as producing pain; but now it is known that the immune system does a lot more than just fight off infection, and actually works in conjunction with the nervous system.

women men pain graphic smallClick to enlargeFor example, many experiments have shown that one immune cell, called microglia, is critical for pain processing. When activated by injury like inflammation or nerve damage, microglia sound the alarm by changing their shape and releasing chemicals. These chemicals communicate with nearby neurons in the spinal cord to turn up the volume knob of pain.

The findings from Sorge and colleagues show that this process only occurs naturally in male mice. Interfering with the function of microglia in a variety of ways blocks pain in male mice, but has no effect whatsoever in female mice. A completely different type of immune cell, called T cells, appears to be responsible for releasing the same chemicals and sending the same signal in female mice. The study also found that females are able to use the male system in instances when the female system is not available or when high levels of testosterone are present.

“Given that women greatly outnumber men as sufferers of chronic pain, one might wonder why it is that this sex difference was not noted until now,” Sorge said. “The reason is that, as in most pain research, the overwhelming majority of the studies of microglia and pain were performed only on male rats and mice.”

The U.S. National Institutes of Health recently unveiled a new policy, similar to one already in force in Canada, to require the use of female animals and cell lines in preclinical research.

“The current findings from this paper are an excellent example of the wisdom of this policy,” said Sorge. “Introducing female animals into research will ensure that we can identify problems and conditions that may be mechanistically differently in each sex.”

The paper detailing the research, “Different immune cells mediate mechanical pain hypersensitivity in male and female mice,” was published today in Nature Neuroscience online.

The work was supported by grants from the Canadian Institutes for Health Research, Louise and Alan Edwards Foundation, and the U.S. National Institutes of Health.

Potential drug lessens neurodegeneration in Parkinson’s disease model
Potential drug lessens neurodegeneration in Parkinson’s disease model
The drug inhibits the activity of a kinase enzyme called LRRK2, and it showed no pathology in rat lungs, kidneys or livers.

andy westAndy WestThe first test in a mammalian model of a potential new class of drugs to treat Parkinson’s disease shows abatement of neurodegeneration in the brains of test rats and no significant toxicities, University of Alabama at Birmingham and Pfizer Inc. researchers report online in The Journal of Biological Chemistry.

At present, there are no therapies to slow or block the progression of Parkinson’s disease, a common neurodegenerative disorder that affects 7 million to 10 million people worldwide.

The rat model overexpresses the protein α-synuclein in one side of the brain. This leads to degeneration of the dopamine-generating neurons of the substantia nigra region of the brain.

“Because our observations were limited to a four-week period, we are not sure whether neurodegeneration associated with α-synuclein is truly prevented or just delayed,” senior author Andrew West, Ph.D., and colleagues wrote. “Either way, any interruption of neurodegeneration associated with Parkinson’s disease might represent a significant therapeutic advance.”

“For a patient with disease onset in the mid-60s, Parkinson’s disease runs its course over 10 to 15 years,” explained West, co-director of the Center for Neurodegeneration and Experimental Therapeutics, and the John A. and Ruth R. Jurenko Professor of Neurology at UAB. “So, if we can slow down the disease by even 50 percent, that may be effectively as good as a cure, given the available symptomatic treatments.”

The rat model used mimics two cardinal features of Parkinson’s disease: degeneration of dopamine neurons in the brain, and the accumulation of alpha-synuclein in surviving neurons. Patients with Parkinson’s have significant degeneration of dopaminergic neurons in the substantia nigra, up to 70 percent losses at even mid-stages of their disease, and abnormal accumulation of α-synuclein in many of the surviving neurons that occurs years earlier. Details of how Parkinson’s begins and how it progresses are still unclear.

“For a patient with disease onset in the mid-60s, Parkinson’s disease runs its course over 10 to 15 years. So, if we can slow down the disease by even 50 percent, that may be effectively as good as a cure, given the available symptomatic treatments.”

The potential new class of drugs is kinase inhibitors that are active against the enzyme “leucine-rich repeat kinase 2” (LRRK2, pronounced “lark two”). Two clues point to LRRK2 as a possible target for therapy in Parkinson’s. First, about 2 percent of Parkinson’s disease patients have a specific mutation in LRRK2 called G2019S that increases the kinase activity of LRRK2; this suggests that increased activity plays a role in progression of the disease. Second, the West lab last year reported that gene “knockout” rats with no LRRK2 are completely protected from neurodegeneration in the α-synuclein-overexpression model, suggesting pharmacological inhibition may be a viable approach.

The model uses rats that express a cloned human G2019S-LRRK2 gene. Then these rats are injected in the brain (specifically a part of the brain called the substantia nigra) with a virus that expresses human α-synuclein. Test rats were fed the test inhibitor for four weeks, beginning at the time of infection. The small-molecule inhibitor easily passes through the blood-brain barrier to reach the brain from the bloodstream. Besides protecting against neurodegeneration, the inhibitor also lessened an inflammatory response by microglial cells seen in the brain in association with G2019S-LRRK2 expression.

West and colleagues also tested the inhibitor in outbred, wild-type rats, animals that are distinct from the strain that has the human G2019S-LRRK2. With the placebo, these rats showed about a 20 percent loss of neurons after four weeks of α-synuclein overexpression; but treatment with the inhibitor completely abated that loss. This result suggests that the inhibitor also has efficacy in the absence of the human G2019S-LRRK2.

“That is important because only 2 percent of Parkinson’s disease patients have the G2019S mutation,” West said. “These wild-type rats really excited us because it suggests the therapeutic action of the drug may extend to the majority of Parkinson’s disease patients. This has invigorated our collaborative efforts with Pfizer Inc. and the Michael J. Fox Foundation for Parkinson’s Research to invest more effort in LRRK2 inhibitors.”

The Pfizer inhibitor is one of a number of LRRK2 inhibitors under development by drug companies, and also at UAB in collaboration with the Southern Research Institute. West says there will be room for several different inhibitors if this class of drugs shows promise in initial clinical trials, which hopefully will occur within the next year.

The next steps for the Pfizer inhibitor will be testing a variety of doses and testing what happens if treatment begins after the α-synuclein expression has already started. West notes that any possible therapy for Parkinson’s disease will need to be incredibly safe because treatment would last for years.

“We have to be very careful with what our models can tell us,” West cautioned about extrapolating from the rat model. “We need to think critically about what type of benefit we can expect to see in humans because there are recent examples where improper clinical trial design have hindered the development of a new class of drugs for years and sometimes decades.”

For example, it is not clear where and how the inhibitor acts in the rat model, especially since inflammatory microglia cells in the brain also express LRRK2. Knowing such information might be critical to the success of these drugs in the clinic. In a separate trail of evidence, researchers, who include David Standaert, M.D.,Ph.D., have found that gene knockout of several neuroinflammatory processes can block α-synuclein neurodegeneration. Thus, the inhibitor may have an effect on just neurons or just microglia, or it may be a two-hit process affecting both neurons and microglia. Standaert is the John N. Whitaker Professor and chair of the Department of Neurology at UAB.

Co-authors of the paper, “LRRK2 Pharmacological Inhibition Abates α-Synuclein Induced Neurodegenerationα-Synuclein Induced Neurodegeneration,” are João Daher, Hisham Abdelmotilib, Xianzhen Hu, Laura Volpicelli-Daley, Ph.D., Mark Moehle and Kyle Fraser, all from the Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, UAB School of Medicine; Elie Needle, Yi Chen and Warren Hirst, of the Pfizer Neuroscience Research Unit; Stefanus Steyn, Pfizer Pharmacokinetics, Dynamics and Metabolism, Cambridge; and Paul Galatsis, Pfizer Worldwide Medicinal Chemistry, Cambridge, Massachusetts.

This study was supported by the Michael J. Fox Foundation for Parkinson’s Disease Research, the National Institute of Neurological Disorders and Stroke, and the American Parkinson’s Disease Association.

Office of Undergraduate Research Summer EXPO to be held July 24
Office of Undergraduate Research Summer EXPO to be held July 24
Hundreds of students will present academic pursuits in cutting-edge research topics.

expo 2015Hundreds of UAB students will present academic pursuits in cutting edge research topics.The University of Alabama at Birmingham’s Office of Undergraduate Research will host nearly 200 student presentations during its Summer Expo on Friday, July 24. 

The EXPO celebrates excellence in research, creative activity and scholarship by showcasing the academic endeavors of undergraduate students covering more than three-quarters of the majors offered at UAB. Undergraduates will have the opportunity to present what they have learned through their research experiences to an audience. This event also provides a forum for students, faculty and the community to discuss cutting-edge research topics and to examine the connection between research and education.

This year’s EXPO will feature a keynote address by Daniel Bullard, Ph.D., director of genetics, genome and bioinformatics in UAB’s Department of Genetics. He will discuss strategies that can be implemented to increase competitiveness for students as they aim to be accepted into top biomedical graduate programs.

Registration, poster setup and student presentations will be held from 7 a.m. to 12:15 p.m. Friday, July 24, in the Campus Recreation Center, 1401 University Blvd. The keynote address will be held at Heritage Hall in Room 102 at 11 a.m. followed by the awards ceremony.

Two major national clinical trials available for lung cancer patients at UAB
Two major national clinical trials available for lung cancer patients at UAB
UAB offers two national clinical trials with customized treatment for lung cancer patients.

ronald alvarezRonald AlvarezThe University of Alabama at Birmingham Comprehensive Cancer Center is enrolling lung cancer patients into two leading national clinical trials, the LUNG-MAP and The Adjuvant Lung Cancer Enrichment Marker Identification and Sequencing Trials, better known as the ALCHEMIST, in which genetic screening is conducted on the tumors of all participants to determine the genetic alterations that drive their specific lung cancer and potentially could be inhibited by a molecularly targeted therapeutic.

In 2014, the National Cancer Institute launched the National Clinical Trials Network, intended to improve treatment for the more than 1.6 million Americans diagnosed with cancer each year. In the same year, after a competitive peer-review application process, UAB was awarded an NCI grant and was chosen as an NCTN Lead Academic Participating Site, one of 30 cancer centers in the nation chosen and one of only five in the Southeast.

Ronald Alvarez, M.D., professor in the UAB Division of Gynecologic Oncology, who applied for the NCI grant, also heads up the NCTN group at UAB. 

“It is because of this grant that UAB could offer significant precision-based clinical trials like this to patients in our community who are affected by lung cancer,” said Alvarez, principal investigator on the NCTN grant. “This clinical trial opportunity is an example of what personalized medicine is all about.”

Lung cancer is the second-most-common cancer in men and women and accounts for about 13 percent of all new cancers. The American Cancer Society estimates that, in 2015, about 221,200 new cases of lung cancer will occur and an estimated 158,040 patients will succumb to this disease. Lung cancer accounts for about 27 percent of all cancer deaths, and each year more people die of lung cancer than of colon, breast and prostate cancers combined.

“With these trials, all our patients are able to receive the best possible treatment, which might include various chemotherapy options or new drugs designed to attack their particular cancer based upon their tumor’s specific characteristics."

“With these trials, all our patients are able to receive the best possible treatment, which might include various chemotherapy options or new drugs designed to attack their particular cancer based upon their tumor’s specific characteristics,” Alvarez said.

LUNG-MAP is a first-of-its-kind clinical trial that uses a multidrug, targeted screening approach to match patients with sub-studies testing investigational new treatments based on the unique tumor profile. For squamous cell lung cancer patients, the clinical trial uses state-of-the-art genomic profiling to match patients to sub-studies of investigational treatments that may target the genomic alterations, or mutations, found to be driving the growth of their cancer. Instead of having to undergo multiple diagnostic tests to determine eligibility for many different studies, enrollees are tested just once according to a master protocol and assigned to one of five different trial sub-studies, each testing a different drug from a different developer.  

“Involvement in these types of clinical trials provides better access for patients to promising drugs and the infrastructure needed to test these investigational drugs here at UAB,” Alvarez said.

The ALCHEMIST are a group of clinical trials for patients with certain types of early-stage non-small-cell lung cancer that has been treated surgically. The ALCHEMIST also involves genetic profiling of tumor specimens removed during surgery and matching patients with specific gene mutations to trials evaluating drugs that target those specific mutations. Patients will already have had surgery and adjuvant therapy proceedings with the ALCHEMIST treatments.

“We want to encourage patients with early-stage lung cancer to enroll in these trials so that we can treat them early with drugs that target their specific genetic mutations, with the hope that we will help increase the number of lung cancer patients who can be cured,” said Francisco Robert, M.D., professor in the UAB Division of Hematology and Oncology and a lung cancer specialist. “In the age of precision medicine and targeted therapy, the primary objective of both these trials is to learn whether a targeted cancer therapy that is matched to the genomic makeup of a patient’s lung cancer tumor is more effective than the current standard therapy in halting or reversing the progress of the disease and extending the patient’s life.”

Patients with lung cancer are encouraged to talk to their doctors about which trial might be appropriate for them.

For detailed information and eligibility requirements for the LUNG-MAP and ALCHEMIST contact Liz Busby, director of Oncology Clinical Trials at the UAB Comprehensive Cancer Center at 205-934-0337 or lizbusby@uab.edu.

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