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UAB News

  • Parkinson’s disease pathogenesis is reduced in a rat model using a cell-signaling inhibitor drug
    Results show that JAK/STAT pathway inhibitors may be a new class of therapeutic treatments for patients with Parkinson’s disease. Acting by reducing inflammation, they prevent neurodegeneration in animal models and may be an important new approach to slow progression of the disease.

    Etty “Tika” BenvenisteUniversity of Alabama at Birmingham researchers report the first documentation that suppressing a key cell-signaling pathway in a rat model of Parkinson’s disease reduces pathogenesis. Oral administration of AZD1480 — one of the JAK/STAT pathway inhibitors generally known as Jakinibs — lessened the destructive inflammation and nerve cell degradation in the area of the brain affected by Parkinson’s.

    At present, there are no therapies available to patients to prevent progression of Parkinson’s disease, the chronic neurodegenerative movement disorder marked by profound loss of dopamine-producing neurons in the brain.

    “We believe Jakinibs may become a viable therapeutic option for Parkinson’s disease patients,” said Etty “Tika” Benveniste, Ph.D., professor in the Department of Cell, Developmental and Integrative Biology and lead author of a paper published May 4 in The Journal of Neuroscience. “They are already being studied for other conditions, are orally bioavailable, seem to be well-tolerated, and do not promote troublesome immunosuppression. Furthermore, there may also be other ways of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegenerative disease.”

    A variety of Jakinibs are in Phase I, II or III clinical trials for several other diseases. The current UAB study, funded by the Michael J. Fox Foundation for Parkinson Research and the National Institutes of Health, is the first to show that disrupting the JAK/STAT pathway prevents the neuroinflammation and neurodegradation specific to Parkinson’s disease.

    “This is a very important advance,” said David Standaert, M.D., Ph.D., professor and chair of the UAB Department of Neurology and a collaborator on the project. “It shows that anti-inflammatory strategies have real potential. The next steps will be to validate some of the inflammatory changes seen in the animals in patients with Parkinson’s disease, which in turn will enable planning of clinical studies of anti-inflammatory therapies in patients with Parkinson’s.”

    “This is a very important advance. It shows that anti-inflammatory strategies have real potential. The next steps will be to validate some of the inflammatory changes seen in the animals in patients with Parkinson’s disease, which in turn will enable planning of clinical studies of anti-inflammatory therapies in patients with Parkinson’s.” — David Standaert, M.D., Ph.D.
    Benveniste and Standaert are part of an interdisciplinary UAB team focusing on neuroinflammatory mechanisms in Parkinson’s disease. The group — co-led by Benveniste, Standaert and Andrew West, Ph.D., associate professor of neurology — seeks to understand how the body’s immune system contributes to the pathology seen in the brains of Parkinson’s disease patients and to the development and progression of the disease. Only recently have researchers begun to suspect an important role for inflammation in the disease, and this is still largely uncharted territory.

    For the current paper, UAB researchers, led by Hongwei Qin, Ph.D., associate professor of cell, developmental and integrative biology, either challenged rat immune cells in vitro with aggregated human α-synuclein, or induced overexpression of α-synuclein carried by a virus vector in brains of rats. Untreated, this in vivo model leads to neuroinflammation in the brain and degradation of dopamine-producing neurons in the substantia nigra, the portion of the midbrain marked by cell death in Parkinson’s patients. Accumulation of α-synuclein in the brains of patients is a core feature of Parkinson’s disease, and this leads to the activation of the brain immune cells called microglia, the production of inflammatory signaling chemicals, and ultimately, neurodegradation.

    In vitro and in vivo experiments showed AZD1480 inhibited JAK/STAT activation and downstream gene induction after a challenge by α-synuclein. The genes that are induced by α-synuclein, but not induced in the presence of α-synuclein and AZD1480, are associated with the proinflammatory phenotype. The inhibition by AZD1480 dampened both innate and adaptive immune responses.

    Altogether, the researchers say, the results show the potential of Jakinibs to protect against the degradation of dopamine-producing neurons.

    Details

    For the in vivo neuroinflammation experiments, α-synuclein overexpression was induced, and two weeks later rats were given AZD1480 by oral gavage for 14 days. Then the researchers analyzed the inflammatory response in the substantia nigra of the midbrain for AZD1480-treated and -untreated animals. AZD1480 prevented the increased numbers of microglia and macrophages seen after α-synuclein overexpression. AZD1480 also prevented inflammatory activation of the microglia, as measured by Iba1-positive cells, and it prevented upregulation of genes for the proinflammatory markers TNF-α, iNOS, IL-6 and CCL2.

    AZD1480 also prevented neurodegradation. For the in vivo neurodegradation experiments, α-synuclein overexpression was induced, and four weeks later — at the peak of neuroinflammation — rats were given a four-week treatment of AZD1480 oral gavage. At 12 weeks, the brains were analyzed for nigral neurons of the substantia nigra. Benveniste and colleagues found that overexpression of α-synuclein caused a 50 percent loss of nigral neurons at three months. But when the α-synuclein rats were also treated with AZD1480, that loss was prevented, and the numbers of nigral cells were similar to those of the controls.

    In Parkinson’s disease, chronic inflammation in the brain makes the blood-brain barrier more permeable, allowing immune system T-cells to infiltrate into the brain from the bloodstream, potentially adding to neuroinflammation. In the rat model, α-synuclein overexpression increased the infiltration of CD4+ T-helper cells and induced activation of the STAT3 signaling protein. AZD1480 treatment inhibited both of these immune responses. AZD1480 also inhibited induction of two genes for proinflammatory markers, CIITA and MHC Class II.

    The UAB researchers further found that α-synuclein overexpression significantly upregulated 186 genes in the midbrains of rats, while AZD1480 treatment of α-synuclein-overexpression rats inhibited the expression levels of 59 genes, the majority being genes that were induced by α-synuclein. Genes induced by α-synuclein overexpression include many that are implicated in cell signaling, inflammatory and neurological diseases, and antigen presentation (a step in the adaptive immune response).

    Besides Benveniste, Qin and Standaert, authors of the paper, “Inhibition of the JAK/STAT pathway protects against α-synuclein-induced neuroinflammation and dopaminergic neurodegeneration,” are Jessica A. Buckley, Yudong Liu, Thomas H. Fox III, Gordon P. Meares, Hao Yu and Zhaoqi Yan, all of the UAB Department of Cell, Developmental and Integrative Biology; Xinru Li and Ashley S. Harms, UAB Department of Neurology; and Yufeng Li, UAB Department of Medicine.

    At UAB, Benveniste holds the Charlene A. Jones Endowed Chair in Neuroimmunology, and Standaert holds the John N. Whitaker Endowed Chair in Neurology. West holds the John A. and Ruth R. Jurenko Endowed Professorship in Neurology.

    Research support came from the M.J. Fox Foundation, and from NIH grants RO1 NS57563-05, P20 NS095230, P30 AR48311, P30 NS47466, P30 CA13148 and P30 AI027767.

  • UAB students win public health scholar bowl in St. Louis
    The undergraduates answered questions on everything from disease outbreaks to community health as they competed against 13 teams from across the country.

    Aarin Palomares, Claire Finney, Sean McMahon, Katherine Hymel and Beenish KamranFive students from the UAB School of Public Health competed against 13 teams from across the United States in the St. Louis University Public Health Scholar Bowl, winning first place in the bowl and tying for second place in the case competition.

    Beenish Kamran, Katherine Hymel, Sean McMahon, Claire Finney and Aarin Palomares won the quiz-bowl-style tournament focused on current public health topics ranging from disease outbreaks to global and community health. The group of undergraduate students competed against teams including Johns Hopkins, George Washington University and Washington University.

    “Beyond academic success in the classroom — which this group has in spades — these students have always pushed the envelope to identify opportunities to practice and display their public health skills in the community,” said Suzanne Judd, Ph.D., assistant dean for undergraduate education in the School of Public Health. “The public health scholars bowl was a natural extension of their commitment to seek out these new opportunities. Competing against students from other universities only enhanced their drive to succeed. I am so proud of the passion and drive within each of these talented undergraduates that led to the success they achieved at the scholars bowl.” 

    During the case competition, UAB’s team worked collaboratively to tackle a current issue causing health problems in a community, sleep deprivation on campus. The team developed a promotional campaign and identified policies that may impact sleep, which landed them in second place.

    “These students have participated in our Wicked Problem Case Competition and the Global Case Competition, and this year a couple of them assisted in writing the case for our wicked competition,” said Max Michael, M.D., dean of the UAB School of Public Health. “Because the cases we use are so complex, our students are well-prepared in thinking through the process of dealing with complicated issues. I’m not at all surprised at their success and how well they represented our school at a national competition.”

  • Health Literacy Partnership of Alabama established
    Governor Robert Bentley has signed an executive order establishing the initiative to improve the health literacy of Alabamians, and UAB faculty will play an important role.

    Alabama Governor Robert Bentley signs an Executive Order establishing the Health Literacy Partnership of Alabama in his office at the State Capitol in Montgomery on Wednesday, April 20, 2016. UAB faculty members Conan Davis, Ann Gakumo and Joy Deupree are at left. (Photo courtesy of the Governor's Office.)Gov. Robert Bentley announced April 26 that he had signed an executive order establishing the Health Literacy Partnership of Alabama.

    The Health Literacy Partnership of Alabama, created by Executive Order 18, will recommend to the governor ways to improve the health literacy of Alabamians. Recommendations may take the form of regulatory or statutory changes, with initial recommendations due before the start of the 2017 regular session of the Alabama Legislature.

    “It is vitally important that people understand their health care needs and how they are treated. This reduces chronic illness and in turn lowers overall health care costs,” Bentley said. “This partnership is important to providing the resources needed by the people of Alabama to ensure they know how to properly seek treatment for any health issues they may have.”

    Joy Deupree, an assistant professor in the UAB School of Nursing and Robert Wood Johnson executive nurse fellow, will chair the Partnership.

    “From diagnosis to medication management and discharge instructions, patients are at risk for poor outcomes because they often do not understand how to use the information," Deupree said. “The support of the governor to establish a meaningful initiative to address health literacy disparities in Alabama is an important development for the health and economic future of our state. I am deeply grateful for his commitment to improve health care outcomes in our state.”

    The Partnership comprises members from health care-focused agencies and organizations across Alabama, including four other UAB faculty members:

    • Nancy E. Dunlap, M.D., professor emerita of medicine
    • Conan Davis, DMD, assistant dean for Community Collaborations and Public Health, UAB School of Dentistry
    • C. Ann Gakumo, assistant professor, UAB School of Nursing; Robert Wood Johnson nurse faculty scholar
    • Kathleen Ladner, adjunct associate professor at UAB School of Nursing
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