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UAB Research 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.

  • First-of-its-kind driving simulator lab at UAB powered by donation from Honda Manufacturing of Alabama and ALDOT
    The facility will enable new distracted-driving research, addressing a major public health issue that is a leading cause of highway and traffic-related injuries and death.

    During Distracted Driving Awareness Month, UAB has opened the first SUV driving simulator laboratory in the world.

    In the development of this lab, UAB partnered with Honda Manufacturing of Alabama, which provided a full-bodied 2016 Honda Pilot built at their factory in Lincoln, Ala., to be retrofitted with state-of-the-art simulator technology funded by the Alabama Department of Transportation. The technology gives UAB researchers the opportunity to conduct important safety studies involving distracted driving practices.

    Representatives from Honda, ALDOT and Alabama’s Office of the Attorney General joined the UAB team to announce the new initiative at a grand opening this week.

    “Honda Manufacturing of Alabama is honored to partner with UAB in this important project, with the goal of saving lives by increasing awareness of distracted driving,” said HMA Vice President Mike Oatridge. “Honda is very pleased we could donate the most advanced Honda Pilot ever built in Alabama, which has a five-star crash safety rating and features Honda most advanced safety features including the full range of Honda Sensing technology.”

    The goal of this effort is to facilitate solutions and best practices in motor-vehicle-related safety and crash prevention, addressing the major public health problem of highway and traffic-related injuries and death. 

    “Data tell us that distracted driving is a factor in nearly 50 percent of car crashes, which translates to one million injury-producing crashes each year,” said Despina Stavrinos, Ph.D., an assistant professor in the Department of Psychology in UAB’s College of Arts and Sciences and director of the UAB Translational Research for Injury Prevention Laboratory. “Ten percent of those crashes result in a fatality. Understanding which factors influence an individual’s likelihood to engage in distracted driving is essential to being able to purposefully address this growing problem. With this new simulator, we will be able to gain new information about how drivers participate in distracted behavior, giving us valuable insight that can increase the effectiveness of educational campaigns and improve driving safety.”

    The core of Stavrinos’ work is the prevention of injury, particularly unintentional injuries like those that result from distracted driving behaviors. She will lead her TRIP Lab in conducting studies with the new simulator.

    The first study, set to begin in a couple of weeks, will focus on teens and adults over 65, two of the most vulnerable populations when it comes to distracted driving.

    The simulator is intended to be available to researchers from all appropriate disciplines throughout UAB, other universities in the state, and even throughout the Southeast. In addition, non-university research scientists will be afforded access to the simulator and its associated support services.

    “UAB really thrives on investing in resources that are going to allow multidisciplinary research to take place,” said Richard Marchase, Ph.D., vice president for research and economic development at UAB. “With this new technology, which we are very thankful to Honda Manufacturing of Alabama and ALDOT for helping us create, we will be able to do just that and make this facility a destination for collaboration and innovation for researchers across campus and beyond. It will be a resource that I’m sure will be game-changing.”

    “Honda Manufacturing of Alabama is honored to partner with UAB in this important project, with the goal of saving lives by increasing awareness of distracted driving,” said HMA Vice President Mike Oatridge. “Honda is very pleased we could donate the most advanced Honda Pilot ever built in Alabama, which has a five-star crash safety rating and features Honda's most advanced safety features, including the full range of Honda Sensing technology.”

    Individuals interested in utilizing these resources or contributing should contact Stavrinos at dstavrin@uab.edu or (205) 934-7861. 

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