The CTBR awarded 5 seed funding projects to full and associate faculty members for our 2013-2014 grant year. The seed funding projects received $20,000 for one year.
mTOR mediation of alcohol neurobiological and behavioral effects: the role phospholipase D
PI: Michael Lewis, Psychology Department
Dr. Lewis’ research is relevant to our understanding of alcohol's effects on the brain and other bodily functions as well as alcohol abuse and dependence. The objective of this project was to investigate the role mTOR signaling in alcohol’s behavioral and physiological effects and, more specifically, to EtOH interaction with PLD in the production of mTOR. The specific aims focused on the role of PLD in alcohol consumption and dependence-related behaviors. The long-term objective of this line of inquiry is to determine the role of PLD-controlled mTOR signaling in not only the behavioral and physiological effects of alcohol, but also its longevity enhancing effects. Results are still pending.
Promoting myelin repair via increased cytoskeletal plasticity
PI: Carmen Melendez-Vasquez, Biology Department
The goal of Dr. Melendez-Vasquez’s project was to promote myelin repair and return of function in multiple sclerosis (MS) a demyelinating disease that targets oligodendrocytes (OL) and the myelin sheaths they produce. Strategies that seek to promote OL maturation and remyelination are central to neuroprotection. Currently, no such therapies exist and the only available treatments are targeted to limit the damage caused by the inflammatory response within demyelinated lesions. Dr. Melendez-Vazquez’s preliminary data indicated that repair of immune-mediated demyelinated lesions is accelerated in mutant mouse lacking myosin II in oligodendrocytes. This is in line with her lab’s previous studies showing improved repair in non-immune mediated model of focal demyelination (Rusielewicz et al., 2014). This seed project resulted in developing a new model of immune-mediated focal demyelination, a publication (referenced below), preliminary data for a grant from the MS Society and a new model of immune-mediated focal demyelination. Dr. Melendez-Vasquez’s studies are of great relevance to regeneration and repair and ideally suited to one of the Center’s goals to build translational/clinical capacity in the areas of Neuro/Behavior, with emphasis on neuroprotection and therapeutics.
Rusielewicz T, Nam J, Damanakis E, John GR, Raine CS, Melendez-Vasquez CV. Accelerated repair of demyelinated CNS lesions in the absence of non-muscle myosin IIB. Glia. 2014 Apr;62(4):580-91. doi: 10.1002/glia.22627. Epub 2014 Jan 28. PMID: 24470341.
Identification of patho-adaptive genomic changes in Pseudomonas aeruginosa
PI: Weigang Qiu, Biology Department
Pseudomonas is a major pathogen causing opportunistic infections in hospitals. Dr. Qiu proposed to identify the genomic basis of pathogenicity of P. aeruginosa by whole-genome sequencing and by comparative analysis of clinical and environmental isolates. Over 40 new genome sequences have been obtained. Dr. Qiu and his lab have built a genome database, developed bioinformatics pipelines, and identified strain-specific genomic elements. This seed project resulted in a NSF CAREER proposal with Dr. Qiu’s collaborator Dr Joao Xavier of MSKCC as the PI. Additionally, the award helped build new bioinformatics and analytical capabilities of the Dr. Qiu’s lab.
Deciphering Specific Risk Behaviors for HIV Transmission in Women
PI: Carol Roye, Hunter-Bellevue School of Nursing
This project compared the behaviors, health and mental health history of recently infected (HIV-positive) women with a matched control of negative women. This is a novel study and may illuminate previous unaddressed risk factors in women, such as heterosexual anal intercourse. As of August 2014 the study is still ongoing and results are pending. Once all data and results have been collected and analyzed Dr. Roye’s research group will be better able to design a risk-reduction intervention.
cAMP/VEGF signaling to prevent & improve cognition and plasticity in TBI
PI: Peter Serrano, Psychology Department
For this project, Dr. Serrano used the controlled cortical impact (CCI) model of TBI, which induces retrograde and anterograde memory deficits, in rats to determine the efficacy of simultaneously activating cAMP/VEGF signaling pathways as a combinatorial therapeutic approach against retrograde amnesia that models the immediate consequences of TBI on cognition and anterograde learning and memory deficits that model long-term deficits in cognition. TBI is a major public health issue that affects each year more than 1 million people in the US. TBIs can cause lifelong deficits in mental health and other impairments, which can require long-term rehabilitation and other services. In lower socioeconomic populations these services often fall short of the need and care of these individuals. TBI is particularly relevant to health disparity populations. According to a CDC report, African Americans exhibit the highest death rate from TBI and with American Indians/Alaska Natives they have the highest TBI hospitalization rates (Langlois, JA, et. al, 2006). TBI is considered the “silent epidemic” as the general population remains largely unaware of it and the deficits are often invisible (Rutland-Brown W, et. al, 2006). Moreover, TBI is considered a major risk factor for the development of Alzheimer disease (AD) (Mortimer JA, et. al, 1991;Fleminger S, et. al, 2003). The Serrano group identified a working memory deficit in rats given PGJ2 as a method to induce inflammation, which models the traumatic brain injury, and poor spatial learning and memory retention when inflammation was induced within the hippocampus. Molecular analyses are currently underway.
The results of this seed funding project will be incorporated into the resubmission of a grant due Nov 2014. This funding allowed the Serrano group to solidify its collaboration with Weill Cornell and prompted more experiments to be executed with these collaborators. Additionally, Dr. David Mozley of Weill Cornell Medical College served as Co-PI on the project and as Dr. Serrano’s mentor. Dr. Mozley’s mentoring increased Dr. Serrano’s knowledge and training on micro-PET, which will be instrumental in furthering his animal model of TBI.