Dr. Milligan Carol

Dr. Milligan Carol

Professor

Neurobiology and Anatomy, Wake Forest School of Medicine
Medical Center Blvd, Winston-Salem, United States of America, 27157

plus Speciality

CELLULAR BIOLOGY

Biography:

Carol Milligan, PhD heads the ALS Center’s TSU coordinating a series of institutional and national grants that fund research for treatments and potential causes of ALS. Dr. Milligan is Professor in the Department of Neurobiology and Anatomy, and an Associate in the Department of Neurology. The overall focus of the research in Dr. Milligan’s lab is to understand the intra- and intercellular mechanisms that mediate motor neuron survival and death during normal development and in ALS and other motor neuron diseases.

Academic positions:

Academic Appointments: Wake Forest University School of Medicine, Wake Forest University: 2009-Present Professor, Department of Neurobiology and Anatomy 2007-Present Member, WFUHS Translational Science Institute 2007-Present Associate, Department of Neurology 2006-Present Associate Faculty, Women’s Health Center of Excellence 2001-2009 Associate Professor, Department of Neurobiology and Anatomy 1997-Present Member, Molecular Genetics Graduate Program 1996-Present Member, Interdisciplinary Neuroscience Graduate Program 1996-Present Graduate School Faculty 1996-2001 Assistant Professor, Department of Neurobiology and Anatomy Professional Experience: 2011-2012 Career Development for Women Leaders Program 2010-present Scientific Board of Advisors, ALS Biopharma, Doylestown, PA 2008-Present Director, Translational Science Unit of the ALS Center 2008-2012- Northeast ALS Consortium (NEALS) Co-Chair Sample Repository Committee Committee member 2012-present NEALS is a National Consortium of Medical Centers and coordinates many of the clinical trials for ALS. As chair of this committee I helped establish a national repository of cerebral spinal fluid, serum, plasma and DNA samples that is now available to investigators world-wide. I also helped establish the application and review processes to distribute the samples. 2007-Present Coordinator, WFUSM ALS Research Group This is a group of investigators whose research and clinical interests focus on ALS. It includes Drs. Caress, Cartwright, Delbono, Oppenheim and myself. 2006 Coordinator, Neuromuscular Research Interest Group This is a group of 20 researchers from seven departments or centers that meets on a monthly basis to discuss current research and potential collaborative projects. 1990 Teaching Assistant - Microanatomy, Department of Anatomy and Neurobiology, The Medical College of Pennsylvania. 1985-1987 Research Associate, NYGene Corporation, Malvern, Pennsylvania. Research Project: Research and development of monoclonal antibodies for use in cancer therapy. Funding Agency Reviewer: NIH: Special Study Section Panel Member, ALS and SMA (12/00) NIH: BDCN-3 Study Section (Member, 3/00-3/04) NIH: MCDN-2 (Ad hoc Member, 10/98) Spinal Cord Research Foundation Nominated for Membership on SCRF's Scientific Board of Advisors for 1998 NSF Muscular Dystrophy Association of Great Britain AIBS/USARMRMC Panel A Two: Amyotrophic Lateral Sclerosis Review Panel (5/04-05/05) NIH: CDIN study section - ad hoc member (6/04) NIH: ZRG1 IFCN A study section - ad hoc member (7/04) NIH: ZNS1 SRB-M - Fellowship review (ad hoc member, 11/04) NIH: CDIN Study Section - member (2006-2009) AIBS/USARMRMC Panel A Two: Amyotrophic Lateral Sclerosis Review Panel (September 2008; December 2009) VA Neurobiology and 2 Integrated Review Group - NURE (Ad hoc member, December 2008-2010) VA Neurobiology and 2 Integrated Review Group - NURE (member, 2010-2012) NIH Neurological Sciences and Disorders B study section- ad hoc member 6/2012

Research interests:

Carol Milligan, Ph.D. Statement of Research Interests Neuronal death is a prominent feature of the developing and pathological central nervous system (CNS). When I established my laboratory, we focused on embryonic chick motoneurons in tissue culture and investigated the intracellular mechanisms mediating motoneuron death. We identified several novel biochemical and molecular events that appear critical to this cell death. One of these events was increased expression of the amyloid precursor protein (APP) in motoneurons deprived of trophic support as compared to healthy counterparts. We were the first lab to identify APP as a substrate for caspases, critical proteases in cell death. This event is now thought to be part of the pathology in Alzheimer’s as well as other neurodegenerative diseases, including those involving motoneurons. Nonetheless, this and many other events occur after the cell becomes committed to die, and specific inhibition of these events, while delaying the death of the cells, does not restore its health or function. Our research on this topic continues on several novel fronts under the premise that a full investigation into events associated with or leading to neuronal cell death will be critical to better understanding many pathologies that affect humans. There are many reasons to conduct basic science research, including pure investigation to determine quite simply how things work. The quest for discovery motivates me as well as the majority of scientists. However, my earliest experience in research immediately after college instilled in me that the goal of my research was to lead to a better understanding of pathologies with the ultimate goal of developing novel and effective therapeutics. Motoneuron pathologies are directly contributory to several nervous system disorders and diseases in humans, notably Amyotrophic Lateral Sclerosis (ALS). ALS is the most debilitating neurodegenerative disease with an adult onset (30-70 years of age with clinical symptoms that result from the selective dysfunction, denervation and ultimate degeneration of cortical and spinal motoneurons. ALS has the same incidence as multiple sclerosis and our ALS Center serves about 120 ALS patients at any given time. There is no treatment that significantly ameliorates or delays progression of disease, and death occurs within 3-5 years from diagnosis. The specific insult, agent and/or genetic abnormality that initiate disease pathology are not known. Ninety-five percent of all cases are sporadic and have a worldwide distribution. Previous ALS research has not been fruitful in developing effective treatments for the disease, perhaps because treatments are initiated too late in the course or because the targets (caspase inhibition, anti-oxidants) are too far down a cascade of events that eventually terminate with cell death. Indeed, in collaborative studies with Ron Oppenheim’s lab, examining the role of motoneuron death in the G93A SOD1 mouse model of ALS, we learned that muscle denervation, rather than cell death, may mediate symptom onset and disease progression. Our research emphasis must now focus not only on the motoneuron cell body and environment in the spinal cord, but also on the neuromuscular junction and muscle. My research focus has evolved and expanded from a relatively straightforward focus on motoneuron cell death mechanisms to the ramifications of motoneuron dysfunction for diseases such as ALS. With this also comes a realization that no single investigator and approach will prove fruitful. For this reason I have worked for the past several years developing collaborative projects and initiating our ALS research group, helping to expand our ALS Center to include active research in addition to superior clinical care. Our group includes senior investigators renowned for their work in motoneuron and muscle biology, clinicians whose expertise is centered on neuromuscular disorders, including ALS. We have also expanded our collaborations to include novel approaches in imaging. There is no doubt that basic science research is essential if we are to understand the underlying events of neurological disorders. Identifying and characterizing these events will be critical to the development of innovative and effective therapeutic strategies. These goals will only be attained through collaborative and interdisciplinary projects utilizing the experience and expertise of basic scientists and clinicians.

What I think of the idea behind WebmedCentral and WebmedCentral plus:

While I am a strong believer of peer-review, I think that biomedical publishing in its conventional form can be improved. Many scientists have valuable results that should be made available to increase our knowledge and in many ways the current peer-review system slows getting this information out to the scientific community. The current system of review by just two or three reviewers mostly working anonymously needs to be broadened in its scope provide more opportunity for evaluation of the published work. I am in support of a system that will instill more rapidity, accountability, and transparency into biomedical publishing and especially to make it as unbiased as possible.