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University of California San Francisco
Neurology
Dr. Rabinovici is the Edward Fein and Pearl Landrith Distinguished Professor of Neurology and Radiology at the University of California San Francisco. His research investigates how structural, functional and molecular brain imaging techniques can be used to improve diagnostic accuracy in dementia and to study the biology of neurodegenerative diseases. He serves as co-Director of the UCSF ADRC, PI of the IDEAS and New IDEAS studies, and co-PI and PET Core lead of the LEADS study, among other projects. Dr. Rabinovici’s work is supported by the National Institutes of Health, the Alzheimer’s Association, the American College of Radiology, the Rainwater Charitable Foundation and additional foundations and industry partners. Awards recognizing his work include the 2015 Christopher Clark Award for human amyloid imaging, the 2012 American Academy of Neurology Research Award in Geriatric Neurology and the 2010 Best Paper in Alzheimer’s Disease Neuroimaging: New Investigator Award from the Alzheimer’s Association.
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QPS Austria GmbH
Neuropharmacology
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University of British Columbia
Michael Smith Laboratories
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Icahn School of Medicine at Mount Sinai
Neurology
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Jahangirnagar University
Biochemistry and Molecular Biology
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Gothenburg University
Dep Psychiatry and neurochemistry, Inst.Neuroscience and physiology, Sahlgrenska Academy
University of California, San Francisco
Radiology
I am Professor of Radiology and Bio-engineering at UCSF, San Francisco. I have more than 15 years experience in computer vision, signal processing, graph theory, medical imaging and informatics. I have had continuous and successive experiences in forming and leading research teams comprising of basic and clinical scientists in executing NIH-funded research projects. I have published more than 100 peer reviewed papers ranging from microwave engineering, superconductivity, image/signal processing, vision, graph theory and neuroscience, and two US patents. I have attracted several NIH grants, on graph algorithms for accelerated MRI, theoretical neuroscience and network modeling of dementia and Parkinson’s. The defining characteristic of my work has been inter-disciplinarity: finding innovative ways to apply computation and algorithms to biomedical applications. My group was an early adopter of mathematical models of brain connectivity networks, a subject that marries computer science with neuroradiology. I have deep interest in the graph properties of brain networks, and how they are altered in neurological disorders like epilepsy, dementia, movement disorders, traumatic brain injury and stroke. A recent project on dementia modeling was selected by the NIH for the prestigious EUREKA award that supports highly innovative but risky research, and another by the BRAIN Initiative. My team has developed novel image reconstruction algorithms for fast MRI, motion correction for MR angiography, and new methods in tractography, Q-ball imaging, brain connectivity networks and computational neurology. My research program focuses nowadays in developing brain network models of neurodegenerative diseases, especially Alzheimer's and Parkinson's.
University of Miami
John P. Hussman Institute for Human Genetics
Dr. Rajabli is an Associate Scientist at the John P. Hussman Institute for Human Genomics (HIHG) at the University of Miami Miller School of Medicine. He has 10 years of experience in machine learning and computational biology, with a primary focus on the neurological disorders of Alzheimer’s disease. During his doctoral and postdoctoral training, he has mastered a variety of techniques including genome-wide association studies, family-based association studies, next-generation sequence analysis methods, population genetics, and whole-exome sequencing.
Instituto de Medicina Molecular João Lobo Antunes
Luísa Lopes lab
I am currently on the last year of my PhD thesis in Neurosciences at iMM, Lisbon (Instituto de Medicina Molecular João Lobo Antunes). My PhD work is focused on Amyloid Precursor Protein (APP), mostly known by its contribution to Alzheimer’s Disease. In this project, we took a step back to understand the physiological role of APP at the synapse, namely by controlling NMDA receptors. Therefore, I am currently focused on synapse biology and working in a collaboration between iMM (Portugal) and Institute of Molecular and Cellular Pharmacology (IPMC, France). During my career path I have worked in other research institutes in Portugal and abroad (Center for Neuroscience and Cell Biology - CNC, Coimbra and University of Oxford) and explored different research fields such as gene therapy. During this trajectory, I have contributed to the publication of two research papers and one review. What truly motivates me is to generate new scientific knowledge with clinical applications. I am also passionate about science communication, discussing ideas and establishing new collaborations.
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TU Kaiserslautern
Human biology and human genetics
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PsychoGenics Inc.
Neurodegeneration
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iMM Instituto de Medicina Molecular João Lobo Antunes
Faculdade de Medicina de Lisboa
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IPMC UMR7275
UCA ED85
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Hospital Clínic de Barcelona-IDIBAPS
Neurology Service, Alzheimer's Disease and other cognitive disorders Unit
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UNIVERSITY OF TEXAS HEALTH SAN ANTONIO
Cell Systems & Anatomy
UCSF
Neurology
Dr. Kamalini Ranasinghe received her medical degree from the University of Peradeniya, Sri Lanka and earned her doctorate degree in Cognition and Neuroscience from the University of Texas at Dallas, under the mentorship of Dr. Michael Kilgard. She completed her Fellowship training at the Memory and Aging Center, UCSF under the mentorship of Drs. Bruce Miller, MD, Keith Vossel, MD and Srikantan Nagarajan, PhD. Dr. Ranasinghe currently is an assistant professor at the Memory and Aging Center. Her research centers on the network dysfunction of neurodegenerative diseases including Alzheimer’s disease and frontotemporal lobar degeneration. Much of her work has been devoted to identifying the spatial and temporal characteristics of network dysfunction using MEG-imaging of the brain.
University of Florida
Center for NeuroGenetics; Molecular Genetics and Microbiology
Dr. Laura P.W. Ranum, is the Kitzman Family Professor of Molecular Genetics and Microbiology, and the Founding Director of the Center for Neurogenetics at the University of Florida. In 2011, her lab overturned long-standing dogma in the field by discovering that an entire class of novel proteins are produced from repeat expansion mutations without canonical AUG-initiation codons. These toxic, repeat-associated, non-AUG (RAN) proteins have been shown to accumulate in a growing number of neurodegenerative diseases including Huntington’s disease, amyotrophic lateral sclerosis, frontotemporal dementia, ataxia and myotonic dystrophy. Mechanistic insights from her recent work have identified novel therapeutic strategies to treat RAN protein disorders. Dr. Ranum’s scientific contributions have been honored by the Hans Steinert Award for Myotonic Dystrophy Research (2017); election as a fellow the American Association for the Advancement of Science (2016); Javits Neuroscience Investigator Award, NIH/NINDS. (2015-2022) and W.F. Keck Award-Repeat Associated Non-ATG Translation: Impact and Biology (2012-2015). Additionally, she has served as Chair/co-Chair of eight international scientific meetings and is an advocate for ataxia, myotonic dystrophy and ALS patients.
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Ageing Epidemiology (AGE) Research Unit, School of Public Health, Faculty of Medicine, The Imperial Collge of Science, Technology and Medicine
School of Public Health, Faculty of Medicine
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Avid Radiopharmaceuticals
Neuroscience
Alkahest Inc
Clinical Development
Alkahest’s therapeutic agents stem from a deep understanding of the changing plasma proteome in healthy aging and in age-related diseases. As we age, the majority of our proteins stay the same. But about 15% of our proteins change substantially as we age, or as we contend with disease. It’s these proteins, the chronokines, which inspire Alkahest science. By targeting chronokines, we develop clinical candidates that either increase or decrease the levels of circulating chronokines to promote innate and natural restorative biological processes or discourage pathological, degenerative processes in age-related diseases.