Dr. Brackett is Director of the Male Fertility Research Program at the Miami Project to Cure Paralysis and Director of the Clinical Andrology Laboratory in the Department of Urology.
Dr. Brackett’s research is focused on treatment of infertility in men with spinal cord injury. Her research has been supported by the National Institutes of Health, the Craig Neilsen Foundation, the State of Florida Department of Health, and the Miami Project to Cure Paralysis.
Dr. Brackett serves on the Editorial Boards of: Fertility and Sterility and Asian Journal of Andrology. She has served on the Board of Directors of the American Society for Reproductive Medicine, and the Executive Council for the American Society of Andrology. She is Past President of the Society for Male Reproduction and Urology and is a frequent invited speaker at international medical conferences she has given more than 80 invited interviews to the lay press on the topic of male fertility following spinal cord injury.
The history of Spinalis began in 1984, when Claes Hultling was involved in a diving accident whereupon he hit his head on a rock and broke his neck, becoming paralyzed from the chest down. At the time of the accident he was working as an anesthesiologist at Karolinska Hospital. He has since dedicated his life to rehabilitation, research and advocacy for people with spinal cord injuries - also in Africa.
His research group is based in the Neurorestoration cluster at the London Bridge campus. He obtained first class honours in his undergraduate degree at the University of Oxford and was awarded his Ph.D. for work relating to the use of chondroitinase ABC in a model of brain injury in Prof. James Fawcett’s lab at the University of Cambridge.
His postdoctoral training was in Prof. Mary Bartlett Bunge’s lab at the Miami Project to Cure Paralysis where in collaboration with Prof. Fred Gage’s lab he identified a novel set of genes which promote regrowth of injured CNS axons in vitro and in vivo.
His lab in London uses rodent models of spinal cord injury and stroke to evaluate candidate therapies for neural repair, including Neurotrophin-3 (www.lawrencemoon.co.uk).
His lab is currently funded by the International Spinal Research Trust, the Brain Research Trust, the Rosetrees Trust and the UK’s Medical Research Council.
For fun and to accelerate research, his team also use 3D printing, custom electronics and artificial neural networks to automate and improve many of the methods they use in the lab. He is a co-founder of Research Devices Ltd (www.ResearchDevices.com) with the goal of providing novel in-cage solutions for rodent behavioural testing.
Dr. Strittmatter has a long-standing interest in ligand–receptor and signal transduction interactions in translational neuroscience. He developed expertise in the biochemistry of neuronal receptors during MD/PhD training with Solomon Snyder at Johns Hopkins. He pursued Neurology residency training at Massachusetts General Hospital under the guidance of John B. Martin, Raymond Adams, and C. Miller Fischer. His clinical practice included an early focus on Movement Disorders working with John Growdin and Kenneth Marek. Recently, he founded the Yale Memory Disorders Clinic leading 4 neurologists plus support personnel.
After Residency training, he developed an interest in the molecular biology of axon growth during a Fellowship with Mark Fishman. In his own laboratory at Yale, the mechanisms of axon guidance were the first focus, and insights into the molecular mechanisms of Semaphorin action during brain development were revealed. This led to an interest in the molecular pathways that inhibit fiber growth and functional rewiring of healthy and damaged adult brain. His work included the identification of Nogo and its receptor NgR1. This pathway was shown to play a role in limiting recovery after spinal cord injury and stroke. A key focus now is the study of brain plasticity and its modulation by NgR1 and by injury. Technically, he utilizes chronic in vivo imaging of neuronal connections, genetic alteration of mice and induction of surgical lesions resembling clinical trauma and stroke.
More recently, Dr. Strittmatter has focused on pathophysiological ligand–receptor pairs in the degenerative dementias. Molecular contributions of particular ligands for these pathologies had been discovered by genetic methods, but their mechanism of action remained poorly understood. Dr. Strittmatter has focused on defining the pathophysiological action of Amyloid-beta (Aβ) peptide oligomers in Alzheimer's disease, and on the role of secreted Progranulin in Fronto-Temporal Lobar Degeneration. For both of these molecules, interaction with the specific receptors on the neuronal surface is crucial. His investigations have led recently to the identification of PrPC and Sortilin as sites for Aß and PGRN, respectively. He has defined a molecular pathway from Aßo through PrPC to mGluR5 and Fyn kinase leading to synaptic dysfunction in AD models. His laboratory utilizes receptor ligand binding assays, expression cloning, electrophysiology, genetics and mouse behavior to study these pathways.
I have been investigating the impact of Spinal Cord Injury (SCI) on autonomic regulation of the cardiovascular system and have published over 60 peer-reviewed manuscripts describing the impact of autonomic nervous system (ANS) impairment on organ system function in persons with chronic SCI.
Recently the focus of my investigatory work has been to describe the impact of ANS impairment on blood pressure regulation and the secondary consequences of hypotension and orthostatic hypotension on cognitive dysfunction and quality of life in persons with SCI.
We were one of the first laboratories to document deficits in memory and information processing in hypotensive individuals with SCI compared to a normotensive SCI cohort, and believe that these deficits may stem, in part, from dysregulation of cerebral blood flow.
Subsequent funding from the New Jersey Commission for Spinal Cord Research, the Veterans Affairs Rehabilitation & Development Service and the Craig H. Neilsen Foundation has supported our continued exploration to describe associations between blood pressure dysregulation, cerebral blood flow and cognitive performance in individuals with SCI.