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Dr. Michael Johnston is a research scientist at Kennedy Krieger Institute. He is also a professor of Neurology and Pediatrics at the Johns Hopkins University School of Medicine.
Biographical Sketch:
Dr. Johnston attended Franklin and Marshall College before going on to medical school at the University of Pittsburgh, from which he graduated cum laude in 1971. His postdoctoral training at the Johns Hopkins Hospital included work in Pediatrics, Neurology, Pharmacology, and Pediatric Neurology. After teaching positions and research work at the University of Michigan Medical School and University of Michigan Hospitals, Dr. Johnston returned to Baltimore in 1988. Today he is Senior Vice President and Chief Medical Officer at Kennedy Krieger Institute, as well as director of both KKI’s Division of Neurology & Developmental Medicine and KKI’s Neuroscience Laboratory. Dr. Johnston is an attending physician at both Johns Hopkins Hospital and Kennedy Krieger Children's Hospital.
Research Summary:
Dr. Johnston and his group, including Drs. Mary Blue, Mary Ann Wilson and Alec Hoon, perform clinical and basic laboratory research focused on developing therapies to reduce brain injury in infants and children as well as to promote recovery by enhancing brain plasticity. His laboratory was one of the first to describe the mechanisms through which the neurotransmitter glutamate triggers brain injury from lack of oxygen, trauma and other insults. If administered early enough, drugs that block the effects of glutamate on one of its receptors called the NMDA receptor can totally prevent brain injury in infants.
His group also recognized that the major role that glutamate plays in injury during development is related to the important role it plays in normal development. During development, glutamate released from nerve terminals helps to refine the synaptic connections that link neurons into circuits. These mechanisms are enhanced during development to shape circuits in response to environmental stimuli and formation of memories, a process called "neuronal plasticity." When the brain is injured, these circuits can be damaged by too much glutamate, much like a computer's chips can be damaged by a power surge during a thunderstorm.
Because injury and plasticity are two sides of the same processes in brain development, Dr. Johnston’s research has grown beyond mechanisms of injury into processes that control brain plasticity. For example, he studies how cerebral cortex is reassigned in response to injury, which is the major mechanism for recovery of function from stroke and other disorders. Even learning and long-term memory are based on these same mechanisms, since it depends on neurons exciting each other with glutamate and changes in synaptic connections. Numerous disorders associated with mental retardation are caused by genetic flaws in these systems, and Dr. Johnston recently completed a project focused on a defect in a neuronal signaling process involved in a form of X-linked mental retardation.
So Dr. Johnston’s initial pursuit of ways to reduce brain injury in infants and children with medications has led to a broader understanding of processes involved in plasticity and recovery from injury. The immature brain's glutamate signaling system, which is enhanced compared to the adult in order to shape its complex neuronal circuitry, proves to be its "Achilles’ Heel" when it is injured. Accordingly, Dr. Johnston’s research has proved to be relevant to a broad range of neurodevelopmental disabilities including cerebral palsy, mental retardation, lead poisoning, genetic metabolic disorders, and epilepsy as well as brain injury from lack of oxygen and trauma.
Recent Publications/Presentations:
Johnston MV and Hoon AH. Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernictus or mitochondrial encephalopathies. J Child Neurology 15:588-591, 2000.
Wilson MA, Johnston MV, Goldstein GG, Blue ME. Neonatal lead exposure impairs development of rodent barrel field cortex. Proc. N. Acad. Sci 97:5540-5545, 2000.
Nakajima W, Ishida A, Lange MS, Gabrielson KL, Wilson MA, Martin LJ, Blue ME and Johnston MV. Apoptosis has a prolonged role in neurodegeneration after hypoxic ishcemia in newborn rat. J.Neuroscience 20:7994-8004, 2000.
Harum KH, Alemi L and Johnston MV. Cognitive impairment in Coffin-Lowry syndrome correlates with reduced RSK 2 activation. Neurology 56:207-214, 2001.
Johnston, MV, Nakajima, W and Hagberg, H. Mechanisms of hypoxic degeneration in the developing brain. The Neuroscientist 8:212-220, 2002.
Johnston MV, Trescher WH, Ishida A, Nakajima W. Neurobiology of hypoxic-ischemic injury in the developing brain. Pediatric Research 49: 735-741, 2001. |
