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The ability to store information and to learn, as well as to adapt to the continuously changing environment, is critical for proper function of the central nervous system (CNS). Indeed, the human brain continuously undergoes structural and functional remodeling, which is the basis for brain plasticity. Plasticity is also the underlying mechanism for functional recovery following brain injury. Brain plasticity has several components. In the uninjured adult mammalian brain, neurogenesis, i.e. generation of new neurons, primarily occurs in two brain regions, the walls of the lateral ventricles and the hippocampus. While in rodents the immature neurons generated in the subventricular zone migrate through the rostral migratory stream to their final destination in the olfactory bulbs, striatum appears to be the main destination for the immature neurons generated in this region in humans. Adult hippocampal neurogenesis seems to be of importance for at least some aspects of learning and memory. Brain injury, such as stroke, can be a strong inducer of neurogenesis, in particular in the subventricular zone and striatum. Synaptogenesis, formation and maturation of new connections between neurons, as well as synapse elimination and changes in neuronal excitability and gene expression are other examples of activity dependent mechanisms of brain plasticity as a means for learning, memory and adaptation. These processes, together with axonal and dendritic collateral sprouting from uninjured neurons and regeneration of damaged axons, are also important for functional recovery after brain damage.

Complement is part of the innate immune response known for its role in the elimination of pathogenic bacteria. Complement proteins are produced by many cell types including astrocytes, microglia and neurons. Complement activation results in the formation of C3-convertase, an enzymatic complex that activates the central molecule of the cascade, the third complement component (C3). The proteolytic activation of C3 by a C3-convertase generates C3a, a 77 amino acid long peptide with anaphylatoxic and pro-inflammatory properties. The larger fragment C3b, binds to the activating surface such as bacterial or cell membrane and triggers the terminal part of the cascade and culminating in the assembly of the cytolytic membrane attack complex on the target cell membrane or other surface. Research during the past 10 years has shown that complement is a major regulator of brain plasticity and function.

The current main focus of Pekna’s lab focuses on the functions of complement in functional recovery after brain ischemia. The long-standing goal is to understand the role of complement activation in ischemia-induced brain plasticity. Towards this goal, the lab uses experimental in vivo and in vitro models of brain ischemia to determine the specific roles of the complement system and its activation products, in particular C3a, in ischemic brain damage and functional recovery after stroke. Pekna’s laboratory showed that the complement system stimulates the formation of new neurons in the adult mammalian brain, both under basal conditions and after ischemia, and thus may contribute to brain repair. They also showed that complement-derived peptide C3a is protective against tissue loss induced by neonatal hypoxia-ischemia. Recently, the lab demonstrated that C3a stimulates post-stroke neural plasticity and that intranasal treatment with C3a promotes functional recovery after stroke and ameliorates cognitive impairment in an experimental model of perinatal asphyxia.

We believe that better understanding of the inflammatory response in cerebral ischemia will provide opportunity for the development of new treatment strategies for patients affected by stroke and birth-asphyxia.

Page Manager: Katinka Almrén|Last update: 2/9/2017

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