Star Trk(B)

The generation and transmission of the information in the central nervous system (CNS) strongly rely on the structural and functional framework formed by neuronal cells. However, astrocytes, the major glial cell type, may profoundly impact on the performance of the framework, as they give metabolic and trophic support to neurons, and regulate synapse formation and function. Under pathological settings astrocytes rapidly respond to injury by promoting the formation of scar tissue and supporting local acute inflammatory reactions—both aspects are essential to confine the lesions, repair the damage and restore tissue homeostasis. Clearly, dysregulation of astrocyte activities may be dangerous for CNS function. In multiple sclerosis (MS), an inflammatory neurodegenerative disorder of the CNS, chronic lesions are characterized by permanent demyelination and neurodegeneration. Here, we observed the upregulation of the neurotrophin receptor TrkB on astrocytes (Fig. 1). Neurotrophins constitute a family of growth factors including NGF, BDNF, NT3 and NT4/5. Since they are important for survival, differentiation and function of neurons, neurotrophins have been regarded as beneficial for neuroprotection and neuroregeneration. Similarly to human MS lesions, astrocyte TrkB was strongly upregulated also in experimental autoimmune encephalomyelitis (EAE), the animal model of MS, indicating that neuroinflammation makes astrocytes more sensitive to neurotrophin action. Interestingly, the main TrkB variant detected in astrocytes both in MS and Star Trk(B) The astrocyte path to neurodegeneration