Juliana Dushanova

Bulgarian Academy of SciencesBulgaria

Dr. Dushanova’s research interests are in motor neurophysiology, pathophysiology of Parkinson’s disease and in the development of approaches for diagnostics. Her works span human and non-human primate research, computational modeling and simulations. She received her MS degree from Sofia University, Bulgaria, Predoctoral fellow by Prof. Pfurtscheller at Department of Medical Informatics, Ludwig Boltzmann Institute for Medical Informatics and Neuroinformatics, Technical University Graz, Austria, PhD from Institute of Neurobiology, Bulgarian Academy of Sciences and studied neurophysiology under Prof. J.P. Donoghue in the Neuroscience Department of Brown University, RI USA. Assoc. Prof. J. Dushanova’s research is in the field of movement disorders and she has been involved in electroencephalography research and practice since 1994.

2books edited

1chapters authored

Latest work with IntechOpen by Juliana Dushanova

Parkinson's disease (PD) results primarily from the death of dopaminergic neurons in the substantia nigra. Current PD medications treat symptoms; none halt or retard dopaminergic neuron degeneration. The main obstacle to developing neuroprotective therapies is a limited understanding of the key molecular mechanisms that provoke neurodegeneration. The discovery of PD genes has led to the hypothesis that misfolding of proteins and dysfunction of the ubiquitin-proteasome pathway are pivotal to PD pathogenesis. Previously implicated culprits in PD neurodegeneration, mitochondrial dysfunction, and oxidative stress may also act in part by causing the accumulation of misfolded proteins, in addition to producing other deleterious events in dopaminergic neurons. Neurotoxin-based models have been important in elucidating the molecular cascade of cell death in dopaminergic neurons. PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process.

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