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Welcome to the Leonidas Stefanis Lab at BRFAA

The interest of the lab lies in the pathogenesis of neurodegenerative conditions, such as Parkinson’s, Alzheimer’s and Huntington’s Diseases, Multiple System Atrophy and Amyotrophic Lateral Sclerosis. We are studying potential mechanisms through which such conditions may initiate and propagate within the nervous system, with the hope that, if these mechanisms are identified, they can be potential targets for neuroprotective therapies. The pathophysiological mechanisms that are more closely studied include protein misfolding, protein aggregation, inclusion formation and dissolution, impairment of protein degradation systems, synaptic dysfunction and neuronal cell death. These processes constitute common threads in such neurodegenerative conditions.  The group is more focused on the pathogenesis of Parkinson’s Disease (PD) and, in particular, in deciphering the link between identified genetic defects and the disease. Activities range from the study of biological material from patients afflicted with PD, up to cell culture and animal models. Models are largely based on the concept of synucleinopathies. Relevant biochemical pathways identified in such models are then examined in patient biological material, while insights from the study of the biological material of patients are then used to develop new models. Experimental therapeutics in synucleinopathies also constitute a major focus of the lab.

Expression of GFP and HA-tagged Lamp2a, the rate-limiting step for CMA activation, in neurons of the rat Anterior Olfactory Nucleus (AON) following injection with respective Adeno-Associated Viruses (AAVs).

Systemically injected Adeno-Associated Viruses (AAVs) downregulate alpha-synuclein expression in mouse dopaminergic neurons of the Substantia Nigra.

Seeding of endogenously expressed WT alpha-synuclein in inducibly expressing SH-SY5Y cells following exposure to alpha-synuclein PFFs.