25 results on '"Fellner, Lisa"'
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2. Emergent creativity in frontotemporal dementia
3. iPS-abgeleitete Kardiomyozyten als therapeutische Hoffnungsträger
4. Models of Multiple System Atrophy
5. Neuroprotection by Epigenetic Modulation in a Transgenic Model of Multiple System Atrophy
6. Limited effects of dysfunctional macroautophagy on the accumulation of extracellularly derived α-synuclein in oligodendroglia: implications for MSA pathogenesis
7. Editorial: Targeting α-Synuclein in Parkinson's Disease and Multiple System Atrophy
8. Targeting α-Synuclein in Parkinson's Disease by Induced Pluripotent Stem Cell Models
9. Guanosine Protects Neuronal PC12 Cells from Serum Deprivation-induced Cell Death
10. Toll-Like Receptor 4 Promotes α-Synuclein Clearance and Survival of Nigral Dopaminergic Neurons
11. Autophagy in α-Synucleinopathies—An Overstrained System
12. The Role of Glia in Alpha-Synucleinopathies
13. The Immanent Evolution of Education: A Neglected Aspect of Comparative Education
14. Glial dysfunction in the pathogenesis of α-synucleinopathies: emerging concepts
15. Models of Multiple System Atrophy
16. Toll-like receptor 4 is required for α-synuclein dependent activation of microglia and astroglia
17. Commentary: Discriminating α-synuclein strains in parkinson's disease and multiple system atrophy
18. Multiple system atrophy – Are cerebrospinal fluid cytokines reliable potential diagnostic marker?
19. Anle138b Partly Ameliorates Motor Deficits Despite Failure of Neuroprotection in a Model of Advanced Multiple System Atrophy
20. Glia and alpha-synuclein in neurodegeneration: A complex interaction
21. Overexpression of α-synuclein in oligodendrocytes does not increase susceptibility to focal striatal excitotoxicity
22. Toll‐like receptor 4 is required for α‐synuclein dependent activation of microglia and astroglia
23. The Role of Glia in Alpha-Synucleinopathies
24. Glia and alpha-synuclein in neurodegeneration: A complex interaction
25. Overexpression of α-synuclein in oligodendrocytes does not increase susceptibility to focal striatal excitotoxicity
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