Joseph R. Mazzulli, Ph.D.
Affiliations: | 2007 | University of Pennsylvania, Philadelphia, PA, United States |
Area:
Neuroscience BiologyGoogle:
"Joseph Mazzulli"Mean distance: (not calculated yet)
Cross-listing: Neurotree
Parents
Sign in to add mentor| Harry Ischiropoulos | grad student | 2007 | Penn | |
| (Catechol oxidation and alpha-synuclein aggregation: Implications for selective dopaminergic neurodegeneration in Parkinson's disease.) | ||||
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Publications
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| Stojkovska I, Mazzulli JR. (2021) Detection of pathological alpha-synuclein aggregates in human iPSC-derived neurons and tissue. Star Protocols. 2: 100372 |
| Cuddy LK, Wani WY, Morella ML, et al. (2019) Stress-Induced Cellular Clearance Is Mediated by the SNARE Protein ykt6 and Disrupted by α-Synuclein. Neuron |
| Kim J, Hu C, Moufawad El Achkar C, et al. (2019) Patient-Customized Oligonucleotide Therapy for a Rare Genetic Disease. The New England Journal of Medicine |
| Tsunemi T, Perez-Rosello T, Ishiguro Y, et al. (2019) Increased lysosomal exocytosis induced by lysosomal Ca channel agonists protects human dopaminergic neurons from α-synuclein toxicity. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience |
| Zunke F, Mazzulli JR. (2019) Modeling neuronopathic storage diseases with patient-derived culture systems. Neurobiology of Disease |
| Zunke F, Moise AC, Belur NR, et al. (2017) Reversible Conformational Conversion of α-Synuclein into Toxic Assemblies by Glucosylceramide. Neuron |
| Stojkovska I, Krainc D, Mazzulli JR. (2017) Molecular mechanisms of α-synuclein and GBA1 in Parkinson's disease. Cell and Tissue Research |
| Burbulla LF, Song P, Mazzulli JR, et al. (2017) Dopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson's disease. Science (New York, N.Y.) |
| Chung SY, Kishinevsky S, Mazzulli JR, et al. (2016) Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation. Stem Cell Reports |
| Mazzulli JR, Zunke F, Tsunemi T, et al. (2016) Activation of β-Glucocerebrosidase Reduces Pathological α-Synuclein and Restores Lysosomal Function in Parkinson's Patient Midbrain Neurons. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 36: 7693-706 |