Lena Burbulla

  • 3232 Citations
20102019
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Personal profile

Research Interests

My research focus is to define key molecular pathways in the pathogenesis of neurodegeneration by studying rare genetic diseases with a goal of identifying converging pathways and specific targets for therapeutic development. Utilizing genetic forms of Parkinson’s disease as a model, the overall objective of my work is to evaluate disease mechanisms in specific subtypes of human neurons in an age-dependent manner. For that I am studying long-term cultures of vulnerable midbrain dopaminergic neurons generated from induced pluripotent stem cells by a combination of genomic approaches and functional physiological assays. One major theme is the investigation of the role of oxidative stress as one possible initiating factor contributing to neurodegeneration in Parkinson’s disease. My goal is to evaluate the consequences of oxidative stress in disease progression by studying associated pathogenic mechanisms such as accumulation of aggregation-prone-proteins and toxic dopamine by-products as well as deficient autophagy and lysosomal degradation. This work also includes identifying specific targets for effective therapeutic intervention in Parkinson's disease.

Training Experience

2013Postdoctoral Fellowship, Massachusetts General Hospital, Harvard Medical School
2018Postdoctoral Fellowship, Northwestern University Feinberg School of Medicine

Education/Academic qualification

PhD, University of Tuebingen, Germany

… → 2011

Keywords

  • Aging
  • Cell Biology
  • Metabolism
  • Neuroscience
  • Parkinson’s Disease
  • Stem Cells

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Research Output 2010 2019

  • 3232 Citations
  • 16 Article
  • 3 Comment/debate
  • 2 Review article
  • 1 Chapter

Conversion of Quinazoline Modulators from Inhibitors to Activators of β-Glucocerebrosidase

Zheng, J., Jeon, S., Jiang, W., Burbulla, L., Ysselstein, D., Oevel, K., Krainc, D. & Silverman, R. B., Feb 14 2019, In : Journal of Medicinal Chemistry. 62, 3, p. 1218-1230 13 p.

Research output: Contribution to journalArticle

Glucosylceramidase
Quinazolines
Parkinson Disease
Mutant Proteins
Structure-Activity Relationship
Glucosylceramidase
Quinazolines

Corrigendum: Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230)

Seibler, P., Burbulla, L., Dulovic, M., Zittel, S., Heine, J., Schmidt, T., Rudolph, F., Westenberger, A., Rakovic, A., Munchau, A., Krainc, D. & Klein, C., Mar 1 2019, In : Brain. 142, 3, p. E10

Research output: Contribution to journalComment/debate

Open Access
Iron Overload
Osteogenesis Imperfecta
Ferritins
Brain
Data Display
6 Citations (Scopus)

Acid ceramidase inhibition ameliorates α-synuclein accumulation upon loss of GBA1 function

Kim, M. J., Jeon, S., Burbulla, L. & Krainc, D., Jun 1 2018, In : Human molecular genetics. 27, 11, p. 1972-1988 17 p.

Research output: Contribution to journalArticle

Acid Ceramidase
Synucleins
Ceramides
Glucosylceramidase
Parkinson Disease
3 Citations (Scopus)

Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells

Seibler, P., Burbulla, L., Dulovic, M., Zittel, S., Heine, J., Schmidt, T., Rudolph, F., Westenberger, A., Rakovic, A., Münchau, A., Krainc, D. & Klein, C., Oct 1 2018, In : Brain. 141, 10, p. 3052-3064 13 p.

Research output: Contribution to journalArticle

Iron Overload
Iron
Autophagy
Oxidative Stress
Induced Pluripotent Stem Cells