Lily Rothschild
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Lily Rothschild has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Aditya Bajaj
Immunology Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
1 shared publication - Colter Giem
Immunology Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
1 shared publication - Jacques Deguine
Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, USA
1 shared publication Jessica W. Luo
Immunology Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
1 shared publicationKimberly L. Carey
Immunology Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
1 shared publication- Ramnik J. Xavier
Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, USA
1 shared publication
Latest Publications
- Open Access
Optical Screening Identifies Chemical Modulators of Intracellular α-synuclein Aggregation
Parkinson’s disease (PD) is a movement disorder characterized by the accumulation of alpha-synuclein aggregates leading to dopaminergic neuron loss in the substantia nigra. While PD has been associated with environmental and microbiome changes, our ability to assess the mechanistic impact of these factors on synuclein aggregation in cells has remained limited. Here, we designed and optimized a high-throughput optical screening system to assess the effect of metabolites and small molecules on synuclein aggregation in cell lines expressing a synuclein-fluorescent protein fusion and treated with pre-formed fibrils (PFFs). Using this assay, we identified several compounds that modulate synuclein aggregate accumulation in cells, including harman, a β-carboline that led to reduced synuclein aggregation. We further investigated the transcriptional effect of harman and PFFs and identified changes in peroxiredoxins as a potential mechanism linking harman to aggregate accumulation. Altogether, this work establishes a pipeline to prioritize small molecules that can impact synuclein aggregate formation.
Open AccessOptical Screening Identifies Chemical Modulators of Intracellular α-synuclein Aggregation
Parkinson’s disease (PD) is a movement disorder characterized by the accumulation of alpha-synuclein aggregates leading to dopaminergic neuron loss in the substantia nigra. While PD has been associated with environmental and microbiome changes, our ability to assess the mechanistic impact of these factors on synuclein aggregation in cells has remained limited. Here, we designed and optimized a high-throughput optical screening system to assess the effect of metabolites and small molecules on synuclein aggregation in cell lines expressing a synuclein-fluorescent protein fusion and treated with pre-formed fibrils (PFFs). Using this assay, we identified several compounds that modulate synuclein aggregate accumulation in cells, including harman, a β-carboline that led to reduced synuclein aggregation. We further investigated the transcriptional effect of harman and PFFs and identified changes in peroxiredoxins as a potential mechanism linking harman to aggregate accumulation. Altogether, this work establishes a pipeline to prioritize small molecules that can impact synuclein aggregate formation.