Aditya Bajaj
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Aditya Bajaj has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Colter Giem
Immunology Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
1 shared publication - Fiona Powrie
The Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK
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- Lily Rothschild
Immunology Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, 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.
- Open Access
- 1 January 2021
- Published by Taylor & Francis in Gut Microbes
- Vol. 13 (1) , 1990827
Gut microbiota: sculptors of the intestinal stem cell niche in health and inflammatory bowel disease
Intestinal epithelium represents a dynamic and diverse cellular system that continuously interacts with gut commensals and external cues. Intestinal stem cells, which lie at the heart of epithelial renewal and turnover, proliferate to maintain a steady stem cell population and differentiate to form functional epithelial cell types. This rather sophisticated assembly-line is maintained by an elaborate micro-environment, sculpted by a myriad of host and gut microbiota-derived signals, forming an intestinal stem cell niche. This complex, yet crucial signaling niche undergoes dynamic changes during homeostasis and chronic intestinal inflammation. Inflammatory bowel disease refers to a chronic inflammatory response toward pathogenic or commensal microbiota, in a genetically susceptible host. Compositional and functional alterations in gut microbiota are pathognomonic of IBD. The present review highlights the modulatory role of gut microbiota on the intestinal stem cell niche during homeostasis and inflammatory bowel disease. We discuss the mechanisms of direct action of gut commensals (through microbiota-derived or microbiota-influenced metabolites) on ISCs, followed by their effects via other epithelial and immune cell types.
- 1 January 2021
- Published by Taylor & Francis in Gut Microbes
- Vol. 13 (1) , 1990827
Open AccessGut microbiota: sculptors of the intestinal stem cell niche in health and inflammatory bowel disease
Intestinal epithelium represents a dynamic and diverse cellular system that continuously interacts with gut commensals and external cues. Intestinal stem cells, which lie at the heart of epithelial renewal and turnover, proliferate to maintain a steady stem cell population and differentiate to form functional epithelial cell types. This rather sophisticated assembly-line is maintained by an elaborate micro-environment, sculpted by a myriad of host and gut microbiota-derived signals, forming an intestinal stem cell niche. This complex, yet crucial signaling niche undergoes dynamic changes during homeostasis and chronic intestinal inflammation. Inflammatory bowel disease refers to a chronic inflammatory response toward pathogenic or commensal microbiota, in a genetically susceptible host. Compositional and functional alterations in gut microbiota are pathognomonic of IBD. The present review highlights the modulatory role of gut microbiota on the intestinal stem cell niche during homeostasis and inflammatory bowel disease. We discuss the mechanisms of direct action of gut commensals (through microbiota-derived or microbiota-influenced metabolites) on ISCs, followed by their effects via other epithelial and immune cell types.