Announcements of Opportunity
SURF: Announcements of Opportunity
Below are Announcements of Opportunity posted by Caltech faculty and JPL technical staff for the SURF program.
Each AO indicates whether or not it is open to non-Caltech students. If an AO is NOT open to non-Caltech students, please DO NOT contact the mentor.
Announcements of Opportunity are posted as they are received. Please check back regularly for new AO submissions! Remember: This is just one way that you can go about identifying a suitable project and/or mentor. Click here for more tips on finding a mentor.
Announcements for external summer programs are listed here.
New for 2021: Students applying for JPL projects should complete a SURF@JPL application instead of a "regular" SURF application.
Students pursuing opportunities at JPL must be
U.S. citizens or U.S. permanent residents.
|Project:||Gut-brain communications in Huntington’s disease (HD)|
Senior Research Scientist, (BBE),
HD patients develop debilitating motor, psychiatric, and cognitive symptoms. Although mutant huntingtin (mHTT) is expressed in all stages of brain development, it usually takes decades for the appearance of clinical symptoms. Moreover, the age of disease onset is highly variable among carriers with a similar polyglutamine (polyQ) length. Thus, other genetic and environmental modifiers may play a role. Inflammation is an environmental factor, which may accelerate the progression of HD symptoms. Pre-manifest HD subjects have activated microglia and elevated levels of pro-inflammatory cytokines including IL-1?, IL-6 and TNF-? in the circulation and in the cerebrospinal fluid several years before the onset of clinical symptoms (1, 2). Transcriptome analysis of Innate immune cells of manifest HD patients has also identified functional gene sets linked to NF-kB deregulation, and elevated expression of inflammatory mediators (). A prominent source of inflammation is the gastrointestinal (GI) tract, which bidirectionally communicates with the immune system and CNS. Disruptions in gut-immune and gut-brain signaling are linked to many biochemical changes implicated in brain disorders (3). Recent studies demonstrate that the GI resident microbes (termed the microbiota, and their collective genomes as the microbiome) influence neuroinflammation and the progression of brain disorders. We predict that an inflammatory GI environment induced by the abnormal growth of yet unknown bacteria may contribute to systemic inflammation in HD and influence the disease progression.
We are using Drosophila and mouse models to examine whether gut-brain interactions are altered in HD. Students will work on the impact of pathogenic bacteria and small therapeutic molecules on disease progression in Drosophila models.
Experience with Drosophila is preferred. Basic aseptic techniques. Knowledge in neurobiology, brain disorders, and amyloid proteins.
This AO can be done under the following programs:
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