About our lab
The Mandel lab applies a diverse set of approaches to questions related to the mechanisms of gene regulation in the healthy and diseased brain. At one end of a spectrum, we use animal models to study the developing and adult mouse brain, as well as to model the severe neurological disorder, Rett Syndrome, to better understand its molecular basis and how we might reverse symptoms. We also use human cell lines and brain tissue to study aging and its relationship to cognitive decline. At the extreme other end of the spectrum, we use high resolution imaging and single cell chromatin and transcriptomic analyses to unravel fundamental principles of gene regulation that extend across all organisms. This wide berth—from molecule to organism—allows us to capture the excitement of biology at more than one level and keeps our research at the forefront of the field.
We're recruiting postdoctoral fellows
The Mandel Lab has openings for postdocs interested in using molecular analyses to understand nervous system adaptations during aging and underlying neurological disease.
- A postdoctoral position is available for understanding the role of transcriptional and chromatin changes in brain during human aging.
- A postdoctoral position is available for exploring new molecular editing approaches toward repair of the neurological disease, Rett Syndrome.
Interested applicants should send a CV and list of references to Gail Mandel at email@example.com. Prior molecular experience is preferred.
Mandel Lab 2019
Members of the Mandel Lab gather for a group photo in the LBRB Courtyard.
(Left to Right) Jessica Yeates, Gabe Haw, Michael Spinner, Mike Jacobson, Michael Linhoff, Gail Mandel, John Sinnamon, Jenna Fisk, James McGann, Abinaya Ravisankar and Aliyih Bristol.
Be sure to check out the lab's most recent paper
In vivo repair of a protein underlying a neurological disorder by Sinnamon et al., Cell Reports, 2020, is the first report showing success of an RNA editing approach, using Adeno Associated Virus delivery to the hippocampus, to restore protein function in neurons affected in a human disease. The work focuses on a patient loss-of-function mutation in the transcription factor, MeCP2, which underlies the neurological disorder, Rett syndrome. Repairing the mutation leads to recovery of chromatin binding of MeCP2 across three different neuronal populations in the hippocampus in the affected mice. Because Rett syndrome in mice is reversible, our study is the first step towards a potential cure for this CNS disease.
Join our lab
If you are interested in working on our projects as a postdoctoral fellow, please send your CV and names of three references to Gail Mandel via email.
Summer Research Opportunities
Occasional and open only to highly motivated students, usually in their senior year of undergraduate studies. If you are interested, contact Gail Mandel via email.