Single-cell transcriptional profiling of Huntington's disease in human and mouse models
Name
1227278096-MIT.pdf
Size
13.51 MB
Format
Adobe PDF
Checksum (MD5)
7f4c5bc1596590a6e5a1ee6d838e6f2d
Author(s)
Pineda, Sergio Sebastian.
Advisor(s)
Manolis Kellis and Myriam Heiman.
Alternative Title
Single-cell transcriptional profiling of HD in human and mouse models
Date Issued
2020
Publisher
Massachusetts Institute of Technology
Abstract
Uncovering the mechanisms that drive cell type-specific vulnerability differences in Huntington's disease (HD) is an imperative prerequisite to finding a reliable therapeutic target. The most affected regions and cell types likely possess vulnerability factors or lack protective factors possessed by other cell types that lead to their early dysfunction and enhanced loss, but such factors remain elusive. In order to characterize the cell type-specific responses induced by mutant huntingtin (mHTT), we applied single-nucleus RNA sequencing to pro- file gene expression changes in human HD and two commonly used mouse models of HD. In the process, we produced the first molecular atlas of the human neostriatum, identified new and previously unobserved cell types, and examined the molecular conservation of this brain region across species. We also developed and documented new computational methods and techniques for curating and analyzing single-cell data from post-mortem human brain samples.
Description
Thesis: S.M., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, September, 2020
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 45-48).
Subjects
Electrical Engineering and Computer Science.
MIT Department
Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science
Terms of Use
MIT theses may be protected by copyright. Please reuse MIT thesis content according to the MIT Libraries Permissions Policy, which is available through the URL provided.
Persistent DSpace Link
