Modulation of mTOR and CREB pathways following mGluR5 blockade contribute to improved Huntington’s pathology in zQ175 mice
Abstract Huntington’s disease (HD) is a neurodegenerative disorder caused by a genetic abnormality in the huntingtin gene that leads to a polyglutamine repeat expansion of the huntingtin protein. The cleaved polyglutamine expansion of mutant huntingtin (mHTT) protein can form aggregates strongly cor...
Main Authors: | Khaled S. Abd-Elrahman, Stephen S. G. Ferguson |
---|---|
Format: | Article |
Language: | English |
Published: |
BMC
2019-04-01
|
Series: | Molecular Brain |
Subjects: | |
Online Access: | http://link.springer.com/article/10.1186/s13041-019-0456-1 |
Similar Items
-
Small, Seeding-Competent Huntingtin Fibrils Are Prominent Aggregate Species in Brains of zQ175 Huntington’s Disease Knock-in Mice
by: Franziska Schindler, et al.
Published: (2021-06-01) -
mGluR5 regulates REST/NRSF signaling through N-cadherin/β-catenin complex in Huntington’s disease
by: Jéssica M. de Souza, et al.
Published: (2020-08-01) -
Reduced mGluR5 Activity Modulates Mitochondrial Function
by: Miguel A. Gonzalez-Lozano, et al.
Published: (2021-06-01) -
Role of TFEB in Huntington’s Disease
by: Javier Ojalvo-Pacheco, et al.
Published: (2024-04-01) -
Prion‐like mechanisms in neurodegenerative disease: Implications for Huntington's disease therapy
by: Bhairavi Srinageshwar, et al.
Published: (2020-05-01)