Excess Rab4 rescues synaptic and behavioral dysfunction caused by defective HTT-Rab4 axonal transport in Huntington’s disease

Excess Rab4 rescues synaptic and behavioral dysfunction caused by defective HTT-Rab4 axonal transport in Huntington’s disease

Abstract Huntington’s disease (HD) is characterized by protein inclusions and loss of striatal neurons which result from expanded CAG repeats in the poly-glutamine (polyQ) region of the huntingtin (HTT) gene. Both polyQ expansion and loss of HTT have been shown to cause axonal transport defects. Whi...

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Bibliographic Details
Main Authors: Joseph A. White, Thomas J. Krzystek, Hayley Hoffmar-Glennon, Claire Thant, Katherine Zimmerman, Gary Iacobucci, Julia Vail, Layne Thurston, Saad Rahman, Shermali Gunawardena
Format: Article
Language:English
Published: BMC 2020-07-01
Series:Acta Neuropathologica Communications
Subjects:
Huntingtin
Rab4
Axonal transport
Synaptic defects
Behavioral deficits
In vivo imaging
Online Access:http://link.springer.com/article/10.1186/s40478-020-00964-z

Internet

http://link.springer.com/article/10.1186/s40478-020-00964-z

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