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...

Celý popis

Podrobná bibliografie

Hlavní autoři:	Joseph A. White, Thomas J. Krzystek, Hayley Hoffmar-Glennon, Claire Thant, Katherine Zimmerman, Gary Iacobucci, Julia Vail, Layne Thurston, Saad Rahman, Shermali Gunawardena
Médium:	Artigo
Jazyk:	Inglês
Vydáno:	BMC 2020-07-01
Edice:	Acta Neuropathologica Communications
Témata:	Huntingtin Rab4 Axonal transport Synaptic defects Behavioral deficits In vivo imaging
On-line přístup:	http://link.springer.com/article/10.1186/s40478-020-00964-z
Tagy:	Přidat tag Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!