Recent research has identified ER stress as a
major mechanism implicated in cytotoxicity in many
neurodegenerative diseases, among them Huntington’s
disease. This genetic disorder is of late-onset, progressive
and fatal, affecting cognition and movement. There is
presently no cure nor any effective therapy for the disease.
This review focuses on recent findings that shed light on
the mechanisms of the advent and development of ER
stress in Huntington’s disease and on its implications,
highlighting possible therapeutic avenues that are being
or could be explored.