Synaptic dysfunction in Huntington's disease: a new perspective

Research output: Contribution to journalReview article


Huntington's disease (HD) is caused by a polyglutamine expansion in the protein huntingtin and is characterized by intraneuronal inclusions and widespread neuronal death at the late stage of the disease. In research, most of the emphasis has been on understanding the cell death and its mechanisms. Until recently, it was believed that the vast majority, if not all, of the symptoms in HD are a direct consequence of neurodegeneration. However, increasing evidence shows that subtle alterations in synaptic function could underlie the early symptoms. It is of particular interest to understand the nature of this neuronal dysfunction. Normal huntingtin interacts with various cytoskeletal and synaptic vesicle proteins that are essential for exocytosis and endocytosis. Altered interactions of mutant huntingtin with its associated partners could contribute to abnormal synaptic transmission in HD. This review describes recent advances in understanding synaptic dysfunction in HD.


Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Cell Biology


  • pathophysiology, neurotransmission, Huntington's disease, exocytosis, synaptic protein, endocytosis
Original languageEnglish
Pages (from-to)1901-1912
JournalCellular and Molecular Life Sciences
Issue number17
Publication statusPublished - 2005
Publication categoryResearch

Bibliographic note

The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041)