Huntington's disease (HD) is an inherited, neurodegenerative disorder caused by 
a single-gene mutation: a CAG expansion in the huntingtin (HTT) gene that 
results in production of a mutated protein, mutant HTT, with a polyglutamine 
tail (polyQ-HTT). Although the molecular pathways of polyQ-HTT toxicity are not 
fully understood, because protein misfolding and aggregation are central 
features of HD, it has long been suspected that cellular housekeeping processes 
such as autophagy might be important to disease pathology. Indeed, multiple 
lines of research have identified abnormal autophagy in HD, characterized 
generally by increased autophagic induction and inefficient clearance of 
substrates. To date, the origin of autophagic dysfunction in HD remains unclear 
and the search for actors involved continues. To that end, recent studies have 
suggested a bidirectional relationship between autophagy and primary cilia, 
signaling organelles of most mammalian cells. Interestingly, primary cilia 
structure is defective in HD, suggesting a potential link between autophagic 
dysfunction, primary cilia and HD pathogenesis. In addition, because polyQ-HTT 
also accumulates in primary cilia, the possibility exists that primary cilia 
might play additional roles in HD: perhaps by disrupting signaling pathways or 
acting as a reservoir for secretion and propagation of toxic, misfolded 
polyQ-HTT fragments. Here, we review recent research suggesting potential links 
between autophagy, primary cilia and HD and speculate on possible pathogenic 
mechanisms and future directions for the field.