Abstract
Huntington's disease (HD) is an inherited autosomal dominant neurodegenerative disorder caused by a polyQ expansion (>36 glutamine repeats) in Huntingtin (Htt) protein. It is believed that dysfunction of corticostriatal system is one of the main pathological events. Special attention is paid to synaptic dysfunction of transmission between cortical and striatal neurons. This review focuses on modern concepts of molecular and cellular mechanisms of HD pathology and especially on alterations in corticostriatal connectivity. Calcium hypothesis of HD and new pharmacological targets are described.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Paper version not known
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Журнал высшей нервной деятельности им. И. В. Павлова
Paper Title
Journal
Date
