INTRODUCTION: Huntington's disease is a neurodegenerative, autosomal dominant 
disease that mainly affects the basal ganglia. The disorder is caused by 
mutation in the gene encoding the huntingtin protein (Htt), producing 
intracellular aggregates. The adult form (chorea with dementia) is the most 
frequent. It is characterized by unpredictable, spasmodic, involuntary and 
constant movements, mostly associated with psychiatric and cognitive 
alterations.
DEVELOPMENT: The main characteristics of Huntington's disease are: neuronal 
loss, glyosis, and accumulations of mutated Htt, all associated with different 
underlying channels in the pathogenesis of the disease, such as: excitotoxicity, 
energy deficit (ATP depletion), reduction in the synthesis and release of 
neurotrophic factors (BDNF and GDNF), and oxidative stress. Oxidative stress is 
involved in the pathogenesis of various neurodegenerative diseases, including 
Huntington's disease, and numerous studies have shown the existence of oxidative 
damage in the plasma and tissue of patients suffering from this disease.
CONCLUSIONS: Oxidative stress in patients with Huntington's disease may be used 
as an evolutionary-prognostic marker of both the disease and therapeutic 
effectiveness, as well as an interesting field of research for the development 
of new therapeutic strategies.