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Introduction Huntington’s disease (HD) is a progressive neurodegenerative disorder caused by an expanded cytosine-adenine-guanine (CAG) trinucleotide repeat on chromosome 4. Exploring sex-related differences in disease manifestation may improve understanding and guide more tailored therapeutic and supportive interventions. Objective To investigate sex differences in the clinical presentation and functional outcomes in a single-center HD cohort, including employment status and use of supportive therapies. Methods We retrospectively analyzed 102 patients with HD who were regularly seen at the Department of Neurology, Medical University of Innsbruck. Exact CAG repeat length was available for 101 participants. Multinomial logistic regression was applied to assess symptom distribution, access to neurorehabilitation, and the impact on employment status. Results We included 44 men and 58 women with genetically confirmed Huntington’s Disease. Among participants with available CAG data ( n  = 101), there was no difference in CAG-Repeat length between male and female patients as well as no differences in the onset of motor or non-motor symptoms (all p-values > 0.05). We found that irritability was significantly more prevalent in female patients ( p  = 0.033). Moreover, women were significantly less likely to be employed than men ( p  < 0.001). No sex differences were observed in the utilization of non-pharmacological therapies such as physiotherapy, occupational therapy, speech therapy, or psychotherapy ( p  > 0.05). Conclusion Female patients with HD showed higher rates of irritability and lower workforce participation, suggesting clinically relevant sex-related differences. These findings highlight the importance of considering sex as a factor in both clinical management and social support strategies.

Background Huntington’s disease (HD) is an autosomal-dominant neurodegenerative disorder and emerging evidence indicates sex-specific differences in disease manifestation and progression. Objective To summarize current evidence on sex-related differences in HD across genetic, clinical, biomarker, and treatment domains and identify gaps in knowledge. Methods A literature search was performed in PubMed and Google Scholar (up to 31.01.2026). Eligible studies examined sex- or gender-related differences in individuals with genetically confirmed HD or those at risk. Meta-analyses, reviews, animal studies, theses, abstracts only, and non-English papers were excluded. After screening and full-text review, secondary citation tracking identified further studies. Sex was defined as the biological classification of participants (male/female) as originally reported, whereas gender was defined as socially constructed roles or identities, where explicitly assessed. Terminology in this review reflects the terminology used in the original publications. Results Fourty-four studies met inclusion criteria. Genetic studies showed similar cytosine-adenine-guanine (CAG) repeat lengths across sexes when parent-of-origin was not considered, while paternal transmission was consistently linked to repeat expansion and earlier disease onset. Clinically, women more frequently exhibited depression, irritability, and greater functional impairment, whereas men more often showed apathy and substance misuse. Medication patterns differed, with women being more likely to receive antidepressants and anxiolytics, and men antipsychotics. Biomarker studies indicated potential sex-related differences in body composition, uric acid, neuroimaging, and hormonal profiles, though available evidence remained heterogeneous and exploratory. Conclusions Sex-related differences in HD are evident in genetic transmission, psychiatric symptoms, functional decline, and medication use. Biomarker findings suggest additional sex-specific biological signatures.

•A review was conducted of 62 patients over 25 years who received tiapride, tetrabenazine, or both.•Tiapride was more often chosen as first-line therapy (69% vs 31%).•Less frequent discontinuation was noted with tiapride because of adverse effects (27% vs 55%).•Adverse effects in combination therapy appeared mostly within the first year.•Reinitiation of either drug was feasible in selected cases. Chorea is a key motor feature of Huntington’s disease (HD). In Germany, Austria, and Switzerland, tiapride and tetrabenazine are established and formally approved for symptomatic management of chorea in HD. However, long-term real-world comparative data are lacking, and early documentation is often incomplete. The purpose of this study was to analyze prescription patterns, tolerability, and reasons for discontinuation of both medications in a retrospective real-world HD cohort and to examine outcomes of reinitiation and combination therapy. We retrospectively reviewed medical records from 140 adults with genetically confirmed HD between 2000 and 2025. Patients receiving tiapride, tetrabenazine, or both were analyzed at the treatment-course level. Exploratory comparisons included Total Motor Score and Total Functional Capacity values closest to treatment initiation. Sixty-two patients received tiapride, tetrabenazine, or both and contributed one or more treatment courses. Tiapride was more frequently used as first-line therapy (69% vs 31%). Documented treatment discontinuation due to adverse effects was less frequent in tiapride courses than in tetrabenazine courses (27% vs 55%; P = 0.005). Fatigue and apathy were the most common adverse effects with tiapride, whereas mood-related adverse events were more frequently recorded as reasons for dose reduction or discontinuation in tetrabenazine-treated patients. Adverse effects in combination therapy appeared mostly within the first year. Reinitiation of either drug was feasible in selected cases. Tiapride was prescribed more frequently and showed fewer documented adverse effect–related discontinuations than tetrabenazine. Reinitiation proved feasible in selected patients. Careful monitoring is needed in the first year of combination therapy. The long timeframe captures evolving clinical practices but also contributes to heterogeneity and incomplete documentation. Prospective studies with standardized psychiatric assessments and chorea ratings are needed to confirm these findings and guide long-term treatment strategies.

Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder and emerging evidence indicates sex-specific differences in disease manifestation and progression. To summarize current evidence on sex-related differences in HD across genetic, clinical, biomarker, and treatment domains and identify gaps in knowledge. A literature search was performed in PubMed and Google Scholar (up to 31.01.2026). Eligible studies examined sex- or gender-related differences in individuals with genetically confirmed HD or those at risk. Meta-analyses, reviews, animal studies, theses, abstracts only, and non-English papers were excluded. After screening and full-text review, secondary citation tracking identified further studies. Sex was defined as the biological classification of participants (male/female) as originally reported, whereas gender was defined as socially constructed roles or identities, where explicitly assessed. Terminology in this review reflects the terminology used in the original publications. Fourty-four studies met inclusion criteria. Genetic studies showed similar cytosine-adenine-guanine (CAG) repeat lengths across sexes when parent-of-origin was not considered, while paternal transmission was consistently linked to repeat expansion and earlier disease onset. Clinically, women more frequently exhibited depression, irritability, and greater functional impairment, whereas men more often showed apathy and substance misuse. Medication patterns differed, with women being more likely to receive antidepressants and anxiolytics, and men antipsychotics. Biomarker studies indicated potential sex-related differences in body composition, uric acid, neuroimaging, and hormonal profiles, though available evidence remained heterogeneous and exploratory. Sex-related differences in HD are evident in genetic transmission, psychiatric symptoms, functional decline, and medication use. Biomarker findings suggest additional sex-specific biological signatures.