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M3 Study participation but not the antidepressant bupropion reduces apathy in huntington’s disease
  1. Harald Gelderblom1,2,
  2. Torsten Wüstenberg3,
  3. Tim McLean4,
  4. Lisanne Mütze4,
  5. Wilhelm Fischer4,
  6. Carsten Saft5,
  7. Rainer Hoffmann5,
  8. Sigurd Süssmuth4,
  9. Peter Schlattmann6,
  10. Erik van Duijn7,
  11. Bernhard Landwehrmeyer4,
  12. Josef Priller1,8
  1. 1Department of Neuropsychiatry, Charité- Universitätsmedizin Berlin, Berlin, Germany
  2. 2Department of Medicine, National Association of Statutory Health Insurance Funds, Berlin, Germany
  3. 3Department of Psychiatry, Charité-Universitätsmedizin Berlin, Berlin, Germany
  4. 4Department of Neurology, University of Ulm, Ulm, Germany
  5. 5Department of Neurology, Huntington-Centre NRW, Ruhr-University, St. Josef Hospital, Bochum, Germany
  6. 6Institute of Medical Statistics, Computer Sciences and Documentation, Universityhospital, Jena, Germany
  7. 7Department of Psychiatry, Leiden University Medical Centre, Leiden, The Netherlands
  8. 8Cluster of Excellence NeuroCure, DZNE and BIH, Berlin, Germany


Background Apathy is the most common neuropsychiatric syndrome in HD and contributes significantly to the burden of disease. This is in contrast to the prevailing therapeutic nihilism, as no effective treatment is at hand. Several single case reports and results of small series suggested the effectiveness of the antidepressant bupropion for the treatment of apathy in HD and other neurodegenerative diseases.

Aim To evaluate the efficacy and safety of bupropion in the treatment of apathy in HD.

Methods In this phase 2 b multi-centre, double-blind, placebo-controlled crossover trial, individuals with HD and clinical signs of apathy according to the Structured Clinical Interview for Apathy–Dementia (SCIA-D), but not depression (n = 40) were randomised to receive either bupropion 150/300 mg or placebo daily for 10 weeks. The primary outcome parameter was a significant change of the Apathy Evaluation Scale (AES) score after ten weeks of treatment as judged by an informant (AES-I) living in close proximity with the study participant. The secondary outcome parameters included changes of 1. AES scores determined by the patient (AES-S) or the clinical investigator (AES-C), 2. psychiatric symptoms (NPI, HADS-SIS, UHDRS-behaviour), 3. cognitive performance (SDMT, Stroop, VFT, MMSE), 4. motor symptoms (UHDRS-m), 5. activities of daily function (TFC, UHDRS-function), and 6. caregiver distress (NPI-D).

Results At baseline, there were no significant treatment group differences in the clinical primary and secondary outcome parameters. At endpoint, there was no statistically significant difference between treatment groups for all clinical primary and secondary outcome variables. Study participation, irrespective of the intervention, lessened symptoms of apathy. Study participants rated their symptoms of apathy (AES-S) as significantly less severe than caregivers (AES-I) and clinical investigators (AES-C).

Conclusion Study participation, but not the antidepressant bupropion alleviates apathy in HD. Our observations document the need for carefully controlled trials when investigating therapeutic interventions for the neuropsychiatric symptoms of HD.

  • apathy
  • neuropsychiatric symptom
  • symptomatic treatment
  • bupropion. IIT

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