Fluoxetine in the treatment of Huntington's disease

Marchi, Nicola; Daniele, Fabiana; Ragone, Maria Antonietta

doi:10.1007/s002130000575

Cited by 49 publications

(27 citation statements)

References 9 publications

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“…From these results, we conclude that antidepressants with a more specific action on serotonin and norephineprine may provide greater protection against 3-NP neurotoxicity. Some clinical studies have also indicated the therapeutic potential of these antidepressants in HD patients (Shoulson, 1981;De Marchi et al, 2001). Jin et al (2009) reported that fluoxetine suppressed kainic acid-induced neurotoxicity in the hippocampus).…”

Section: Discussionmentioning

confidence: 97%

Nitric oxide mechanism in the protective effect of antidepressants against 3-nitropropionic acid-induced cognitive deficit, glutathione and mitochondrial alterations in animal model of Huntington's disease

Kumar

Kalonia²,

Kumar³

2010

Behavioural Pharmacology

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Huntington's disease (HD), a basal ganglia disorder, is characterized not only by a spectrum of motor deficits, but also by emotional, cognitive and psychiatric manifestations. Cognitive impairment is one of the serious manifestations of this disease in the later stage of life. Although there is currently no cure for HD, there has been a surge of clinical trials involving patients with HD over the past 5 years. However, cognitive measures have generally been lacking from these trials. The beneficial effect of antidepressants in HD has been suggested in recent clinical trials. However, their mechanism of action is still not clear. Therefore, this study was designed to elucidate and compare the mechanistic role of different classes of antidepressants (sertraline, venlafaxine, imipramine and trazodone) against 3-nitropropionic acid (3-NP)-induced cognitive impairment, oxidative stress (glutathione) and mitochondrial dysfunction in rat hippocampus. Systemic treatment with 3-NP (10 mg/kg for 14 days) significantly impaired memory performance (both in the Morris water maze and elevated plus maze escape retention test), oxidative defence (glutathione redox status) and mitochondrial enzyme complex activities in rat hippocampus. Sertraline, venlafaxine, imipramine and trazodone treatments significantly improved performance in both cognitive tasks and glutathione redox status, and restored mitochondrial enzyme complex activities, as compared with the 3-NP treated group. L-arginine (50 mg/kg) pretreatment for 14 days together with a subeffective dose of sertraline (10 mg/kg), venlafaxine (10 mg/kg), imipramine (10 mg/kg) or trazodone (10 mg/kg) partially attenuated their protective effects. Further, G-nitro-L-Arginine-Methyl Ester (10 mg/kg) pretreatment together with subeffective dose of sertraline (10 mg/kg), venlafaxine (10 mg/kg), imipramine (10 mg/kg) and trazodone (10 mg/kg) significantly enhanced their efficacy. The results of this study suggest that nitric oxide modulation is involved in their protective effect of antidepressants against 3-NP induced cognitive dysfunction in rats.

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Section: Discussionmentioning

confidence: 97%

Nitric oxide mechanism in the protective effect of antidepressants against 3-nitropropionic acid-induced cognitive deficit, glutathione and mitochondrial alterations in animal model of Huntington's disease

Kumar

Kalonia²,

Kumar³

2010

Behavioural Pharmacology

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“…Olanzapine [80•] Open trial, 11 Improvement in five patients on "overall behavior"; irritability improved, aggression unchanged; depression, anxiety, and obsessions also improved in some patients Olanzapine [81] Case report, 1 Improvement in aggression and irritability (symptoms disappeared after 5 months of olanzapine treatment) Fluoxetine [82] Case report, 1 with irritability and agression (second patient also treated with fluoxetine for movements only) Improvement in irritability and aggression; authors suggest that this may be due to treatment of underlying obsessive-compulsive disorder Olanzapine and divalproex [83] Case reports, 2 Improvement (psychotic symptoms with aggression) Buspirone [84] Case report, 1 Improvement Sertraline [85] Case reports, 2 Improvement Clozapine [78] Retrospective case reviews, 2 with aggression, 2 with delusions (eight patients total, four tried clozapine for chorea only) Improvement in aggression and delusions; considerable sedation in seven of eight patients…”

Section: Comments and Outcome On Target Symptomsmentioning

confidence: 98%

An overview of psychiatric symptoms in Huntington’s disease

Anderson

Marder

2001

Curr Psychiatry Rep

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Huntington's disease (HD) is an inherited autosomal dominant disorder characterized by neurologic, cognitive, and psychiatric symptomatology. Psychiatric symptoms in HD are often amenable to treatment, and relief of these symptoms may provide significant improvement in quality of life. This review will briefly describe neurologic, neuropsychologic and brain imaging data, and then review psychiatric syndromes seen in HD and their treatment.

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“…A report of two patients with genetically confirmed HD from the same extended pedigree were administered fluoxetine 20 mg/day for disabling obsessive-compulsive disorder. 98 Both patients had a sustained improvement in UHDRS chorea score (by 8 and 5 points), with prompt worsening on attempts to discontinue the drug. However, in the case of a 46-year-old man with genetically confirmed HD who was treated with fluoxetine 20 mg daily for new-onset disabling obsessive-compulsive disorder, chorea worsened within several days after initiating the treatment, although his decline was not quantified.…”

Section: Antidepressantsmentioning

confidence: 91%

Symptomatic Treatment of Huntington Disease

2008

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Summary: Huntington disease (HD) is a progressive heredoneurodegenerative disease manifested by chorea and other hyperkinetic (dystonia, myoclonus, tics) and hypokinetic (parkinsonism) movement disorders. In addition, a variety of psychiatric and behavioral symptoms, along with cognitive decline, contribute significantly to the patient's disability. Because there are no effective neuroprotective therapies that delay the progression of the disease, symptomatic treatment remains the cornerstone of medical management. Several classes of medications have been used to ameliorate the various symptoms of HD, including typical and atypical neuroleptics, dopamine depleters, antidepressants, antiglutamatergic drugs, GABA agonists, antiepileptic medications, acetylcholinesterase inhibitors, and botulinum toxin. Recently, surgical approaches including pallidotomy, deep brain stimulation, and fetal cell transplants have been used for the symptomatic treatment of HD. The selected therapy must be customized to the needs of each patient, minimizing the potential adverse effects. The primary aim of this article is to review the role of the different therapies, both available and investigational, for the treatment of the motor, psychiatric, behavioral, and cognitive symptoms of HD, and to examine their impact on the patient's functionality and quality of life.

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Fluoxetine in the treatment of Huntington's disease

Cited by 49 publications

References 9 publications

Nitric oxide mechanism in the protective effect of antidepressants against 3-nitropropionic acid-induced cognitive deficit, glutathione and mitochondrial alterations in animal model of Huntington's disease

Nitric oxide mechanism in the protective effect of antidepressants against 3-nitropropionic acid-induced cognitive deficit, glutathione and mitochondrial alterations in animal model of Huntington's disease

An overview of psychiatric symptoms in Huntington’s disease

Symptomatic Treatment of Huntington Disease

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