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Amantadine and Huntington's disease

Amantadine and Huntington's disease


Medication and Treatment for Huntington's disease


Susceptibility to Oseltamivir and Amantadine of Human Influenza Viruses Circulating in Portugal

Background:
Since 2002, increasing incidence of amantadine resistance has been detected worldwide. In a minor extent, emergence of oseltamivir-resistant strains has been identified during 2007/2008 winter season.
This study aims to contribute to global surveillance on antiviral resistance and to risk assessment of drug use with continuous liberation of national data. Its main objective is to evaluate influenza virus susceptibility to oseltamivir and amantadine during 2004/2005-2007/2008, in Portugal.

Methods:
Susceptibility to oseltamivir was evaluated by fluorescence assay in 233 strains from 2004/2005-2007/2008. NA and HA1 gene sequencing was performed in statistical outliers and in 30% of susceptible strains, identified by fluorescence.
Resistance to amantadine was evaluated by pyrosequencing in 128 strains from 2004/2005-2006/2007.

Results:
All 89 A(H3N2) and 94 B influenza strains tested shown to be oseltamivir-susceptible. Of the 50 A(H1N1) strains tested, 3 of the 14 from 2007/2008 were drug-resistant by exhibiting fluorescence-IC50 values approximately 400 times higher than the median value and mutation H274Y in NA sequence.
Susceptibility to amantadine was detected in all 23 A(H1N1) strains tested. Resistance was found, by identification of mutation S31N in M2 sequence, in 24 of the 105 A(H3N2) strains tested: in the single strain from 2005/2006 and in 23 of the 35 strains from 2006/2007.

Discussion:
The origin of oseltamivir-resistant A(H1N1) strains in Portugal (2007/2008), and concurrently in other European countries, remains unclear. Their persistence through influenza seasons and their effect in viral evolution could become clearer with subsequent and continuous data analysis. Conversely, emergence of amantadine resistance in Portugal, identified in 2005/2006 and persistent through 2006/2007, probably derived from global spread of A(H3N2) virus bearing mutation S31N.

These preliminary findings can presently contribute to monitor international dispersion of resistant viruses. Continuous and timely input of national data onto global surveillance constitutes the basis for risk assessment on antiviral drug use.

Author(s): V. Correia, H. Rebelo-de-Andrade, L. Santos, M. Gíria
Affiliation: Centro Nacional da Gripe, Instituto Nacional de Saúde (Research grant supported by Calouste Gulbenkian Foundation - Portugal), Lisboa, Portugal


Source: http://www.setbb.com/phpbb/viewtopic.php?mforum=fluwiki2&p=1078#1078


The U.S. Food and Drug Administration (FDA) has approved Xenazine (tetrabenazine) for the treatment of chorea in people with Huntington’s disease. Chorea is the jerky, involuntary movement that occurs in people with this disease.

Xenazine is the first medication of any kind approved in the U.S. by the FDA for the treatment of any symptom of Huntington’s disease. According to the FDA, “Serious side effects reported with use of Xenazine include depression and suicidal thoughts and actions.”

Huntington's disease, which affects about 30,000 people in the U.S., is a rare, inherited neurological disorder that causes degeneration of brain cells. The deterioration of brain cells causes the uncontrolled movements, loss of intellectual powers, and emotional difficulties. Huntington’s disease is passed from parent to child and each child of a parent with the disease has a 50% chance of inheriting the condition.

Huntington’s disease is an autosomal dominant inherited disorder characterized by a triad of motor, cognitive, and psychopathological symptoms (1). Currently, the only treatment options available for the disease are symptomatic. Aripiprazole is a novel antipsychotic drug that possesses the pharmacological characteristics of a partial agonist of the dopamine D2 and serotonin 5-HT1A receptors and antagonist of the 5-HT2A receptor. We report the use of aripiprazole in the treatment of psychotic symptoms in a patient with Huntington’s disease whose diagnosis was confirmed by DNA analysis.
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