How Xanax works
Huntington’s is a rare inherited disease caused by mutations in the huntingtin (HTT) gene. This results in the formation of a misfolded protein, which is then degraded by the cell, leading to the formation of toxic protein fragments. These fragments cluster inside nerve cells and cause neurodegeneration, causing the symptoms of Huntington’s disease.
Xanax is a benzodiazepine, a family of chemicals that binds to two benzodiazepine receptors in the central nervous system. The receptor BNZ1 regulates sleep, while BNZ2 affects muscle relaxation, motor coordination, anticonvulsant activity, and memory. Both receptors are bound to the gamma-aminobutyric acid (GABA) receptors; when bound to benzodiazepines, BNZ1 and BNZ2 enhance the effects of GABA by increasing the affinity of the receptor for GABA. When Xanax is bound to BNZ1 and BNZ2, GABA is more likely to bind to the GABA receptor.
GABA is an inhibitory neurotransmitter. It works to decrease the excitability of neurons, decreasing the nerve signal emitted. By enhancing the activity of GABA, Xanax decreases muscle tremors and anxiety, but also may cause drowsiness.
Xanax in clinical trials
Initial clinical trials conducted in 1980s compared Xanax oral tablets to placebo in a four-week, double-blind clinical study in patients with anxiety or anxiety-associated depression. Up to 4 mg per day of Xanax was significantly more efficient than placebo at reducing anxiety as determined by patient and physician impressions using the Hamilton anxiety rating scale.
Xanax can cause several side effects, including ataxia (difficulty moving and balancing), drowsiness, fatigue, memory impairment, changes in weight or appetite, and blurred vision.
Xanax should not be used in combination with alcohol, as the combination can severely depress the central nervous system.
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