Nabiximols, a combined THC and cannabidiol (CBD) product that is formulated as an oral (buccal) spray, has been shown to improve withdrawal symptoms without improving abstinence rates. Oral CBD has not shown efficacy in reducing the signs or symptoms of cannabis use, and likely has no benefit in cannabis use withdrawal symptoms. The CB-1 receptor antagonist rimonabant has shown efficacy in reducing the effects of cannabis in users, but with a risk for serious psychiatric side effects.Naltrexone, a mu opioid receptor antagonist, has shown mixed results for cannabis use disorder—both increasing the subjective effects of cannabis when given acutely, but potentially decreasing the overall use of cannabis with chronic administration. N-acetylcysteine (NAC) has shown some limited benefit in decreasing cannabis use in adolescents, though not with adults. Lithium, a mood stabilizer, has shown mixed results for treating symptoms of cannabis withdrawal, but is likely ineffective. Quetiapine, a second-generation antipsychotic, has been shown to treat cannabis withdrawal related insomnia and decreased appetite at the expense of exacerbating cravings. Oxytocin, a neuropeptide that the body produces, has shown some benefit in reducing the use of cannabis when administered intranasally in combination with motivational enhancement therapy sessions, though the treatment effect did not persist between sessions.Finally, CB1 antagonists such as rimonabant have been tested for utility in CUD. These drugs are effective at blocking the subjective effects of cannabis intoxication as well as the somatic components. This is accomplished by preventing THC binding to the CB1 receptor, effectively eliminating the ability to get high.
Collins bodies form in cortical and subcortical neurons where they disrupt the cells normal functioning and ultimately lead to cell death. Progressive dementia results from this gradual loss of nerve cells in certain parts of the brain. Researchers believe that a buildup of related, potentially toxic substances in nerve cells may also contribute to the signs and symptoms of this condition.This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In many cases, an affected person has a parent with the condition. References

National Library of Medicine. Genetics Home Reference - Familial encephalopathy with neuroserpin inclusion bodies


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