OBJECTIVE: To explore the change and impact factors of craving for heroin in patients after 6 month methadone maintenance treatment (MMT). METHODS: The questionnaire of craving for heroin was used to measure the level of craving for heroin when patients just entered the study and were treated for 6 months. The influence of MMT on craving in patients were analyzed. RESULTS: The total score and score for other factors decreased except the factor "self-control" after MMT. The craving for high dose patients decreased significantly after 6 month treatment (P<0.05). The degree of craving for heroin in males and females all decreased after MMT, but no significant difference was shown (P>0.05). The craving degree for heroin in patients with long drug use was higher than that of patients with short drug use. After the treatment, the improvement of craving was more significant for the long drug users. CONCLUSION MMT can decline the craving for heroin in drug users. Dosage for methadone and gender may be the risk factors of craving change.
Adult ; China ; Female ; Heroin Dependence ; drug therapy ; psychology ; rehabilitation ; Humans ; Male ; Methadone ; therapeutic use ; Substance Withdrawal Syndrome ; drug therapy ; psychology ; Surveys and Questionnaires ; Young Adult

Genetic mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to a variety of neurodegenerative diseases including Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia and Parkinson’s disease. In the brain, TREM2 is highly expressed on the cell surface of microglia, where it can transduce signals to regulate microglial functions such as phagocytosis. To date, mechanisms underlying intracellular trafficking of TREM2 remain elusive. Mutations in the presenilin 1 (PS1) catalytic subunit of the γ-secretase complex have been associated with increased generation of the amyloidogenic Aβ (amyloid-β) 42 peptide through cleavage of the Aβ precursor amyloid precursor protein. Here we found that TREM2 interacts with PS1 in a manner independent of γ-secretase activity. Mutations in TREM2 alter its subcellular localization and affects its interaction with PS1. Upregulation of PS1 reduces, whereas downregulation of PS1 increases, steady-state levels of cell surface TREM2. Furthermore, PS1 overexpression results in attenuated phagocytic uptake of Aβ by microglia, which is reversed by TREM2 overexpression. Our data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function.