Background: and Purpose: As it becomes an aging society, interest in senile diseases is increasing. Alzheimer’s dementia (AD) and osteoporosis are representative senile diseases.Various studies have reported that AD and osteoporosis share many risk factors that affect each other’s incidence. This aimed to determine if active medication treatment of AD could affect the development of osteoporosis. Methods: The Health Insurance Review and Assessment Service provided data consisting of diagnosis, demographics, prescription drug, procedures, medical materials, and healthcare resources. In this study, data of all AD patients in South Korea who were registered under the national health insurance system were obtained. The cohort underwent conversion to an Observational Medical Outcomes Partnership–Common Data Model version 5 format. Results: This study included 11,355 individuals in the good persistent group and an equal number of 11,355 individuals in the poor persistent group from the National Health Claims database for AD drug treatment. In primary analysis, the risk of osteoporosis was significantly higher in the poor persistence group than in the good persistence group (hazard ratio, 1.20 [95% confidence interval, 1.09–1.32]; p<0.001). Conclusions We found that the good persistence group treated with anti-dementia drugs for AD was associated with a significant lower risk of osteoporosis in this nationwide study. Further studies are needed to clarify the pathophysiological link in patients with two chronic diseases.

Synthetic cannabinoids are one of most abused new psychoactive substances. The recreational use of abused drug has aroused serious concerns about the consequences of these drugs on infection. However, the effects of synthetic cannabinoid on resistance to tetanus toxin are not fully understood yet. In the present study, we aimed to determine if the administration of synthetic cannabinoids increase the susceptibility to tetanus toxin-induced motor behavioral deficit and functional changes in cerebellar neurons in mice. Furthermore, we measured T lymphocytes marker levels, such as CD8 and CD4 which against tetanus toxin. JWH-210 administration decreased expression levels of T cell activators including cluster of differentiation (CD) 3ε, CD3γ, CD74p31, and CD74p41. In addition, we demonstrated that JWH-210 induced motor impairment and decrement of vesicle-associated membrane proteins 2 levels in the cerebellum of mice treated with tetanus toxin. Furthermore, cerebellar glutamatergic neuronal homeostasis was hampered by JWH-210 administration, as evidenced by increased glutamate concentration levels in the cerebellum. These results suggest that JWH-210 may increase the vulnerability to tetanus toxin via the regulation of immune function.
Animals ; Cannabinoids ; Cerebellar Diseases* ; Cerebellum ; Glutamic Acid ; Homeostasis ; Immunosuppression* ; Mice* ; Neurons ; R-SNARE Proteins ; T-Lymphocytes ; Tetanus ; Tetanus Toxin