Antidepressants are the most commonly and widely used medication for its effectiveness in the treatment of anxiety and depression. A few epidemiological studies have documented that antidepressant is associated with increased risk of dementia so far. Here, our aim is to assess the association between antidepressant use and risk of dementia in elderly patients. We searched articles through MEDLINE, EMBASE, Google, and Google Scholar from inception to December 1, 2017, that reported on the association between antidepressant use and dementia risk. Data were collected from each study independently, and study duplication was checked by at least three senior researchers based on a standardized protocol. Summary relative risk (RR) with 95% CI was calculated by using a random-effects model. We selected 9 out of 754 unique abstracts for full-text review using our predetermined selection criteria, and 5 out of these 9 studies, comprising 53,955 participants, met all of our inclusion criteria. The overall pooled RR of dementia was 1.75 (95% CI: 1.033–2.964) for SSRIs whereas the overall pooled RR of dementia was 2.131 (95% CI: 1.427–3.184) for tricyclic use. Also, MAOIs showed a high rate of increase with significant heterogeneity. Our findings indicate that antidepressant use is significantly associated with an increased risk of developing dementia. Therefore, we suggest physicians to carefully prescribe antidepressants, especially in elder patients. Additionally, treatment should be stopped if any symptoms related to dementia are to be noticed.

The present study was carried out to further examine the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO(2)) on experimental spinal cord injury (SCI). Rats were divided into three major groups: (1) sham operation (laminectomy only); (2) laminectomy + SCI + normobaric air (NBA; 21% oxygen at 1 ATA); and (3) laminectomy + SCI + HBO(2) (100% oxygen at 2.5 ATA for 2 h). Spinal cord injury was induced by compressing the spinal cord for 1 min with an aneurysm clip calibrated to a closing pressure of 55 g. HBO(2) therapy was begun immediately after SCI. Behavioral tests of hindlimb motor function as measured by the Basso, Beattie, and Bresnahan (BBB) locomotor scale was conducted on days 1-7 post-SCI. The triphenyltetrazolium chloride staining assay and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick-end labeling assay were also conducted after SCI to evaluate spinal cord infarction and apoptosis, respectively. Cells positive for glial cell line-derived neurotrophic nerve growth factor (GDNF) and vascular endothelial growth factor (VEGF) and cytokines in the injured spinal cord were assayed by immunofluorescence and commercial kits, respectively. It was found that HBO(2) therapy significantly attenuated SCI-induced hindlimb dysfunction, and spinal cord infarction and apoptosis, as well as overproduction of spinal cord interleukin-1beta and tumor necrosis factor-alpha. In contrast, the numbers of both GDNF-positive and VEGF-positive cells and production of spinal cord interleukin-10 after SCI were all significantly increased by HBO(2). These data suggest that HBO(2) may attenuate experimental SCI by stimulating production of GDNF, VEGF, and interleukin-10.

The findings suggested that LIPUS could be useful as a physical stimulation of cell metabolism for the repair of the AF.