Objective The objectives of the current study are to evaluate the prevalence of depression symptoms among breast cancer patients in Jordan and impact of the disease on patient’s quality-of-life. Methods A cross-sectional survey-based study was conducted over a 6-month period among breast cancer patients attending two major hospitals in Jordan. A validated questionnaire was used to evaluate the prevalence of depression symptoms and quality-of-life aspects among those patients utilizing Beck’s Depression Inventory-II score and 36-Item Survey Form (SF-36) score, respectively. Results The mean age±SD of patients (n=169) was 49.12±6.48 years. Depression symptoms were reported in 30.2% of patients. As for quality-of-life, the physical functioning (PF) subscale was significantly associated with the patient’s age ( P =0.03). The role-physical (RP) subscale was associated with number of sleeping hours ( P =0.038). Marital status of breast cancer patients was significantly associated with role-emotional (RE) ( P =0.015) and mental health (MH) ( P =0.009) subscales. The number of patient’s siblings was significantly associated with daily habits such as PF ( P =0.031) and RP ( P =0.005) subscales. Moreover, the occupation of patients was associated with the PF ( P =0.041) and MH ( P =0.049). Conclusion About one-third of breast cancer patients reported depression symptoms. Quality-of-life subscales among those patients were associated with multiple social and health determinants, such as age, marital status, number of siblings, occupation, and number of sleeping hours. There is urgent need to support this group of patients to help them to cope with depression symptoms and to improve their quality-of-life.

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that can happen after exposure to a traumatic event. Post-traumatic stress disorder is common among mental health disorders that include mood and anxiety disorders. Omega-3 fatty acids (OMGs) are essential for the maintenance of brain function and prevention of cognition dysfunctions. However, the possible effect of OMG on memory impairment induced by PTSD has not been studied. In here, such an effect was explored using a rat model of PTSD. The PTSD-like behavior was induced in animals using a single-prolonged stress (SPS) rat model of PTSD (2 h restraint, 20 min forced swimming, 15 min rest, 1–2 min diethyl ether exposure). The OMG was administered orally at a dose of 100 mg omega-3 polyunsaturated fatty acid (PUFA)/100 g body weight/day. Spatial learning and memory were assessed using the radial arm water maze (RAWM) method. Changes in oxidative stress biomarkers, thiobarbituric acid reactive substances (TBARS), and brain derived neuroptrophic factor (BDNF) in the hippocampus following treatments were measured. The results revealed that SPS impaired both short- and long-term memory (p < 0.05). Use of OMG prevented memory impairment induced by SPS. Furthermore, OMG normalized SPS induced changes in the hippocampus that reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratios, the activity of catalase, glutathione peroxidase (GPx), and TBARSs levels. In conclusion, the SPS model of PTSD-like behavior generated memory impairment, whereas OMG prevented this impairment, possibly through normalizing antioxidant mechanisms in the hippocampus.

Introduction: Psychosocial stress (STS) negatively influences memory. This might be associated to oxidative stress-induced progressive destruction of numerous brain structures and functions. L-carnitine (L-CAR) is a widely used antioxidant compound that is endogenously made in mammalian species. The current study investigated the effect of L-CAR on STS-induced memory impairment in the rat hippocampus. Methods: The STS was induced using intruder model, where two rats were randomly switched from each one cage to another, once/day for 6 weeks. Concurrently, L-CAR (300mg/kg/day) was intraperitoneally administered for 6 weeks. After that, radial arm water maze (RAWM) was used to assess spatial learning memory in rats. Hippocampal biomarkers of oxidative stress, including thiobarbituric acid reactive substance (TBARs), oxidized glutathione (GSSG), reduced glutathione (GSH), glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD), and Brain-derived neurotrophic factor (BDNF) were examined. Results: The results showed impairment of short-term memory (P < 0.05) during STS, whereas L-CAR treatment protected against this effect. Furthermore, while no change was observed in GSH, GSSG, GPx, catalase, and SOD, L-carnitine normalized STS-induced reduction in the hippocampal BDNF levels and increase in TBARS levels. Discussion: Chronic psychosocial stress-induced memory impairment was prevented via L-CAR administration, which could have been achieved via normalizing changes in lipid peroxidation (TBARs) and BDNF levels in the hippocampus.

Background: Psychosocial stress (STS) is a common stress in modern societies. Chronic STS is associated with impairment of a broad range of cognitive functions in humans and with prolonged abnormalities in memory. Matrix metalloproteinases (MMPs), a protein family of zinc-containing endopeptidases, are essential in neuro-inflammation and involved in neurodegenerative diseases. L-Car possesses neuroprotective, antioxidant, and anti-inflammatory properties and was shown to modulate MMPs. Objective: The current study aimed to examine the protective effect of L-Carnitine (L-CAR) on STS-induced changes in serum corticosterone levels, MMP-2, -9, and -12 protein and mRNA expression in the hippocampus as a possible mechanism for L-CAR protective effect on STS-induced memory impairment. Methods: The chronic STS and L-CAR (300mg/kg/day, i.p) were simultaneously administered for 6 weeks to adult male Wistar rats. Serum corticosterone and protein levels of MMP-2, -9 and -12 were evaluated using ELISA. Real-Time PCR techniques were used to determine the mRNA levels of MMP-2, -9 and -12 in the hippocampus. Results: The findings showed that serum corticosterone levels and MMP-2 and -9 protein levels were significantly increased (P<0.05) in STS group compared to the control. Similarly, RT-PCR findings showed that the mRNA of those proteinases significantly increased (P<0.05) following the intruder method. On the other hand, the administration of L-CAR restored the alterations in corticosterone levels and MMPs gene and protein expression induced by chronic STS. Conclusions: STS induced elevations in corticosterone and MMP-2 and -9 levels in the hippocampus. L-CAR, on the other hand, exhibited protective effects against the STS-induced changes in MMP-2 and -9.