Family Dynamics and Grandparents' Anxiety and Depression in Intergenerational Rearing Families: A Correlational Study.

Background: In China, intergenerational rearing is a ubiquitous phenomenon based on unique national conditions. This study aimed to explore family dynamics in intergenerational rearing families as well as their correlation with older household members' anxiety and depression. Methods: The elderly from intergenerational (n = 141) and non-intergenerational rearing families (n = 266) were investigated using the following scales: the general information questionnaire, Self-Rating Scale of Systemic Family Dynamics, Geriatric Depression Scale, and Self-Rating Anxiety Scale. Results: Scores from the four dimensions (family atmosphere, system logic, individuation, and the concept of disease) of the structure of family dynamics were computed. The comparison of these dimensions scores and the total scores of grandparents' anxiety and depression for the two groups were not statistically significant (p > 0.05). In Pearson's correlation analysis, no significant correlation between the family atmosphere dimension and the total score of the grandparents' depression and anxiety scales was observed. The system logic aspect was negatively correlated with depression and anxiety scale scores. The individual dimension was positively correlated with the anxiety scale scores. The disease concept dimension was positively correlated with depression and anxiety scale scores. Hence, the results were statistically significant. Conclusion: There were no significant differences in terms of family dynamics and risk of anxiety and depression among grandparents between the two family types. The system logic, individuation, and disease concept dimensions were correlated with their anxiety and depression.

Endomorphin-1 attenuates Aß42 induced impairment of novel object and object location recognition tasks in mice.

A growing body of evidence suggests that the agglomeration of amyloid-ß (Aß) may be a trigger for Alzheimer׳s disease (AD). Central infusion of Aß42 can lead to memory impairment in mice. Inhibiting the aggregation of Aß has been considered a therapeutic strategy for AD. Endomorphin-1 (EM-1), an endogenous agonist of µ-opioid receptors, has been shown to inhibit the aggregation of Aß in vitro. In the present study, we investigated whether EM-1 could alleviate the memory-impairing effects of Aß42 in mice using novel object recognition (NOR) and object location recognition (OLR) tasks. We showed that co-administration of EM-1 was able to ameliorate Aß42-induced amnesia in the lateral ventricle and the hippocampus, and these effects could not be inhibited by naloxone, an antagonist of µ-opioid receptors. Infusion of EM-1 or naloxone separately into the lateral ventricle had no influence on memory in the tasks. These results suggested that EM-1 might be effective as a drug for AD preventative treatment by inhibiting Aß aggregation directly as a molecular modifier.

The role of apelin-13 in novel object recognition memory.

Apelin and its receptor APJ (apelin receptor) are prominently expressed in brain regions involved in learning and memory. However, the role of apelin in cognition was largely unclear. Here, the role of apelin-13 in memory processes was investigated in mice novel object recognition task. Post-training injection of apelin-13 (0.3 and 1 nmol) dose-dependently impaired short-term memory (STM), however, pre-training infusion of apelin-13 (1 nmol) did not affect STM, suggesting apelin-13 blocks formation but not acquisition of STM. Apelin-13 (1 nmol) administered immediately, 30, 60 or 120 min post-training impaired long-term memory (LTM) in a time-dependent manner (30 min), however, both pre-training and pre-test infusion of apelin-13 (1 nmol) did not affect LTM, suggesting apelin-13 impaired consolidation but not acquisition and recall of LTM. Taken together, for the first time, our results indicate that apelin-13 blocks STM formation and LTM consolidation in novel object recognition task.

Neuropeptide S interacts with the basolateral amygdala noradrenergic system in facilitating object recognition memory consolidation.

The noradrenergic activity in the basolateral amygdala (BLA) was reported to be involved in the regulation of object recognition memory. As the BLA expresses high density of receptors for Neuropeptide S (NPS), we investigated whether the BLA is involved in mediating NPS's effects on object recognition memory consolidation and whether such effects require noradrenergic activity. Intracerebroventricular infusion of NPS (1nmol) post training facilitated 24-h memory in a mouse novel object recognition task. The memory-enhancing effect of NPS could be blocked by the ß-adrenoceptor antagonist propranolol. Furthermore, post-training intra-BLA infusions of NPS (0.5nmol/side) improved 24-h memory for objects, which was impaired by co-administration of propranolol (0.5µg/side). Taken together, these results indicate that NPS interacts with the BLA noradrenergic system in improving object recognition memory during consolidation.

Hypercholesterolemia blocked sevoflurane-induced cardioprotection against ischemia-reperfusion injury by alteration of the MG53/RISK/GSK3ß signaling.

BACKGROUND: Recent studies have demonstrated that volatile anesthetic preconditioning confers myocardial protection against ischemia-reperfusion (IR) injury through activation of the reperfusion injury salvage kinase (RISK) pathway. As RISK has been shown to be impaired in hypercholesterolemia, we investigate whether anesthetic-induced cardiac protection was maintained in hypercholesterolemic rats. METHODS: Normocholesteolemic or hypercholesterolemic rat hearts were subjected to 30 min of ischemia and 2 h of reperfusion. Animals received 2.4% sevoflurane during three 5 min periods with and without PI3K antagonist wortmannin (10 µg/kg, Wort) or the ERK inhibitor PD 98059 (1 mg/kg, PD). The infarct size, apoptosis, p-Akt, p-ERK1/2, p-GSK3ß were determined. RESULTS: Two hundred and six rats were analyzed in the study. In the healthy rats, sevoflurane significantly reduced infarct size by 42%, a phenomenon completely reversed by wortmannin and PD98059 and increased the phosphorylation of Akt, ERK1/2 and their downstream target of GSK3ß. In the hypercholesterolemic rats, sevoflurane failed to reduce infarct size and increase the phosphorylated Akt, ERK1/2 and GSK3ß. In contrast, GSK inhibitor SB216763 conferred cardioprotection against IR injury in healthy and hypercholesterolemic hearts. CONCLUSIONS: Hyperchoesterolemia abrogated sevoflurane-induced cardioprotection against IR injury by alteration of upstream signaling of GSK3ß and acute GSK inhibition may provide a novel therapeutic strategy to protect hypercholesterolemic hearts against IR injury.

Neuropeptide S enhances memory and mitigates memory impairment induced by MK801, scopolamine or Aß1₋42 in mice novel object and object location recognition tasks.

Neuropeptide S (NPS), the endogenous ligand of NPSR, has been shown to promote arousal and anxiolytic-like effects. According to the predominant distribution of NPSR in brain tissues associated with learning and memory, NPS has been reported to modulate cognitive function in rodents. Here, we investigated the role of NPS in memory formation, and determined whether NPS could mitigate memory impairment induced by selective N-methyl-D-aspartate receptor antagonist MK801, muscarinic cholinergic receptor antagonist scopolamine or Aß1₋42 in mice, using novel object and object location recognition tasks. Intracerebroventricular (i.c.v.) injection of 1 nmol NPS 5 min after training not only facilitated object recognition memory formation, but also prolonged memory retention in both tasks. The improvement of object recognition memory induced by NPS could be blocked by the selective NPSR antagonist SHA 68, indicating pharmacological specificity. Then, we found that i.c.v. injection of NPS reversed memory disruption induced by MK801, scopolamine or Aß1₋42 in both tasks. In summary, our results indicate that NPS facilitates memory formation and prolongs the retention of memory through activation of the NPSR, and mitigates amnesia induced by blockage of glutamatergic or cholinergic system or by Aß1₋42, suggesting that NPS/NPSR system may be a new target for enhancing memory and treating amnesia.