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Objective: To explore the intrinsic mechanism of enriched environment- induced improvement of memory in rats with chronic cerebral ischemia. Method: Forty-eight healthy male SD rats were randomly divided into chronic cerebral ischemia+standard environment group (CCH+SE), chronic cerebral ischemia+rich environment group (CCH+EE), and Sham surgery+ standard environment group (Sham+SE) with 16 rats in each group. The CCH+SE group and CCH+EE group were given bilateral common carotid artery ligation surgery and a rat model of chronic cerebral ischemia was constructed. The Sham+SE group performed the same procedures as the model group without ligating bilateral common carotid arteries. Three groups of rats were raised in corresponding environments for 21 days, and their spatial learning and memory functions were tested using a water maze test. Protein immunoblotting and immunofluorescence techniques were used to detect changes of BDNF, GAP-43, and SYN proteins expressions in the CA3 region of the rat hippocampus. Result: Compared with the standard environment group, the learning and memory functions of the enriched environment group were significantly improved, with a statistically significant difference (P<0.05). The expression levels of BDNF, GAP-43, and SYN proteins in the CA3 region of the hippocampus were significantly increased, with a statistically significant difference (P<0.05). Conclusion: Enriched environment intervention can improve learning and memory ability in rats with chronic cerebral ischemia, and its underlying mechanism may be promoting synaptic remodeling in the hippocampal CA3 region. [ABSTRACT FROM AUTHOR]

Objective To explore the correlation between abnormal thalamic functional connectivity (FC) and memory loss in maintenance hemodialysis patients with end-stage renal disease (ESRD). Methods An auditory verbal learning test (AVLT-H) was conducted on 22 patients with ESRD and 28 age-, sex-, and education-matched healthy controls (HC) to evaluate memory function. After that, resting-state functional magnetic resonance imaging (rs-fMRI) data were gathered, and a whole-brain FC analysis centered on the thalamus was executed to discern variations in thalamic FC between the two groups. Finally, Pearson and Spearman correlation analyses were carried out. Results Compared to the HC group, the ESRD group exhibited notably lower scores in IR-S (P=0.002), SR-S (P<0.001), and LR-S (P=0.005). Concurrently, the ESRD group demonstrated diminished FC of the right thalamus with the left superior frontal gyrus, the left parietal lobule, the right suproccipital gyrus, the right anterior cuneus, and the right middle frontal gyrus (P<0.05, TFCE correction). Additionally, reduced FC were observed between the left thalamus and the left gyrus rectus, the left parietal lobule, and the right parietal lobule in the ESRD group (P<0.05, TFCE correction). Moreover, the FC values between the left thalamus and the left gyrus rectus in the ESRD group displayed significant negative correlations with IR-S (r=-0.499), SR-S (r=-0.458), and LR-S (r=-0.455) (all P<0.05). Conclusion Memory impairment is evident in ESRD patients undergoing maintenance hemodialysis, and it appears to be intricately linked to anomalous FC within the left thalamus and the left gyrus rectus. These findings offer potential imaging markers for monitoring memory dysfunction in individuals with ESRD. [ABSTRACT FROM AUTHOR]

Objective To study the mechanism of learning and memory impairment in aged female mice caused by chronic stress. Methods Twenty-month-old ICR mice were randomly divided into four groups: control females, control males, stressed females, and stressed males. Chronic stress was applied to the stress group for 30 days. The learning and memory ability was measured by novel object recognition test and Morris water maze test. Damage to hippocampal neurons was observed with Nissl staining, and dendrites of hippocampal neurons were observed with Golgi-Cox staining microscopy, the expression of the mammalian target of rapamycin (mTOR) and p-mTOR in hippocampal tissue was measured by Western blot, and the level of serum corticotropin-releasing hormone (CRH) was measured by ELISA. Results There was a significant decrease in the learning and memory ability only in the stressed female group after applied stress. In the Morris water maze, after a 6-day swimming training, the escape latency decreased in the control female group, the control male group and in the stressed male group(P＜0.001, P＜0.001, P＜0.05), but not in the stressed female group. The swimming speed was consistent across groups, but the number of platform crossings and the number of target quadrant crossings were significantly lower in the stressed female group than those in the control female and stressed male groups(P＜0.001).There was significant damage to neurons in the hippocampal CA3, CA1, and DG regions of mice in the stressed female group. The expression of hippocampal m-TOR and p-mTOR protein was significantly decreased in the stressed female group of mice(P＜0.05). In addition, chronic stress caused a significant increase in serum CRH levels in aged female mice(P＜0.05). Conclusions Chronic stress caused learning and memory impairment and pathological damage of the hippocampus in aged female mice, but not in aged male mice, which may be related to a fact that chronic stress elevates CRH and inhibits the hippocampal m-TOR signaling pathway in aged female mice.

Objective To establish an animal model to investigate the relationship between cell division cycle 42 (CDC42) and cognitive deficits in hippocampal neurons. Methods Adenovirus with CDC42 mutant gene was packaged to infect excitatory neurons in the hippocampus of healthy mice by microinjection. The cognitive phenotypes of mice under various behavioral patterns were detected. Results Adenovirus specifically enhanced or decreased the expression activity of CDC42 protein in excitatory neurons in the hippocampus. After the inhibition of CDC42 protein in the hippocampus, the conditioned memory of the mice decreased,significantly at 24 hours and 96 hours, and enhancing CDC42 activity in the hippocampus made mice show an obvious anxiety behavior. However, neither enhancement nor inhibition of the CDC42 activity in the hippocampus had a significant effect on social behavior (P > 0.05). Conclusions The mice with altered CDC42 activity in hippocampal excitatory neurons may present a fear conditioning memory defect and significant anxiety behavior, this may suggest the relationship between cytoskeletal protein CDC42 and cognitive phenotypes. This regulatory model may provide new methods and ideas for the establishment of research models for mental disorders such as SZ and CDC42 is expected to become a new molecular target for the treatment of memory impairment or anxiety. [ABSTRACT FROM AUTHOR]

To investigated the mechanisms underlying the effects of modified Kaixin San(MKXS) on improving memory and synaptic damage of Alzheimer's disease(AD) mouse model with conditional presenilin 1/2 conditional double knockout(PS cDKO). Specifically, 60 PS cDKO mice(3-3.5 months old) and their age-matched wild-type(WT) littermates were randomized into three groups: WT group(n=20), PS cDKO group(n=20), and PS cDKO+MKXS group(n=20). Mice in WT and PS cDKO groups were fed with standard chow and those in PS cDKO+MKXS group were given chow containing MKXS(at 2.55 g·kg~(-1)) for 60 days. Novel object reco-gnition task was employed to detect the recognition memory of mice, and Western blot to detect the protein levels of synapse-associated proteins in the hippocampus(HPC) of mice, such as NR1, NR2 A, NR2 B, p-αCaMKⅡ, tau, and p-tau. Microglial morphology in the HPC CA1 of mice was observed based on immunohistochemistry. Quantitative real time-PCR(qRT-PCR) was employed to detect the mRNA levels of the pro-inflammatory factors and synapse-associated proteins in the HPC of mice, including COX-2, iNOS, IL-1β, IL-6, TNF-α, PSD95, NR1, NR2 A, NR2 B, and MAP2. The protein levels of IL-1β, TNF-α, and IL-6 were tested by enzyme-linked immunosorbent assay(ELISA). The interaction between PSD95 and αCaMKⅡ and between PSD95 and p-αCaMKⅡ was tested by co-immunoprecipitation(Co-IP). The results showed that PS cDKO+MKXS demonstrated significantly higher preference index and recognition index of the new objects, lower protein level of p-tau(ser 396/404) and mRNA levels of COX-2, iNOS, TNF-α, IL-1β, and IL-6 in HPC, higher protein levels of NR1, NR2 A, NR2 B, and p-αCaMKⅡ and mRNA levels of NR1, NR2 A, NR2 B, PSD95, and MAP2, and stronger interaction of αCaMKⅡ with PSD95 and interaction of p-αCaMKⅡ with PSD95 than the PS cDKO group. Immunohistoche-mical staining showed that MKXS inhibited the activation of microglia. In conclusion, MKXS improves memory and synaptic damage in mice with AD by modulating αCaMKⅡ-PSD95 protein binding through inhibition of neuroinflammation.

Dementia causes semantic and episodic memory impairments that limit patients' activities of daily living (ADL) and increase caregiver burden. Spaced retrieval training uses repetitive retrieval to strengthen cognitive and motor skills intuitively in mild / moderate dementia patients who retain preserved implicit / non-declarative memory. This article describes and discusses the operative mechanism, influencing variables, and practical applications of spaced retrieval training. We hope this article increases professional understanding and application of this training approach to improve dementia patient ADL and improve quality of life for both caregivers and patients. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protection effect of dexamethasone (DXMS) on the memory impairment and neuronal damage of neonate rats that caused by sevoflurane (SEVO) exposure., Methods: 5-days-old newborn SD rats were randomly divided into normal group (NC group) (10 rats), SEVO group (10 rats) and SEVO+DXMS group (10 rats). Rats of SEVO group and SEVO+DXMS group were exposed to 2.5% SEVO 2 h per day for 1 week, meanwhile the rats of SEVO+DXMS group were given 20 mg/kg DXMS treatment before exposure and the normal group was given the same amount of placebo and carrier gas as control. All rats were fed normally till infancy. Then the Morris water maze test was used to assess the learning and memory function of rats of each group. HE and Nissl staining were used to observe the histomorphology and neuronal changes in the hippocampus of rats. ELISA was performed to test the changes in nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) level in brain tissues. The expression of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor-γ coactivator-1α ( PGC -1 α ), fork head protein transcription factor 3α ( FOXO 3 α ) mRNA in brain tissue was detected by qRT-PCR. Western blot was used to explore the changes in SIRT1 and caspase-3 protein expression of hippocampus., Results: Compared with the NC group, the pathologic damage of hippocampus tissues was severely in SEVO group, and the number of neuronal cells was decreased as well. After SEVO intervention, the degree of pathologic damage was alleviated, and the number of neuronal cells was significantly increased. The Morris water maze test showed that the escape latency, number of platform crossing and target quadrant retention time between SEVO group and SEVO+DXMS group were significant different. The level of NO and MDA in brain of SEVO+DXMS group was significantly decreased than that of SEVO group, while the level of SOD was increased. qRT-PCR showed that the mRNA levels of SIRT1, PGC -1 α and FOXO 3 α in SEVO+DXMS group were significantly higher those in SEVO group, but mRNA level of SIRT1 was still significantly lower than that of NC group. Western blot showed that the expression of SIRT1 protein in SEVO+DXMS group was significantly higher than that of SEVO group, and the expression of caspase-3 was reduced in SEVO+DXMS compared with SEVO group., Conclusion: DXMS could reduce the level of oxidative stress and suppress the apoptosis of neuronal cells, reduce SEVO-induced brain damage in neonatal rats and improve learning and memory ability in infant rats., (Copyright© by Editorial Board of Journal of Sichuan University (Medical Science Edition).)

In order to study the potential application value of lavender volatile oil (LVO), the chemical composition of the volatile oil of lavender was analyzed by GC-MS, and the mouse model of Alzheimer's disease (AD) was established. Additionally, the antioxidant enzymes activity of T-SOD, GSH-PX, CAT and MDA content were studied. Experimental results showed that 55 kinds of chemical constituents including terpene, terpene alcohol and ester compounds from LVO were identified, and the content of linalool and linalyl acetate was the highest, accounting for 49.71% of the total volatile oil. The ability of mouse platform memory was improved significantly. The levels of GSH-PX, CAT and T-SOD of mouse brain tissue in the treatment group were significantly higher than those in the model group (P<0.05). The level of MDA reached the maximum value in the model group, while there was no notable difference between the levels of MDA in the drug group and the normal group. The result indicated the significant oxidative activity of LVO, the possibility of induced oxidative stress reduction in neurons, and the reversal effect of memory acquired disorder., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)