METHODS: Memory deficiency was produced by AlCl3 (100 mg/kg; p.o.) in experimental animals. Learning and memory activity was measured using Morris water maze (MWM) test model. Central cholinergic activity was evaluated through the measurement of brain acetylcholinesterase (AChE) activity. In addition to the above, oxidative stress was determined through assessment of brain thiobarbituric acid-reactive species (TBARS) and glutathione (GSH) levels.
RESULTS: AlCl3 administration prompted significant deficiency of learning and memory in rats, as specified by a noticeable reduction in MWM presentation. AlCl3 administration also produced a significant deterioration in brain AChE action and brain oxidative stress (increase in TBARS and decrease in GSH) levels. Treatment with morusin (5.0 and 10.0 mg/kg, dose orally) significantly overturned AlCl3- induced learning and memory shortages along with diminution of AlCl3-induced rise in brain AChE activity and brain oxidative stress levels.
CONCLUSION: It may be concluded that morusin exerts a memory-preservative outcome in mental discrepancies of rats feasibly through its various activities.
METHODS: PsycINFO, Web of Science, and PubMed databases were searched for articles published between January 1998 and December 2018. Fifty-seven studies met the inclusion criteria. All studies implemented the generative retrieval strategy by inducing memories through cue words or pictures, the life-stage method, or open-ended retrieval method. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Statement guidelines were followed for this review.
RESULTS: Most studies reported that patients with schizophrenia retrieve less specific autobiographical memories when compared to a healthy control group, while only three studies indicated that both groups performed similarly on memory specificity. Patients with schizophrenia also exhibited earlier reminiscence bumps than those for healthy controls. The relationship between comorbid depression and autobiographical memory specificity appeared to be independent because patients' memory specificity improved through intervention, but their level of depression remained unchanged. The U-shaped retrieval pattern for memory specificity was not consistent. Both the connection between the history of attempted suicide and autobiographical memory specificity, and the relationship between psychotic symptoms and autobiographical memory specificity, remain inconclusive. Patients' memory specificity and coherence improved through cognitive training.
CONCLUSIONS: The overgeneral recall of autobiographical memory by patients with schizophrenia could be attributed to working memory, the disturbing concept of self, and the cuing method implemented. The earlier reminiscence bump for patients with schizophrenia may be explained by the premature closure of the identity formation process due to the emergence of psychotic symptoms during early adulthood. Protocol developed for this review was registered in PROSPERO (registration no: CRD42017062643).
METHODS: Male Sprague Dawley rats were subjected to permanent bilateral occlusion of common carotid arteries (PBOCCA) or sham surgery. Then, PBOCCA rats received ip injections with, either vehicle (control group), the muscarinic receptor agonist oxotremorine (0.1 mg/kg), or the acetylcholinesterase inhibitor physostigmine (0.1 mg/kg). Cognitive functions were evaluated using a passive avoidance task and the Morris water maze test. In addition, hippocampal LTP was recorded in vivo under anaesthesia.
RESULTS: The PBOCCA rats exhibited significant deficits in passive avoidance retention and spatial learning and memory tests. They also showed a suppression of LTP formation in the hippocampus. Oxotremorine and physostigmine significantly improved the learning and memory deficits as well as the suppression of LTP in PBOCCA rats.
CONCLUSIONS: The present data suggest that the cholinergic system plays an important role in CCH-induced cognitive deficits and could be an effective therapeutic target for the treatment of VaD.
MATERIALS AND METHODS: In this study, DET (0.625. 1.25 and 2.5 mg/kg, i.p.) was administered in rats for 21 days and those animals were challenged with single injection of LPS (250 μg/kg, i.p.) for 7 days. Cognitive and behavioral assessment was carried out for 7 days followed by molecular assessment on brain hippocampus. Statistical significance was analyzed with one-way analysis of variance followed by Dunnett's test to compare the treatment groups with the control group.
KEY FINDINGS: DET ameliorated LPS-induced neuroinflammation by suppressing major pro-inflammatory mediators such as iNOS and COX-2. Furthermore, DET enhanced the anti-inflammatory cytokines and concomitantly suppressed the pro-inflammatory cytokines and chemokine production. DET treatment also reversed LPS-induced behavioral and memory deficits and attenuated LPS-induced elevation of the expression of AD markers. DET improved synaptic-functionality via enhancing the activity of pre- and post-synaptic markers, like PSD-95 and SYP. DET also prevented LPS-induced apoptotic neurodegeneration via inhibition of PARP-1, caspase-3 and cleaved caspase-3.
SIGNIFICANCE: Overall, our studies suggest DET can prevent neuroinflammation-associated memory impairment and neurodegeneration and it could be developed as a therapeutic agent for the treatment of neuroinflammation-mediated and neurodegenerative disorders, such as AD.