Results: According to the results of repeated measure variance analysis, it was found that both the between- group variable (group) and within-group variable (n) had significant main effects, and the interaction between the between-group variable and the within-group variable was also significant. After Z-transformation, mean (sd) working memory scores of patients with MAP and schizophrenia were 0.91 (0.77) and -0.91 (2.11) respectively, and the difference between these two groups were statistically significant (F=19.253, p<0.001). The relevance between working memory deficits and clinical characteristics was low in both the patients with MAP and patients with schizophrenia.
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Delirium is an acute, severe neuropsychiatric syndrome, characterized by cognitive deficits, that is highly prevalent in aging and dementia and is frequently precipitated by peripheral infections. Delirium is poorly understood and the lack of biologically relevant animal models has limited basic research. Here we hypothesized that synaptic loss and accompanying microglial priming during chronic neurodegeneration in the ME7 mouse model of prion disease predisposes these animals to acute dysfunction in the region of prior pathology upon systemic inflammatory activation. Lipopolysaccharide (LPS; 100 μg/kg) induced acute and transient working memory deficits in ME7 animals on a novel T-maze task, but did not do so in normal animals. LPS-treated ME7 animals showed heightened and prolonged transcription of inflammatory mediators in the central nervous system (CNS), compared with LPS-treated normal animals, despite having equivalent levels of circulating cytokines. The demonstration that prior synaptic loss and microglial priming are predisposing factors for acute cognitive impairments induced by systemic inflammation suggests an important animal model with which to study aspects of delirium during dementia.
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These memory-load specific effects may explain why other studies did not find WM problems in adolescents with ASD. For example, the spatial span that Sally Ozonoff et al. used in their spatial memory-span task  had only a limited working-memory load. Participants had to remember the location of one, three or five colored geometric shapes over a 1,000 or 5,000 ms delay. This low task load on WM did not reveal any difficulties. In other WM studies, problems only appeared when six or eight stimuli had to be memorized [49,54]. Thus, a task using a maximum of five stimuli might simply not uncover spatial WM problems in high-functioning adolescents with ASD. Geurts and colleagues  failed to find an increase in working memory problems with increasing WM load on a self-ordered pointing task (SoP) in high-functioning adolescents with ASD compared with a control group. However, as they compared both groups on differences in beta weights (with difficulty level as the predictor and the number of errors as the dependent variable), no conclusions can be drawn about possible differences between the groups regarding the number of errors made on each load (6, 8, 10, or 12 items). Presumably, the stress placed on the WM system plays an important role in information-processing problems in adolescents with ASD, perhaps even more than the overall functioning of WM. The higher the information load in WM, as is the case with complex and rapidly changing social information, the more problems related to ASD emerge .
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In profiling of working memory endophenotypes in schizophrenia (Tuulio et al., 2003; Hambrecht et al., 2002) and bipolar disorder (Glahn et al., 2008; Thermenos et al., 2010; Glahn et al., 2010), visual memory deficits in the unaffected relatives have been chronicled. However there is no literature to support or oppose the current findings that both verbal and visual working memory are impaired in the patients with ATPD and their unaffected relatives. Interestingly enough, in the performance of the task of spatial working memory, it was not the working memory that was impaired but the constrictive ability ie., visuospatial perception. This can be explained by the observation (Mervis, Robinson, and Pani, 1999) that there is an association between tests of visualization and visuospatial construction. But this does not explain why spatial working memory was not affected contrary to the expectations. Right now what can be deduced is that the poor constructive ability is an index of overall poor cognitive abilities, and the association seen in this study points to the general cognitive decline in both the probands and their unaffected relatives.
Cognitive training methods are an innovative avenue to improve working memory among children who have suffered cognitive deficits related to chronic illness. Most studies of cognitive training programs are tailored toward the specific needs of individual illness populations, however, a more generalized program focused on symptoms and level of impairment would reach more children with working memory deficits and use resources more efficiently. According to Sherr and Langenbahn, level of impairment and symptoms are more important than diagnosis when determining cognitive retraining program techniques (1992). In addition, in a study of patients with brain injury, stroke, or other neurological conditions, Stringer found that cognitive retraining was successful regardless of illness severity and across diagnostic groups (2011). Finally, most children followed for a diagnosis of SCD or cancer attend the same Hematology/Oncology clinic, so a program that fits the needs of both populations would be beneficial. Consequently, the current study will include both children with cancer and SCD who demonstrate impairment on measures of working memory.
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While pre-existing chronically elevated levels of prostaglandins appear important for the deficits observed, there is also a role for acutely elevated IL-1␤. Although there is evidence for direct effects of IL-1 ␤ on hippocampal neurons (Cunningham et al., 1996) and these apparently mediate deficits in the contextual fear-conditioning par- adigm (Cibelli et al., 2010; Frank et al., 2010; Terrando et al., 2010), we have shown here that systemically administered IL-1␤ induces working memory deficits in diseased animals and that systemically administered IL-1RA protects against LPS-induced deficits, suggest- ing a systemic role for IL-1 ␤ . The contextual fear-conditioning task is reliant on slow protein synthesis-dependent consolidation of memory, and inflammation-induced impairment is associated with late-phase long-term potentiation disruption (Chapman et al., 2010). This is manifestly different in nature to the T-maze alternation deficits shown here, which reflect a failure of working memory or short-term habituation and attentional processes (Sanderson et al., 2010). These tasks are therefore predicted to rely on different neural processes, and the current data are con- sistent with distinct inflammatory mechanisms.
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Because most of the available evidence is derived from tasks not specifically developed to probe working mem- ory per se, we wanted to investigate whether working memory deficits may be detected across different para- digms . Within this perspective, a deeper understand- ing of the performance of schizophrenia patients on the self-ordered pointing task (SOPT) [7-9] and the visual conditional associative learning task (VCALT) [9-12] seems appropriate, given that these two tasks have been less extensively studied than others.
change in FS interneurons upon chronic SSRI treatment. Changes in sIPSC frequency or altered inhibitory drive relative to excitatory drive have been observed in other animal models of neurodevelopmental disorders in which working memory deficits have also been reported [29, 46–48]. Our findings support the hypothesis that environmental changes induced by a single drug during pregnancy elicits an imbalance in the inhibitory/excita- tory drive onto major output neurons in the L5 micro- circuits within the PFC and subsequently alters animal behavior through non-genetic, compensatory upregula- tion of unique classes of 5-HT receptors in specific neuronal types. However, the potential mechanism of this compensatory 5-HT-receptor upregulation in FS in- terneurons needs to be addressed. Furthermore, studies to determine whether L2/3 neurons in the mPFC or
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declines as the period of abstinence from cocaine increases. This was true for source memory for spatial position (the position measure) and, on an unadjusted basis, for presentation format source memory (the case measure). While the deficit was apparently related to the frequency with which cocaine was used, the effects observed do not appear to relate to recent use since the source and item memory outcomes either appear unrelated to recent cocaine use or the current frequency effect observed remains significant following statistical control for aspects of recent use. Three of the other measures of cocaine use were associated with various source and item memory outcomes at p<.05 or p<.10 two tailed although these failed to reach significance at the adjusted alpha level. As far as the authors are aware the present study is the first to link recreational use of cocaine with source memory deficits.
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Of all the discourse genres, the ability to tell a story is particularly important for school age children; narrative ability has been linked to better outcomes both socially (Davidson, Walton, & Cohen, 2013; Davidson, Walton, Kansal, & Cohen, 2017; Dray, Selman, & Schultz, 2009) and academically (Fazio, Naremore, & Connell, 1996; Griffin, Hemphill, Camp, & Wolf, 2004). The cognitive demands of generating or retelling a narrative are quite high, requiring support from a range of cognitive-linguistic resources (Duinmeijer, de Jong, & Scheper, 2012; Montgomery, Polunenko, & Marinellie, 2009). One population that has particular difficulty with narratives is children with specific language impairment (SLI), who demonstrate linguistic deficits despite otherwise typical neurological development, normal hearing, and adequate exposure to language models (Leonard, 2014). Children with SLI have demonstrated difficulty with many aspects of narration, such as making logical connections between story events (e.g., Reilly, Losh, Bellugi, & Wulfeck, 2003), establishing a sense of continuity (e.g., Liles, 1985), or describing characters’ feelings or intentions (e.g., Klecan-Aker & Kelty, 1990). Because of the importance of narratives in both social and academic realms, recent research has explored various narrative interventions for children with SLI. Results, however, have not always been favourable (e.g., Green & Klecan-Aker, 2012), possibly due in part to
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who compared adult heavy and long-term cannabis users (smoked at least 5000 times in their lives and were daily smokers at study entry) and controls (who had smoked no more than 50 times in their lives) regarding their performance on neurocognitive measures at three different time-points after the first assessment. On days 0, 1, and 7, cannabis users significantly differed in terms of task performance compared to controls, and the learning and recall deficits across time points were related to ∆ 9-THC-creatinine ratios at first assessment. However, by day 28, the two groups did not dif- fer any longer, and initial ∆ 9-THC concentrations were not related to task performance, suggesting that memory impair- ments in long-term cannabis users may not persist beyond the impact of ∆ 9-THC-induced “residual effects.” This is in line with more recent studies implicating that the severity of deficits in memory and immediate recall associated with cannabis use decreased over time following abstinence; 58,74–76
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COX-1 inhibitor piroxicam protects against this LPS-induced working memory deficit in animals with neurodegeneration while the COX-2-specific inhibitor nimesulide does not. The latter is consistent with evidence that COX-2 inhibition actually exacerbates the CNS consequences of systemic inflammation (Blais et al. 2005) while the former is congruent with our observation of up-regulation of COX-1 in both microglia and PVMs during disease progression (Skelly & Cunningham, unpublished data) and the recently described role of COX-1-positive PVMs as transducers of systemic inflammatory signals to the brain (Garcia-Bueno et al. 2009). Thus, an amplification of the prostaglandin system in micro- glia and PVMs may be a key facet of this susceptibility of aging and/or neurodegeneration. Inhibition of COX-1 may be more attractive than inhibition of COX-2 for both physiolog- ical and inflammatory reasons. It is striking that the COX-1 inhibition reported in our recent studies reduced PGE2 levels but did not lead to any reduction of blood or brain IL-1β, TNF-α, IL-6 or CXCL1 (mouse homolog of IL-8), all of which were previously associated with delirium in clinical studies. Levels of prostaglandins have never been measured in studies of delirium and the role of the cyclooxygenase pathway should be investigated in this population. Given the wide array of prostanoids arising from COX activity (Fig. 3) and the side effects that can be associated with COX inhibitors it will be important to be as precise as possible about which elements of these pathways one might want to inhibit. In this
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It has been suggested that an age-related decrease in the ability to bind and retain conjunctions of features may account for some of the pronounced decline of visual working memory across the adult life-span. So far the evidence for this proposal has been mixed with some suggesting a specific deficit in binding to location, while the retention of surface feature conjunctions (e.g. color-shape) appears to remain largely intact. The present experiments follow up on the results of an earlier study, which found that older adults were specifically poor at detecting conjunction changes when they were mixed with trials containing changes to individual features, relative to when these trials were blocked (Cowan et al., 2006, Dev. Psychol., 42, pp. 1089). Using stimuli defined by conjunctions of color and shape (Experiment 1), and color and location (Experiment 2) we find no evidence that older adults are less accurate at detecting binding changes when trial types are mixed. Further, analysis of estimates of discriminability provides substantial-to-strong evidence against this suggestion. We discuss these findings in relation to previous studies addressing the same question and suggest that much of the evidence for specific age-related VWM binding deficits is not as strong as it first appears.
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17 users may find it difficult to perform an action that is cued by another event, for example remembering to make a dentist appointment when cued by driving past the dental surgery, remembering to return a library book when cued by walking past the library. Research shows that these two types of prospective memory (event based cued by an external event, and time based cued by the time elapsed) utilise distinct neural processes/areas in addition to the shared medial temporal regions mentioned previously. Burgess et al. (2003) and Gilbert et al. (2005) found that event-based PM activates frontopolar areas, and frontal patients perform particularly poorly in this aspect of PM tasks (Fleming et al. 2008). While time-based tasks do utilise frontopolar structures, the areas activated are more diverse (Okuda et al. 2007). Consequently, any cannabis-related neuronal changes could be localised in these areas and future research should seek to confirm this.
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supplements, as well as in certain foods. Amongst the various functions of the brain, one of the most interesting is the ability to acquire new information and store it for further retrieval. Several Central Nervous System disorders (CNS) are often associated with impairment in cognitive functions. Alzheimer’s disease (AD), a complex, multifactoral, progressive, neurodegenerative disease primarily affecting the elderly population is estimated to account for 50–60% of dementia cases in persons over 65 years of age. According to the World Health Organisation around 35 million people in industrialized countries suffered from AD by 2010. Alzheimer’s disease has a primary impact on learning and memory. Other disorders like schizophrenia, bipolar depression are associated with secondary deficits in learning and memory functions. The mechanisms underlying learning and memory include an interaction between the various neurotransmitter systems, amongst which the central cholinergic function is known to play a prominent role. Estimation of acetylcholinesterase (AChE) activity provides a relatively easy and valuable assessment of cholinergic function. 6 Recently, the interest in the use of herbal products has grown dramatically in the western world as well as in developing countries. 4
The review focuses on several natural m emory enhancing agents acting on dementia. Dementia is a syndrom e usually occurs with impairment in memory, thinking, orientation and judgement. In majority of the studies, the underlying mechanism was found to be anti acetylcholinesterase activity and free radical scavenging activity with the facilitation of the cholinergic transmission. The typical scientific approach for selecting plants to investigate for the treatment of these disorders is relatively rational method to develop more acceptable and better substitute to the present pharmacotherapy. The collection of herbal plants showing the nootropic activity were tabulated from the various journals and were reported above as we can conclude that herbal plants are very rich source of substance which are responsible of increasing nootropic activity.
Chotosan (CTS, Diaoteng San) is a Kampo (ie Chinese medicine) formula consisting of ten medicinal herbs and gypsum fibrosum. It has long been used to treat chronic headache and hypertension, particularly in middle-aged or older patients with weak physical constitutions, chronic headache, painful tension of the shoulders and cervical muscles, vertigo, morning headache, a heavy feeling of the head, flushing, tinnitus, and insomnia . In a double-blind and placebo-controlled clinical study , CTS showed an ameliorative effect on cognitive dys- functions in stroke patients. CTS and tacrine (a choli- nesterase inhibitor) exhibit a preventive effect on cognitive deficits in a mouse model of transient cerebral ischemia and a therapeutic effect on learning and mem- ory impairments in a mouse model of chronic cerebral hypoperfusion [2,3]. These findings suggest that CTS may be used as an anti-dementia drug. However, since the beneficial effects of CTS have been demonstrated in young animals from eight to 15 weeks old, it is still unclear whether CTS is applicable to treat cognitive dys- function caused by ischemic insult in aged animals.
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Impaired memory is a state in which a person is unable to remember or recall bits of information or behavioral skills. It can be acute or progressive and chronic. In acute there is sudden memory loss can occur many times, it is naturally reversed or progressive and chronic type of memory impairment causes permanent damage the brain and is usually difficult to be reversed. Memory loss is usually caused by brain trauma, stroke, or as a side effect of medications like statin drugs and chemotherapy, brain infections, brain surgery, or electroconvulsive therapy. Alzheimer's disease (AD), Parkinsonism, dementia complex cause extensive damage to the nervous system, including the impairment of learning and memory (1).
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Qi, L., Ke, L., Liu, X., Liao, L., Ke, S., Wang, Y., Lin, X., Zhou, Y., Wu, L., Chen, Z., Liu, L., 2016. Subcutaneous administration of liraglutide ameliorates learning and memory impairment by modulating tau hyperphosphorylation via the glycogen synthase kinase-3beta pathway in an amyloid beta protein induced alzheimer disease mouse model. Eur J Pharmacol 783, 23-32. Ryder, J., Su, Y., Ni, B., 2004. Akt/GSK3beta serine/threonine kinases: evidence for a signalling
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Chapters 4-10 present the findings of several experiments which have ex- amined various aspects of attentional processing. In Chapter 4, visual selective attention is measured using a visual search paradigm. Both response time and accuracy of target detection as a function of set size were examined. A diffi- culty was demonstrated by the dyslexia cases only where searching involved a conjunction of stimulus features. However, while suggesting a compromised at- tentional system the nature of the visual search difficulties were not addressed in this experiment. For example, attention involves a number of processes, each of which may be responsible for the observed deficits in performance. Further- more, the deficits may also be due to a slower attentional system, and/or relate to the processing of spatial and/or object information, and/or vary with visual field of presentation.
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