Short-term Spatial Memory Research Articles

Modulatory Role of Curcumin on Cobalt-Induced Memory Deficit, Hippocampal Oxidative Damage, Astrocytosis, and Nrf2 Expression.

Chemical overexposure is a growing environmental risk factor for many medical issues. Cobalt toxicity from environmental, industrial, and medical exposure has previously been linked to neurological impairment. Hence, the current study looked into the neuroprotective potential of curcumin, a natural polyphenol contained in the spice turmeric, against cobalt-induced neurotoxicity. Adult rats were randomly divided into six groups as follows: control, 40mg/kg cobalt chloride (CoCl2) only, 240mg/kg curcumin only, 120mg/kg or 240mg/kg curcumin, or 100mg/kg vitamin C co-administered with CoCl2. The administration was via oral route daily for 4weeks. After that, neurobehavioral tests were undertaken to evaluate short-term spatial memory. Biochemical investigation was performed to determine the hippocampal levels of status via measures of SOD, CAT, GST, and LPO. Furthermore, immunohistochemical assessment of the expression of GFAP and Nrf2 in the hippocampus was carried out. In the CoCl2 group, the results showed altered behavioral responses, a decrease in antioxidant activities, increased expression of GFAP and the number of activated astrocytes, and decreased immunoexpression of Nrf2. These effects were mitigated in the curcumin- and vitamin C-treated groups. These results collectively imply that curcumin enhances memory functions in rats exposed to cobalt possibly by attenuating oxidative responses, mitigating astrocytosis, and modulating Nrf2 signaling.

Carotid Body Resection Prevents Short-Term Spatial Memory Decline in Prediabetic Rats Without Changing Insulin Signaling in the Hippocampus and Prefrontal Cortex.

Individuals who develop type 2 diabetes (T2D) at an early age are at higher risk of developing neurodegenerative disorders such as Alzheimer's and Parkinson's disease. A shared dysfunctional characteristic between T2D and these neurodegenerative disorders is insulin resistance. Recently, it was shown that prediabetes animals and patients exhibited increased carotid body (CB) activity. Moreover, these organs are deeply involved in the development of metabolic diseases, since upon abolishment of their activity via carotid sinus nerve (CSN) resection, several dysmetabolic features of T2D were reverted. Herein, we investigated if CSN resection may also prevent cognitive impairment associated with brain insulin resistance. We explored a diet-induced prediabetes animal model where Wistar rats are kept in a high fat-high sucrose (HFHSu) diet for 20weeks. We evaluated CSN resection effects on behavioral parameters and on insulin signaling-related proteins levels, in the prefrontal cortex and the hippocampus. HFHSu animals exhibited impaired short-term memory evaluated by the y-maze test. Remarkably, CSN resection prevented the development of this phenotype. HFHSu diet or CSN resection did not promote significant alterations in insulin signaling-associated proteins levels. Our findings suggest that CBs modulation might have a role in preventing short-term spatial memory deficits associated with peripheral dysmetabolic states.

Brain Factor-7® Improves Cognitive Impairment Following Transient Ischemia and Reperfusion Injury in Gerbil Forebrain through Promoting Remyelination and Restoring Cholinergic and Glutamatergic Neurotransmission in the Hippocampus.

Ischemia and reperfusion injury in the brain triggers cognitive impairment which are accompanied by neuronal death, loss of myelin sheath and decline in neurotransmission. In this study, we investigated whether therapeutic administration of Brain Factor-7® (BF-7®; a silk peptide) in ischemic gerbils which were developed by transient (five minutes) ischemia and reperfusion in the forebrain (tFI/R) improved cognitive impairment. Short-term memory and spatial memory functions were assessed by passive avoidance test and Barnes maze test, respectively. To examine neuronal change in the hippocampus, cresyl violet staining, immunohistochemistry for neuronal nuclei and fluoro Jade B histofluorescence were performed. We carried out immunohistochemistry for myelin basic protein (a marker for myelin) and receptor interacting protein (a marker for oligodendrocytes). Furthermore, immunohistochemistry for vesicular acetylcholine transporter (as a cholinergic transporter) and vesicular glutamate transporter 1 (as a glutamatergic synapse) was done. Administration of BF-7® significantly improved tFI/R-induced cognitive impairment. tFI/R-induced neuronal death was found in the Cornu Ammonis 1 (CA1) subfield of the hippocampus from five days after tFI/R. Treatment with BF-7® following tFI/R did not restore the death (loss) of CA1 neurons following tFI/R. However, BF-7® treatment to the ischemic gerbils significantly improved remyelination and proliferation of oligodendrocytes in the hippocampus with ischemic injury. Treatment with BF-7® to the ischemic gerbils significantly restored vesicular acetylcholine transporter-immunoreactive and vesicular glutamate transporter 1-immunoreactive structures in the hippocampus with ischemic injury. Based on these results, we suggest that BF-7® can be utilized for improving cognitive impairments induced by ischemic injury as an additive for health/functional foods and/or medicines.

Evaluating the effects of low-dose simulated galactic cosmic rays on murine hippocampal-dependent cognitive performance.

Space exploration has advanced substantially over recent decades and plans to increase the duration of deep space missions are in preparation. One of the primary health concerns is potential damage to the central nervous system (CNS), resulting in loss of cognitive abilities and function. The majority of ground-based research on space radiation-induced health risks has been conducted using single particle simulations, which do not effectively model real-world scenarios. Thus, to improve the safety of space missions, we must expand our understanding of the effects of simulated galactic cosmic rays (GCRs) on the CNS. To assess the effects of low-dose GCR, we subjected 6-month-old male BALB/c mice to 50 cGy 5-beam simplified GCR spectrum (1H, 28Si, 4He, 16O, and 56Fe) whole-body irradiation at the NASA Space Radiation Laboratory. Animals were tested for cognitive performance with Y-maze and Morris water maze tests 3 months after irradiation. Irradiated animals had impaired short-term memory and lacked spatial memory retention on day 5 of the probe trial. Glial cell analysis by flow cytometry showed no significant changes in oligodendrocytes, astrocytes, microglia or neural precursor cells (NPC's) between the sham group and GCR group. Bone marrow cytogenetic data showed a significant increase in the frequency of chromosomal aberrations after GCR exposure. Finally, tandem mass tag proteomics identified 3,639 proteins, 113 of which were differentially expressed when comparing sham versus GCR exposure (fold change > 1.5; p < 0.05). Our data suggest exposure to low-dose GCR induces cognitive deficits by impairing short-term memory and spatial memory retention.

Effects of ghrelin on sulfite induced changes in lipid peroxidation, spatial memory, and locomotor activity in rats

ABSTRACT Background Humans are constantly exposed to sulfites and their derivatives, both endogenously and exogenously. Recent studies have shown that sulfite and its derivatives can cause oxidative stress. . Ghrelin has been reported to possess antioxidant properties and stimulates neurogenesis in hippocampal progenitor cells. This study aimed to investigate the effects of ghrelin on sulfite-induced changes in hippocampal oxidative status, spatial learning and locomotor activity in rats. Methods Forty male albino Wistar rats were randomized into four groups as follows; Group 1: Control (C); Group 2: Sodium metabisulfite (Na2S2O5) treated (S); Group 3: Ghrelin treated (G); Group 4: Na2S2O5 + Ghrelin treated (SG). Sodium metabisulfite (100 mg/kg/day) was given by gastric gavage, and ghrelin (20 µg/kg/day) was administered intraperitoneally for 5 weeks. Thiobarbituric acid reactive substances (TBARS) were measured through fluorometric method. The spatial memory and locomotor activity of the rats were evaluated by Y-maze test. Results Y-maze results revealed an enhancement of short-term spatial learning and memory in S and SG groups compared to C group. TBARS levels were increased significantly in S group with respect to C group. The increase in TBARS levels induced by sulfite was completely prevented by ghrelin in SG group. Conclusion We suggest that systemic ghrelin administration might ameliorate ingested sodium metabisulfite-induced hippocampal oxidative damage without providing any changes in spatial learning, memory and locomotion. Further investigation concerning the mechanism of ghrelin action in hippocampus might provide valuable information for developing new therapeutic approaches to attenuate oxidative stress in hippocampal tissue.

Methamphetamine-induced locomotor sensitization in mice is not associated with deficits in a range of cognitive, affective and social behaviours: interaction with brain-derived neurotrophic factor Val66Met genotype.

Chronic methamphetamine (Meth) abuse may induce psychosis similar to that observed in schizophrenia. Brain-derived neurotrophic factor (BDNF) has been implicated in the development of psychosis. We have previously shown long-term protein expression changes in mice treated chronically with Meth depending on BDNF Val66Met genotype. The aim of this study was to investigate if these protein expression changes were associated with differential changes in a range of behavioural paradigms for cognition, anxiety, social and other behaviours. Male and female Val/Val, Val/Met and Met/Met mice were treated with an escalating Meth dose protocol from 6 to 9 weeks of age, with controls receiving saline injections. Several overlapping cohorts were tested in the Y-maze for short-term spatial memory, novel-object recognition test, context and cued fear conditioning, sociability and social preference, elevated plus maze for anxiety-like behaviour and prepulse inhibition (PPI) of acoustic startle. Finally, the animals were assessed for spontaneous exploratory locomotor activity and acute Meth-induced locomotor hyperactivity. Acute Meth caused significantly greater locomotor hyperactivity in mice previously treated with the drug than in saline-pretreated controls. Meth-pretreated female mice showed a mild increase in spontaneous locomotor activity. There were no Meth-induced deficits in any of the other behavioural tests. Val/Met mice showed higher overall social investigation time and lower PPI compared with the Val/Val genotype independent of pretreatment. These results show limited long-term effects of chronic Meth on a range of cognitive, affective and social behaviours despite marked drug-induced locomotor sensitization in mice. There was no interaction with BDNF Val66Met genotype.

Effects of Ornithine Aspartate and Empagliflozin on Memory Deficit Symptoms in Experimental Steatohepatitis

In this study, L-ornithine L-aspartate and empagliflozin were evaluated in terms of their potential effects on the hippocampus-dependent memory status in non-alcoholic steatohepatitis (NASH) in C57Bl/6 mice. NASH was found to be associated with an early transient decrease in the short-term recognition memory as well as a progressive reduction in the short-term spatial memory. L-ornithine L aspartate effectively prevented the impairment of recognition, rather than spatial, memory. At the same time, empagliflozin failed to improve the memory status of the animals.

Neuronal Nitric Oxide Synthase Regulates Depression-like Behaviors in Shortening-Induced Obese Mice.

Shortening is mainly derived from the partial hydrogenation of palm oil and widely used in fast food. Food processed with shortening contains high levels of industrial trans fatty acids. Studies have shown that there is a correlation between industrial trans fatty acids, obesity, and depression. However, the regulatory effect of neuronal nitric oxide synthase (nNOS) on depression in obese patients is still unknown. The purpose of this study was to explore mood changes in obese mice fed a high shortening diet, and to determine the regulatory effect of nNOS on depressive-like behaviors in obese mice. We used a high shortening diet-induced obesity mouse model to systematically assess the metabolic response, behavioral changes, prefrontal and hippocampal nNOS protein levels, and the effect of nNOS inhibitors (7-nitroindole) on depression-like behavior in obese mice. Interestingly, obese mice on a 9-week high-shortening diet developed short-term spatial working memory impairment and anxiety-like behavior, and obesity may be a risk factor for cognitive impairment and mood disorders. In animals fed a high shortening diet for 12 weeks, obese mice developed depression-like behavior and had significantly elevated levels of nNOS protein expression in the hippocampus and prefrontal lobe. Administration of the nNOS inhibitor 7-nitroindole could improve depression-like behaviors in obese mice, further suggesting that inhibition of nNOS is helpful for depression associated with obesity.

Prefrontal parvalbumin interneurons deficits mediate early emotional dysfunction in Alzheimer's disease.

Alzheimer's disease (AD) is the most common neurodegenerative disease and has an insidious onset. Exploring the characteristics and mechanism of the early symptoms of AD plays a critical role in the early diagnosis and intervention of AD. Here we found that depressive-like behavior and short-term spatial memory dysfunction appeared in APPswe/PS1dE9 mice (AD mice) as early as 9-11 weeks of age. Electrophysiological analysis revealed excitatory/inhibitory (E/I) imbalance in the prefrontal cortex (PFC). This E/I imbalance was induced by significant reduction in the number and activity of parvalbumin interneurons (PV+ INs) in this region. Furthermore, optogenetic and chemogenetic activation of residual PV+ INs effectively ameliorated depressive-like behavior and rescued short-term spatial memory in AD mice. These results suggest the PFC is selectively vulnerable in the early stage of AD and prefrontal PV+ INs deficits play a key role in the occurrence and development of early symptoms of AD.

Using zebrafish (&lt;i&gt;Danio rerio&lt;/i&gt;) to assess short-term memory: the habituation and the homebase tests

Environmental novelty is one of the most potent stressors in animals and is often used in behavioral neuroscience to study affective and cognitive impairments. However, in the process of studying an unfamiliar environment in experimental animals, there is a decrease in stress due to habituation (adaptation, habituation). In various behavioral tests in zebrafish, this manifests as swimming in areas that pose a potential danger to them: the upper part of the aquarium in the novel tank test and the central part in the open field test. When building an effective survival strategy, it is important to navigate in an unfamiliar environment from a home base the safest area that serves as a starting point in exploring a novel arena. Both discussed here, habitation and establishing the home base, are important for assessing cognitive behavioral traits in zebrafish related to short-term spatial working memory.

Neuropsychological correlates of P300 parameters in individuals with aphasia.

Aphasia is often accompanied by impairment of non-language cognitive functions. Assessment of cognitive capacity in people with aphasia (PWA) with standard neuropsychological methods may be problematic due to their language difficulties. Numerous experimental studies indicate that P300 may be considered as an index of cognitive capacity in both healthy and clinical samples. Accordingly, the measurement of event-related potentials enables the investigation of behaviourally non-observable mental processes underlying the cognitive functions that are assessed with neuropsychological tests. To investigate in PWA the relationship between P300 parameters and cognitive function efficiency measured with neuropsychological methods. A total of 25 PWA after left-hemispheric stroke participated in the study. Electrophysiological (EEG) signals were recorded during the performance of a visual Go-No Go task. P300 was identified on nine electrodes, which were then pooled in three lines: left (F3, C3, P3), central (Fz, Cz, Pz) and right (F4, C4, P4). The neuropsychological assessment of cognitive functions included mental speed, short-term memory, divided attention, executive functions, auditory language comprehension and expression. P300 latency correlated with indices of several cognitive functions: temporal resolution, psychomotor speed, spatial short-term memory, planning, word and sentence comprehension, as well as verbal fluency. Shorter P300 latencies were accompanied by greater efficiency of the abovementioned functions. In contrast, significant correlations between P300 amplitudes and cognitive measures were fragmentary. In PWA, P300 latency might be related to cognitive functioning, especially to measures that rely heavily on the speed of information processing. However, P300 seems to be unrelated to more complex cognitive functions. P300 latency may be used as a neurophysiological correlate of cognitive efficiency in PWA and might have potential applications in monitoring the effects of therapeutic interventions in this patient group. What is already known on the subject P300 parameters have been reported to be associated with cognitive performance in both healthy individuals and clinical groups (e.g., patients with Alzheimer's disease). Previous studies show that the presence of P300 at the early post-stroke stage may be a predictor of better recovery of comprehension in PWA. What this paper adds to existing knowledge Our results show for the first time that P300 may be used as a neurophysiological correlate of cognitive efficiency in PWA. In our study, P300 latency was associated with several languages and non-language cognitive functions, especially with those whose effectiveness depends mainly on processing speed. In PWA, shorter latency corresponded to more efficient cognitive functioning. What are the potential or actual clinical implications of this work? P300 measurement may be potentially useful in assessing the efficiency of certain cognitive functions in PWA. It may be also used to monitor the recovery process of PWA and to verify the effects of therapeutic interventions.

Dichrocephala integrifolia Aqueous Extract Antagonises Chronic and Binges Ethanol Feeding-Induced Memory Dysfunctions: Insights into Antioxidant and Anti-Inflammatory Mechanisms.

Ethanol consumption is widely accepted despite its addictive properties and its mind-altering effects. This study aimed to assess the effects of Dichrocephala integrifolia against, memory impairment, on a mouse model of chronic and binges ethanol feeding. Mice were divided, into groups of 8 animals each, and received distilled water, Dichrocephala integrifolia aqueous extract (25; 50; 100; or 200 mg/kg) or memantine (200 mg/kg) once a day, while fe, with Lieber-DeCarli control (sham group only) or Lieber-DeCarli ethanol diet ad libitum for 28 days. The Y maze and the novel object recognition (NOR) tests were used to evaluate spatial short-term and recognition memory, respectively. Malondialdehyde, nitric oxide, glutathione levels, and proinflammatory cytokines (Il-1β, TNF-α, and Il-6) were evaluated in brain homogenates following behavioral assessments. The results showed that chronic ethanol administration in mice was associated with a significant (p < 0.001) reduction in the spontaneous alternation percentage and the discrimination index, in the Y maze and the NOR tests, respectively. It significantly (p < 0.01) increased oxidative stress and inflammation markers levels in the brain. Dichrocephala integrifolia (100 and 200 mg/kg) as well as memantine (200 mg/kg) significantly (p < 0.001) increased the percentage of spontaneous alternation and the discrimination index, in the Y maze and NOR tests, respectively. Dichrocephala integrifolia (100 and 200 mg/kg) likewise memantine (200 mg/kg) significantly (p < 0.01) alleviated ethanol-induced increase, in the brain malondialdehyde level, nitric oxide, Il-1β, TNF-α, and Il-6. From these findings, it can be concluded that Dichrocephala integrifolia counteracted memory impairment, oxidative stress, and neuroinflammation induced by chronic ethanol consumption in mice.

Error-prone protein synthesis recapitulates early symptoms of Alzheimer disease in aging mice.

Age-related neurodegenerative diseases (NDDs) are associated with the aggregation and propagation of specific pathogenic protein species (e.g., Aβ, α-synuclein). However, whether disruption of synaptic homeostasis results from protein misfolding per se rather than accumulation of a specific rogue protein is an unexplored question. Here, we show that error-prone translation, with its frequent outcome of random protein misfolding, is sufficient to recapitulate many early features of NDDs, including perturbed Ca2+ signaling, neuronal hyperexcitability, and mitochondrial dysfunction. Mice expressing the ribosomal ambiguity mutation Rps9 D95N exhibited disrupted synaptic homeostasis resulting in behavioral changes reminiscent of early Alzheimer disease (AD), such as learning and memory deficits, maladaptive emotional responses, epileptiform discharges, suppressed circadian rhythmicity, and sleep fragmentation, accompanied by hippocampal NPY expression and cerebral glucose hypometabolism. Collectively, our findings suggest that random protein misfolding may contribute to the pathogenesis of age-related NDDs, providing an alternative framework for understanding the initiation of AD.

Andrographolide Attenuates Short-Term Spatial and Recognition Memory Impairment and Neuroinflammation Induced by a Streptozotocin Rat Model of Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder clinically manifested by a gradual cognitive decline. Intracerebroventricular injection (ICV) of streptozotocin (STZ), a model of sporadic AD (sAD), shows many aspects of sAD abnormalities (i.e., neuroinflammation, oxidative stress, protein aggregation), resulting in memory impairment. Andrographolide (ANDRO), a natural diterpene lactone, has numerous bioactivities including anti-inflammatory and antioxidant properties. Studies in rodents revealed that ANDRO has neuroprotective properties and restores cognitive impairment. In the present study, we investigated the effects of ANDRO in the ICV-STZ model relative to short-term spatial memory (object location test (OLT) and Y maze test), short-term recognition memory (object recognition test (ORT)), locomotor activity (open field test (OFT)), expression of amyloid precursor protein (APP), and activation of astrocytes (glial fibrillary acidic protein (GFAP) expression) and microglia (ionized calcium-binding adapter molecule-1 (Iba-1) immunohistochemistry) in the prefrontal cortex (PFC) and hippocampus (HIP). Wistar rats were injected ICV with STZ (3mg/kg) or vehicle and treated with ANDRO (2mg/kg, i.p.; three times per week). After four weeks, ANDRO attenuated the impairments of the Y maze and ORT performances, and the increase of astrocyte activation in the PFC induced by the ICV-STZ model. In addition, ANDRO decreased the number of activated microglia cells in the HIP of STZ-injected rats. The APP expression was not altered, neither by the STZ nor ANDRO. ANDRO showed a beneficial effect on memory impairment and neuroinflammation in the STZ model of AD.

Acute Vagus Nerve Stimulation Facilitates Short Term Memory and Cognitive Flexibility in Rats.

Vagus nerve stimulation (VNS) causes the release of several neuromodulators, leading to cortical activation and deactivation. The resulting preparatory cortical plasticity can be used to increase learning and memory in both rats and humans. The effects of VNS on cognition have mostly been studied either in animal models of different pathologies, and/or after extended VNS. Considerably less is known about the effects of acute VNS. Here, we examined the effects of acute VNS on short-term memory and cognitive flexibility in naïve rats, using three cognitive tasks that require comparatively brief (single session) training periods. In all tasks, VNS was delivered immediately before or during the testing phase. We used a rule-shifting task to test cognitive flexibility, a novel object recognition task to measure short-term object memory, and a delayed spontaneous alternation task to measure spatial short-term memory. We also analyzed exploratory behavior in an elevated plus maze to determine the effects of acute VNS on anxiety. Our results indicate that acute VNS can improve memory and cognitive flexibility relative to Sham-stimulation, and these effects are independent of unspecific VNS-induced changes in locomotion or anxiety.

Investigation of memory-enhancing effects of Streptococcus thermophilus EG007 in mice and elucidating molecular and metagenomic characteristics using nanopore sequencing

Over the past decades, accumulating evidences have highlighted the gut microbiota as a key player in the brain functioning via microbiota–gut–brain axis, and accordingly, the beneficial role of several probiotic strains in cognitive ability also have been actively investigated. However, the majority of the research have demonstrated the effects against age-related cognitive decline or neurological disease. To this end, we aimed to investigate lactic acid bacteria strains having beneficial effects on the cognitive function of healthy young mice and elucidate underlying characteristics by carrying out nanopore sequencing-based genomics and metagenomics analysis. 8-week consumption of Streptococcus thermophilus EG007 demonstrated marked enhancements in behavior tests assessing short-term spatial and non-spatial learning and memory. It was revealed that EG007 possessed genes encoding various metabolites beneficial for a health condition in many aspects, including gamma-aminobutyric acid producing system, a neurotransmitter associated with mood and stress response. Also, by utilizing 16S–23S rRNA operon as a taxonomic marker, we identified more accurate species-level compositional changes in gut microbiota, which was increase of certain species, previously reported to have associations with mental health or down-regulation of inflammation or infection-related species. Moreover, correlation analysis revealed that the EG007-mediated altered microbiota had a significant correlation with the memory traits.

Central FGF21 production regulates memory but not peripheral metabolism.

SUMMARYFibroblast growth factor 21 (FGF21) is a liver-derived endocrine hormone that functions to regulate energy homeostasis and macronutrient intake. Recently, FGF21 was reported to be produced and secreted from hypothalamic tanycytes, to regulate peripheral lipid metabolism; however, rigorous investigation of FGF21 expression in the brain has yet to be accomplished. Using a mouse model that drives CRE recombinase in FGF21-expressing cells, we demonstrate that FGF21 is not expressed in the hypothalamus, but instead is produced from the retrosplenial cortex (RSC), an essential brain region for spatial learning and memory. Furthermore, we find that central FGF21 produced in the RSC enhances spatial memory but does not regulate energy homeostasis or sugar intake. Finally, our data demonstrate that administration of FGF21 prolongs the duration of long-term potentiation in the hippocampus and enhances activation of hippocampal neurons. Thus, endogenous and pharmacological FGF21 appear to function in the hippocampus to enhance spatial memory.

Therapeutic potential of hair follicle-derived stem cell intranasal transplantation in a rat model of ischemic stroke

BackgroundStem cell-based therapy has received considerable attention as a potential candidate in the treatment of ischemic stroke; however, employing an appropriate type of stem cells and an effective delivery route are still challenging. In the present study, we investigated the therapeutic effect of safe, noninvasive, and brain-targeted intranasal administration of hair follicle-derived stem cells (HFSCs) in a rat model of ischemic stroke.MethodsStem cells were obtained from the adult rat hair follicles. In experiment 1, stroke was induced by 30 min middle cerebral artery occlusion (MCAO) and stem cells were intranasally transplanted immediately after ischemia. In experiment 2, stroke was induced by 120 min MCAO and stem cells were administered 24 h after cerebral ischemia. In all experimental groups, neurological performance, short-term spatial working memory and infarct volume were assessed. Moreover, relative expression of major trophic factors in the striatum and cortex was evaluated by the quantitative PCR technique. The end point of experiment 1 was day 3 and the end point of experiment 2 was day 15.ResultsIn both experiments, intranasal administration of HFSCs improved functional performance and decreased infarct volume compared to the MCAO rats. Furthermore, NeuN and VEGF expression were higher in the transplanted group and stem cell therapy partially prevented BDNF and neurotrophin-3 over-expression induced by cerebral ischemia.ConclusionsThese findings highlight the curative potential of HFSCs following intranasal transplantation in a rat model of ischemic stroke.

A SLAM-based augmented reality app for the assessment of spatial short-term memory using visual and auditory stimuli

A SLAM-based Augmented Reality (AR) app has been designed, developed, and validated to assess spatial short-term memory. Our app can be used with visual and auditory stimuli and can run on mobile devices. It can be used in any indoor environment. The anchors and data of the app are persistently stored in the cloud. As an authoring tool, the type of stimulus, its number, and specific positions in the real environment can be customized for each session. A study involving 48 participants was carried out to analyze the performance outcomes comparing the location and remembering of stimuli in a real environment using visual versus auditory stimuli. The number of objects placed correctly was similar for the two different stimuli used. However, the group that used the auditory stimulus spent significantly more time completing the task and required significantly more attempts. The performance outcomes were independent of age and gender. For the auditory stimuli, correlations among all of the variables of the AR app and the variables of two other tasks (object-recall and map-pointing) were found. We also found that the greater the number of correctly placed auditory stimuli, the greater the perceived competence and the less mental effort required. The greater the number of errors, the less the perceived competence. Finally, the auditory stimuli are valid stimuli that may benefit the assessment of the memorization of spatial-auditory associations, but the memorization of spatial-visual associations is dominant, as our results suggest.

An Improved Model of Moderate Sleep Apnoea for Investigating Its Effect as a Comorbidity on Neurodegenerative Disease.

Sleep apnoea is a highly prevalent disease that often goes undetected and is associated with poor clinical prognosis, especially as it exacerbates many different disease states. However, most animal models of sleep apnoea (e.g., intermittent hypoxia) have recently been dispelled as physiologically unrealistic and are often unduly severe. Owing to a lack of appropriate models, little is known about the causative link between sleep apnoea and its comorbidities. To overcome these problems, we have created a more realistic animal model of moderate sleep apnoea by reducing the excitability of the respiratory network. This has been achieved through controlled genetically mediated lesions of the preBötzinger complex (preBötC), the inspiratory oscillator. This novel model shows increases in sleep disordered breathing with alterations in breathing during wakefulness (decreased frequency and increased tidal volume) as observed clinically. The increase in dyspnoeic episodes leads to reduction in REM sleep, with all lost active sleep being spent in the awake state. The increase in hypoxic and hypercapnic insults induces both systemic and neural inflammation. Alterations in neurophysiology, an inhibition of hippocampal long-term potentiation (LTP), is reflected in deficits in both long- and short-term spatial memory. This improved model of moderate sleep apnoea may be the key to understanding why this disorder has such far-reaching and often fatal effects on end-organ function.