Long-term Memory Performance Research Articles

Multivariable System Prediction Based on TCN-LSTM Networks with Self-Attention Mechanism and LASSO Variable Selection.

Intelligent prediction of key output variables that are difficult to measure online in complex systems has important research significance. In this paper, by using the least absolute shrinkage and selection operator (LASSO) algorithm to analyze the principal elements of input variables, a temporal convolutional network fused with long short-term memory (TCN-LSTM) network and self-attention mechanism (SAM) is designed to realize dynamic modeling of multivariate feature sequences. For complex processes with multiple input variables, each variable has different effects on the output, so it is necessary to use the LASSO algorithm to perform regression analysis on the input and output data for selecting the principal component variables and reducing the redundancy and computation burden of the network. The TCN network is used to extract the features of the input variables efficiently. The long-term memory performance of time series is enhanced by applying an LSTM network. The multihead SAM is used to optimize the network, and the role of key features is enhanced by assigning weights with probability to further improve the accuracy of sequence prediction. Finally, by comparison with the existing network model, the offline data generated by the high and low converters in the synthetic ammonia industry is used to predict the CO content so as to verify the superiority and applicability of the proposed network model.

Abstract 15835: Inhibition of Soluble Epoxide Hydrolase Reduces Cognitive Impairment and Improves Cerebral Hemodynamics in AD/ADRD

Alzheimer's Disease and Alzheimer's Disease-Related Dementias (AD/ADRD) is an emerging global healthcare crisis. However, underlying mechanisms have not been understood well enough to translate into precision medicine. Recent human genetic evidence indicated that soluble hydrolase (sEH) is linked to AD/ADRD. Inhibition of sEH has been reported to improve cognition in AD mice due to its anti-inflammatory and neuronal protective effects. Here, we examined whether inhibition of sEH with TPPU could reduce cognitive impairments by improving cerebral hemodynamics in 18-month-old diabetes (DM)-related ADRD rats and 6 months of TgF344-AD rats. The myogenic responses of the middle cerebral artery (MCA) were impaired in both AD and ADRD rats and were normalized with TPPU. The inner diameters of MCA increased by 49.16 ± 17.02 % in DM rats but decreased by 16.06 ± 2.46% and 11.24 ± 0.05% in age-matched control and TPPU-treated DM rats when pressure was elevated from 40 to 180 mmHg. Similarly, TPPU-treated AD rats significantly enhanced the MCA constriction by 25%. Forced dilatation occurred at pressures > 140 mmHg in MCAs in both rats and was rescued with TPPU treatment. Endothelial denuded MCAs from TPPU-treated DM rats constricted to 75.15 ± 4.25 % at a perfusion pressure of 140 mmHg and further constricted to 74.66 ± 4.01 % at 180 mmHg, compared to dilation of 155.48 ± 17.35 % and 172.78 ± 13.36 % in DM rats at the same pressures. The percentage of time spent with the novel object was 43.32 ± 8.04% and 83.23 ± 8.70% in DM and TPPU-treated DM rats, versus 75.68 ± 3.33% in non-DM rats. Impaired learning and short and long-term memory function examined with an 8-arm water maze in both DM and AD rats were rescued with TPPU treatment. These results provide the first evidence demonstrating that inhibition of sEH reverses cerebrovascular dysfunction and cognitive impairments in AD/ADRD.

Distinct effects of AMPAR subunit depletion on spatial memory

Pharmacological studies established a role for AMPARs in the mammalian forebrain in spatial memory performance. Here we generated global GluA1/3 double knockout mice (Gria1/3-/-) and conditional knockouts lacking GluA1 and GluA3 AMPAR subunits specifically from principal cells across the forebrain (Gria1/3ΔFb). In both models, loss of GluA1 and GluA3 resulted in reduced hippocampal GluA2 and increased levels of the NMDAR subunit GluN2A. Electrically-evoked AMPAR-mediated EPSPs were greatly diminished, and there was an absence of tetanus-induced LTP. Gria1/3-/- mice showed premature mortality. Gria1/3ΔFb mice were viable, and their memory performance could be analyzed. In the Morris water maze (MWM), Gria1/3ΔFb mice showed profound long-term memory deficits, in marked contrast to the normal MWM learning previously seen in single Gria1-/- and Gria3-/- knockout mice. Our results suggest a redundancy of function within the pool of available ionotropic glutamate receptors for long-term spatial memory performance.

The comprehensive mechanism underlying Schisandra polysaccharide in AD-like symptoms of Aβ25-35-induced rats based on hippocampal metabolomics and serum lipidomics techniques

As is well documented, Alzheimer's disease (AD) is the most prevalent neurodegenerative disease. Meanwhile, Schisandra polysaccharide (SCP) has been reported to exert a protective effect on the nervous system and can regulate metabolic disorders in AD-like symptoms of amyloid β-peptide (Aβ) 25–35-induced rats. Nevertheless, the underlying mechanisms and metabolic markers for the diagnosis of AD are yet to be determined. This study aimed to explore the neuroprotective effect and potential mechanism of action of SCP in AD-like symptoms of Aβ25–35-induced rats by combining pharmacodynamics, metabolomics, and lipidomics. The pharmacodynamic results revealed that SCP significantly improved the spatial learning and long-term memory function and the morphology of neurons in the hippocampal CA1 region, alleviated inflammatory damage and oxidative stress, inhibited the activation of microglia and astrocytes, and increased the proportion of mature neurons of AD-like symptoms of Aβ25–35-induced rats. The results of hippocampal metabolomics and serum lipidomics showed 46 and 48 potential biomarkers were identified for the SCP treatment of AD, respectively. The involved pathways principally comprised lipid metabolism, amino acid metabolism, and energy metabolism. This study elucidates the neuroprotective effect of SCP in AD and its mechanism from the perspective of metabolomics and lipidomics and provides a theoretical basis for the therapeutic effect of SCP in AD.

Abstract 013: Hippocampal Neuroinflammation Occurs After Focal Cerebral Ischemic Stroke That May Contribute To Post-Stroke Memory Loss

Chronic hypertension is a leading risk factor for ischemic stroke. Post-stroke dementia occurs in up to 80% of stroke survivors, and its prevalence is increasing due to an aging population. Memory is impaired in rodent models of transient middle cerebral artery occlusion (tMCAO). However, the impact of cerebral ischemia on brain regions involved in memory that are distant from the ischemic site, such as the hippocampus, remains unclear, but may involve neuroinflammation that is known to disrupt memory. We tested the hypothesis that neuroinflammation occurs in the hippocampus after tMCAO, contributing to memory dysfunction, and is more severe during chronic hypertension. Adult normotensive male Wistar rats and spontaneously hypertensive rats (SHR) underwent 45 minutes of ischemia induced using the intravascular filament method of tMCAO and seven days of reperfusion (or sham; n=6-8/group). A novel object recognition task was used days 5-7 post-tMCAO, and recognition index calculated to assess long-term memory function. Neuroinflammation in the hippocampal CA1 region of ipsi- and contralesional hemispheres was assessed immunohistochemically: microglial activation using Iba1 staining and neuronal expression of tumor necrosis factor alpha (TNFα). Data are mean ± SEM and comparisons made via a two-way ANOVA to determine the interaction between hypertension and stroke with a post-hoc Tukey test. Sham operated SHR and Wistar rats performed similarly well in the memory task and had recognition indices 0.65-0.70. However, memory was impaired in rats that had tMCAO, with recognition indices decreasing to 0.52±0.02 in Wistar rats and 0.52±0.03 in SHR (F 1,24 =21.60; p<0.01). Ischemia increased the number of TNFα expressing neurons regardless of hypertensive status in hippocampus of ipsi- (F 1,25 =7.87; p<0.01) and contra-lesional hemispheres (F 1,25 =4.22; p<0.05). There was a significant effect of ischemia on microglial activation in the hippocampus of both SHR and Wistar rats that only occurred ipsi-lesionally (F 1,24 =5.48; p<0.05). These findings demonstrate that hippocampal neuroinflammation is present seven days after transient focal cerebral ischemia that may contribute to post-stroke memory impairment.

Codium fragile Suppresses PM2.5-Induced Cognitive Dysfunction by Regulating Gut-Brain Axis via TLR-4/MyD88 Pathway.

This study was conducted to evaluate the cognitive dysfunction improvement effect of aqueous extract of Codium fragile (AECF) by regulating the imbalance of the gut-brain axis in chronic particulate matter (PM)2.5-exposed mice. The physiological compounds of AECF were identified as hexadecanamide, oleamide, octadecanamide, stearidonic acid, and linolenic acid by the ultra-performance liquid chromatography-quadrupole time of flight mass spectrometry (UPLC Q-TOF MSE) analysis. To evaluate the effect of PM2.5 on the antioxidant system, superoxide dismutase (SOD) contents, reduced glutathione (GSH) contents, and malondialdehyde (MDA) contents were measured in colon and brain tissues. AECF significantly ameliorated the imbalance of the antioxidant systems. Also, AECF improved intestinal myeloperoxidase (MPO) activity, the abundance of the gut microbiome, short-chain fatty acids (SCFAs) contents, and tight junction protein expression against PM2.5-induced damage. In addition, AECF prevented PM2.5-induced inflammatory and apoptotic expression via the toll-like receptor-4 (TLR-4)/myeloid differentiation primary response 88 (MyD88) pathway in colon and brain tissues. Additionally, AECF enhanced the mitochondrial function, including the mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) contents in brain tissues. Furthermore, AECF regulated the cholinergic system, such as acetylcholine (ACh) contents, acetylcholinesterase (AChE) activity, and protein expression levels of AChE and choline acetyltransferase (ChAT) in brain tissues. To evaluate the effect of cognitive dysfunction caused by PM2.5-induced intestinal dysfunction, behavior tests such as Y-maze, passive avoidance, and Morris water maze tests were performed. From the results of the behavior tests, AECF ameliorated spatial learning and memory, short-term memory, and long-term learning and memory function. This study confirmed that AECF reduced PM2.5-induced cognitive dysfunction by regulating gut microbiome and inflammation, apoptosis, and mitochondrial function by enhancing the gut-brain axis. Based on these results, this study suggests that AECF, which contains fatty acid amides, might be a potential material for ameliorating PM2.5-induced cognitive dysfunction via gut-brain axis improvement.

TMEM175 downregulation participates in impairment of the autophagy related lysosomal dynamics following neonatal hypoxic-ischemic brain injury.

The mechanism underlying long-term cognitive impairment caused by neonatal hypoxic-ischemic brain injury (HIBI) remains unclear. Autophagy is a closely related mechanism and may play a role in this process. We aimed to investigate the role of lysosomal transmembrane protein 175 (TMEM175) in the autophagy-lysosome pathway in neonatal rats with HIBI. A neonatal rat model of HIBI was established, hypoxia was induced, followed by left common carotid artery ligation. Expression levels of TMEM175 and the corresponding proteins involved in autophagy flux and the endolysosomal system fusion process were measured. Rats were administered TMEM175 plasmid via intracerebroventricular injection to induce overexpression. Brain damage and cognitive function were then assessed. TMEM175 was downregulated in the hippocampal tissue, and the autophagy-lysosome pathway was impaired following HIBI in neonatal rats. Overexpression of TMEM175 significantly mitigated neuronal injury and improved long-term cognitive and memory function in neonatal rats with HIBI. We found that improvement in the autophagy-lysosome pathway and endolysosomal system homeostasis, which are TMEM175 related, occurred via regulation of lysosomal membrane dynamic fusion. TMEM175 plays a critical role in maintaining the autophagy-lysosome pathway and endolysosomal homeostasis, contributing to the amelioration of neuronal injury and impaired long-term cognitive function following neonatal HIBI.

Hippocampus Prosthesis for Memory Impairment

Abstract: Hippocampus is the area of the brain that is vital for functions as learning, memory and mood setting. It also reacts to injury or neurodegeneration with robust plasticity. Damage to the hippocampus leads to loss of ability to convert short-term memory to new long-term memories. This can happen due to epilepsy, stroke, dimentia or head injuries. Hippocampal injuries typically lead to cognitive dysfunction, depression, and/or epilepsy. Neural stem cell grafting early after injury has promise for preventing neurological deficits. It modulates aberrant hippocampal post-injury plasticity.and adds new inhibitory GABA-ergic interneurons into the hippocampus. Hippocampal memory prosthesis is a Brain Machine Interface (BMI) device developed for restoring or enhancing memory functions. The objective is to restore the long-term memory function in a stimulus-specific manner by using a multi-input, multi-output (MIMO) nonlinear dynamical model which might serve as a boon for patients suffering from Alzheimer’s disease.

Changes in myelinated fibers in the hippocampus of streptozotocin-induced diabetic rats: a stereological investigation.

Diabetes causes cognitive impairment, and the hippocampus is important for long-term and permanent memory function. However, the mechanism of their interaction is still unclear. In this study, rat models of diabetes mellitus were generated by a single injection of streptozotocin (STZ). This study aims to explore the changes in myelinated fibers in the hippocampus of type 1 diabetic rats. The unbiased stereological methods and transmission electron microscopy were used to obtain the total volume of the hippocampus, the total volume of the myelin sheath, the total length of the myelinated nerve fibers, the distribution of the length with different diameters of the myelinated fibers, and the distribution of the length with different thickness of the myelin sheath. Stereological analysis revealed that, compared to that of the control group, the total myelinated fibers volumes and the total myelinated fibers length were decreased slightly, while the total volume and the thickness of myelin sheaths were significantly decreased in the diabetic group. Finally, when compared with the control group, the total length of myelinated fibers in the diabetes group was significantly reduced, with diameters ranging from 0.7 to 1.1 μm and thicknesses of myelin sheaths from 0.15 to 0.17 μm. This study provides the first experimental evidence by stereological means to demonstrate that myelinated nerve fibers may be the key factor in cognitive dysfunction in diabetes.

Effect of 40 Hz light flicker on behaviors of adult C57BL/6J mice

40 Hz light flicker can activate multiple brain regions of wild-type mice. However, there are no systematic studies on the behavioral effects of 40 Hz light flicker on wild-type mice. Adult wild-type C57BL/6J mice were treated with 40 Hz light flicker (200 lx, 40 Hz, 1 h/day for 3 weeks) to evaluate its effects on several behaviors, including mood, locomotor activity, memory, social interaction, mechanical pain, and sense of smell. In the open field test, the elevated zero-maze test, forced swimming test, and tail suspension test, 40 Hz mice showed no anxiety and depression-like behaviors. In the rotarod test, no differences were found between the anti-fatigue ability and motor coordination ability. In memory-related tests, 40 Hz mice showed the short-term cognitive enhancement in the novel object recognition test. Interestingly, 40 Hz mice showed no enhanced the long-term memory performance in the contextual fear conditioning test, and tone-cued fear conditioning test. Besides, 40 Hz mice increased their exploration of social cues that were unfamiliar to them and differed significantly from their own experiences. In terms of sensory abilities, 40 Hz mice had unchanged pain sensitivity in the von Frey fiber test and significant enhancement in the olfactory ability in the food-seeking test. In conclusion, this 40 Hz light stimulation paradigm has high safety and can improve the specific behavioral ability, which provides a theoretical basis for the future use of 40 Hz light flicker as a disease prevention or treatment method.

The clock gene Per1 may exert diurnal control over hippocampal memory consolidation.

The circadian system influences many different biological processes, including memory performance. While the suprachiasmatic nucleus (SCN) functions as the brain's central pacemaker, downstream "satellite clocks" may also regulate local functions based on the time of day. Within the dorsal hippocampus (DH), for example, local molecular oscillations may contribute to time-of-day effects on memory. Here, we used the hippocampus-dependent Object Location Memory task to determine how memory is regulated across the day/night cycle in mice. First, we systematically determined which phase of memory (acquisition, consolidation, or retrieval) is modulated across the 24 h day. We found that mice show better long-term memory performance during the day than at night, an effect that was specifically attributed to diurnal changes in memory consolidation, as neither memory acquisition nor memory retrieval fluctuated across the day/night cycle. Using RNA-sequencing we identified the circadian clock gene Period1 (Per1) as a key mechanism capable of supporting this diurnal fluctuation in memory consolidation, as learning-induced Per1 oscillates in tandem with memory performance in the hippocampus. We then show that local knockdown of Per1 within the DH impairs spatial memory without affecting either the circadian rhythm or sleep behavior. Thus, Per1 may independently function within the DH to regulate memory in addition to its known role in regulating the circadian system within the SCN. Per1 may therefore exert local diurnal control over memory consolidation within the DH.

Effects of schema on the relationship between post-encoding brain connectivity and subsequent durable memory

Schemas can facilitate memory consolidation. Studies have suggested that interactions between the hippocampus and the ventromedial prefrontal cortex (vmPFC) are important for schema-related memory consolidation. However, in humans, how schema accelerates the consolidation of new information and relates to durable memory remains unclear. To address these knowledge gaps, we used a human analogue of the rodent spatial schema task and resting-state fMRI to investigate how post-encoding brain networks can predict long-term memory performance in different schema conditions. After participants were trained to obtain schema-consistent or schema-inconsistent object-location associations, they learned new object-location associations. The new associations were tested after the post-encoding rest in the scanner and 24 h later outside the scanner. The Bayesian multilevel modelling was applied to analyse the post-encoding brain networks. The results showed that during the post-encoding, stronger vmPFC- anterior hippocampal connectivity was associated with durable memory in the schema-consistent condition, whereas stronger object-selective lateral occipital cortex (LOC)-ventromedial prefrontal connectivity and weaker connectivity inside the default mode network were associated with durable memory in the schema inconsistent condition. In addition, stronger LOC-anterior hippocampal connectivity was associated with memory in both schema conditions. These results shed light on how schemas reconfigure early brain networks, especially the prefrontal-hippocampal and stimuli-relevant cortical networks and influence long-term memory performance.

Child word learning in song and speech.

Listening to sung words rather than spoken words can facilitate word learning and memory in adults and school-aged children. To explore the development of this effect in young children, this study examined word learning (assessed as forming word-object associations) in 1- to 2-year olds and 3- to 4-year olds, and word long-term memory (LTM) in 4- to 5-year olds several days after the initial learning. In an intermodal preferential looking paradigm, children were taught a pair of words utilising adult-directed speech (ADS) and a pair of sung words. Word learning performance was better with sung words than with ADS words in 1- to 2-year olds (Experiments 1a and 1b), 3- to 4-year olds (Experiment 1a), and 4- to 5-year olds (Experiment 2b), revealing a benefit of song in word learning in all age ranges recruited. We also examined whether children successfully learned the words by comparing their performance against chance. The 1- to 2-year olds only learned sung words, but the 3- to 4-year olds learned both sung and ADS words, suggesting that the reliance on music features in word learning observed at ages 1-2 decreased with age. Furthermore, song facilitated the word mapping-recognition processes. Results on children's LTM performance showed that the 4- to 5-year olds' LTM performance did not differ between sung and ADS words. However, the 4- to 5-year olds reliably recalled sung words but not spoken words. The reliable LTM of sung words arose from hearing sung words during the initial learning rather than at test. Finally, the benefit of song on word learning and the reliable LTM of sung words observed at ages 3-5 cannot be explained as an attentional effect.

Hippocampal vascular dysfunction occurs prior to the onset of age-related memory decline during chronic hypertension

Chronic hypertension causes cerebrovascular disease and accelerates age-related cognitive decline. However, little is known about how hypertension and age impact the arterioles supplying deep brain regions involved in memory and cognition, such as the hippocampus, that may contribute to vascular dementia. The aim of the current study was to investigate age-related hippocampal vascular dysfunction during chronic hypertension and its relationship to cognitive decline. We hypothesized that vasodilation of hippocampal arterioles (HAs) to mediators of neurovascular coupling would be impaired during chronic hypertension and worsen with age. We further hypothesized that hypertension-induced HA dysfunction would be associated with impaired memory function. HAs were studied isolated and pressurized from 4 mo. male Wistar rats and compared to male spontaneously hypertensive rats (SHR) at 4, 6 and 12 months of age (n=6/group). Reactivity to mediators of neurovascular coupling were determined, including nitric oxide (NO) and adenosine, and structural remodeling measured under fully relaxed conditions. A novel object recognition task was used and recognition index calculated to assess long-term memory function. Data are mean±SEM. Differences between groups were determined by one-way analysis of variance (ANOVA) with a post-hoc Tukey test. Chronic hypertension impaired vasodilation of HAs to a NO donor regardless of age, as vasoreactivity was similarly blunted in HAs from SHR at 4 mo. (13±3%), 6 mo. (24±4%), and 12 mo. (9±4%) compared to arterioles from Wistar rats (43±7%; p<0.05). Vasodilation to adenosine was also significantly impaired during chronic hypertension at all ages studied, with HA reactivity being ~35-45% in HAs from SHR compared to 70±3% in HAs from normotensive rats. Fully relaxed HAs from Wistar rats had lumen diameters of 65±2 μm at 120mmHg intravascular pressure. Lumen diameters were smaller in HAs from SHR at 4 mo. (54±2 μm) and 6 mo. (53±4 μm), and smallest in arterioles from 12 mo. SHR (46±3 μm; p<0.01). Long-term memory function was similar between 4 mo. SHR and Wistar rats that had recognition indices > 0.70. However, memory was impaired in older SHR, with recognition index being 0.52±0.02 in 6 mo. SHR and 0.47±0.05 in 12 mo. SHR (p<0.01). Overall, chronic hypertension caused inward remodeling and impaired vasoreactivity of HAs to mediators of neurovascular coupling that may disrupt basal and/or activity-dependent changes in blood flow in the hippocampus. Importantly, HA dysfunction was present at an age prior to the onset of memory dysfunction in SHR. These findings suggest these arterioles have a causal role in hypertension- and age-related cognitive decline, and represent a therapeutic target to slow memory loss and reduce vascular contributions to cognitive impairment and dementia. NIH NINDS 1R01 NS127284 and AHA 20CDA35310239 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Fingolimod Administration Following Hypoxia Induced Neonatal Seizure Can Restore Impaired Long-term Potentiation and Memory Performance in Adult Rats

Neonatal seizures commonly caused by hypoxia can lead to long-term neurological outcomes. Early inflammation plays an important role in the pathology of these outcomes. Therefore, in the current study, we explored the long-term effects of Fingolimod (FTY720), an analog of sphingosine and potent sphingosine 1-phosphate (S1P) receptors modulator, as an anti-inflammatory and neuroprotective agent in attenuating anxiety, memory impairment, and possible alterations in gene expression of hippocampal inhibitory and excitatory receptors following hypoxia-induced neonatal seizure (HINS). Seizure was induced in 24 male and female pups (6 in each experimental group) at postnatal day 10 (P10) by premixed gas (5% oxygen/ 95% nitrogen) in a hypoxic chamber for 15 minutes. Sixty minutes after the onset of hypoxia, FTY720 (0.3 mg/kg) or saline (100 µl) was administered for 12 days (from P10 up to P21). Anxiety-like behavior and hippocampal memory function were assessed at P90 by elevated plus maze (EPM) and novel object recognition (NOR), respectively. Long-term potentiation (LTP) was recorded from hippocampal dentate gyrus region (DG) following stimulation of perforant pathway (PP). In addition, the hippocampal concentration of superoxide dismutase activity (SOD), malondialdehyde (MDA), and thiol as indices of oxidative stress were evaluated. Finally, the gene expression of NR2A subunit of N-Methyl-D-aspartic acid (NMDA) receptor, GluR2 subunit of (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) AMPA receptor and γ2 subunit of γ-Aminobutyric acid (GABAA) receptor were assessed at P90 by the quantitative real-time PCR. FTY720 significantly reduced later-life anxiety-like behavior, ameliorated object recognition memory and increased the amplitude and slope of the field excitatory postsynaptic potential (fEPSP) in the rats following HINS. These effects were associated with restoration of the hippocampal thiol content to the normal values and the regulatory role of FTY720 in the expression of hippocampal GABA and glutamate receptors subunits. In conclusion, FTY720 could restore the dysregulated gene expression of excitatory and inhibitory receptors. It also increased the reduced hippocampal thiol content, which was accompanied with attenuation of HINS-induced anxiety, reduced the impaired hippocampal related memory, and prevented hippocampal LTP deficits in later life following HINS.

In sight, out of mind? Disengagement at encoding gradually reduces recall of location.

Disengaging from the external world-a phenomenon referred to as mind wandering-is a common experience that has been shown to be associated with detriments in cognitive performance across a large range of tasks. In the current web-based study, we used a continuous delayed estimation paradigm to investigate the impact of task disengagement at encoding on subsequent recall of location. Task disengagement was assessed with thought probes on a dichotomous (off- vs. on-task) and a continuous response scale (from 0% to 100% on-task). This approach allowed us to consider perceptual decoupling in both a dichotomous and a graded manner. In the first study (n = 54), we found a negative relationship between levels of task disengagement at encoding and subsequent recall of location measured in degrees. This finding supports a graded perceptual decoupling process rather than a decoupling that happens in an all-or-none manner. In the second study (n = 104), we replicated this finding. An analysis of 22 participants showing enough off-task trials to fit the data with the standard mixture model revealed that in this particular subsample, being disengaged from the task at encoding was related to worse long-term memory performance in terms of likelihood to recall but not in terms of precision with which information is recalled. Overall, the findings suggest a graded nature of task disengagement that covaries with fine-grained differences in subsequent recall of location. Going forwards, it will be important to test the validity of continuous measures of mind-wandering.

Super-steep synapses based on positive feedback devices for reliable binary neural networks

This work proposes positive feedback (PF) device-based synaptic devices for reliable binary neural networks (BNNs). Due to PF operation, the fabricated PF device shows a high on/off current ratio (2.69 × 107). The PF device has a charge-trap layer by which the turn-on voltage (Von) of the device can be adjusted by program/erase operations and a long-term memory function is implemented. Also, due to the steep switching characteristics of the PF device, the conductance becomes tolerant to the retention time and the variation in turn-on voltage. Simulations show that high accuracy (88.44% for CIFAR-10 image classification) can be achieved in hardware-based BNNs using PF devices with these properties as synapses.

Altered spreading of neuronal avalanches in temporal lobe epilepsy relates to cognitive performance: A resting-state hdEEG study.

Large aperiodic bursts of activations named neuronal avalanches have been used to characterize whole-brain activity, as their presence typically relates to optimal dynamics. Epilepsy is characterized by alterations in large-scale brain network dynamics. Here we exploited neuronal avalanches to characterize differences in electroencephalography (EEG) basal activity, free from seizures and/or interictal spikes, between patients with temporal lobe epilepsy (TLE) and matched controls. We defined neuronal avalanches as starting when the z-scored source-reconstructed EEG signals crossed a specific threshold in any region and ending when all regions returned to baseline. This technique avoids data manipulation or assumptions of signal stationarity, focusing on the aperiodic, scale-free components of the signals. We computed individual avalanche transition matrices to track the probability of avalanche spreading across any two regions, compared them between patients and controls, and related them to memory performance in patients. We observed a robust topography of significant edges clustering in regions functionally and structurally relevant for the TLE, such as the entorhinal cortex, the inferior parietal and fusiform area, the inferior temporal gyrus, and the anterior cingulate cortex. We detected a significant correlation between the centrality of the entorhinal cortex in the transition matrix and the long-term memory performance (delay recall Rey-Osterrieth Complex Figure Test). Our results show that the propagation patterns of large-scale neuronal avalanches are altered in TLE during the resting state, suggesting a potential diagnostic application in epilepsy. Furthermore, the relationship between specific patterns of propagation and memory performance support the neurophysiological relevance of neuronal avalanches.

Reversal of chronic restraint stress-induced memory impairment by Japanese sake yeast supplement in mice: Role of adenosine A1 and A2A receptors

Controversial studies indicate the adenosine compound (a neuromodulator with neuroprotective activity) intervention on cognitive performance. On the other hand, Japanese sake yeast has been enriched with oral adenosine analogs as a novel natural agent. As the first report, we aimed to evaluate the effects of Japanese sake yeast supplement in a mouse model of chronic restraint stress-induced cognitive dysfunction. Mice were subjected to a one-week stress protocol and concomitantly treated orally with sake yeast at the dose level of 100, 200 and 300 mg/kg once daily for a week. The spatial and conditioned fear memory functions were evaluated with the Morris Water Maze (MWM) and the Passive Avoidance Learning (PAL) test, respectively. In all dosing regimens, improvements in spatial cognition were observed significantly in the MWM. 200 and 300 mg/kg of sake yeast significantly improved short- and long-term fear memory functions in the PAL test. Memory-enhancing effect of sake yeast was potentiated by the injection of ZM241385 (15 mg/kg), a selective adenosine A2A receptor (A2AR) antagonist, but completely disappeared by the injection of 8-cyclopentyltheophylline (CPT-8, 10 mg/kg), a selective adenosine A1 receptor (A1R) antagonist. The findings of the present study demonstrate the efficacy of sake yeast in acting as a cognitive performance-enhancing agent. Eventually, sake yeast and its ingredient S-adenosyl methionine (SAM) may be useful in improving memory in patients suffering from many dementia forms including Alzheimer's disease (AD).

Elaboration by superposition: From interference in working memory to encoding in long-term memory.

Distraction embedded in working memory tasks leads to impaired performance. This impairment is mitigated when targets and distractors that follow them share common features-a signature effect of interference by superposition. Here we propose that target-distractor similarity modulates not only forgetting from working memory but also encoding into long-term memory. In five experiments, we test this elaboration-by-superposition hypothesis, demonstrating that semantic relatedness between targets and distractors benefits delayed category-cued recall performance (Experiments 1a and 1b), which is not due to carry-over effects from working memory testing (Experiment 2). Just as in the case of working memory, this long-term memory effect is reduced when distractors precede targets (Experiment 3). Finally, we show that while high target-distractor similarity reduces forgetting from working memory, it produces net benefits for long-term memory performance (Experiment 4). Together, the results suggest that common mechanisms underlie encoding into working and long-term memory, and that bindings between features of spatiotemporal context and features of to-be-remembered items play a crucial role. (PsycInfo Database Record (c) 2022 APA, all rights reserved).