Entrainment emerges when oscillatory movements synchronize with environmental stimuli processing. The purpose of this experiment was to assess how cognitive-motor entrainment during a dual-task would influence the quality of gait and affect episodic long-term memory. Twenty-one participants (22.56 y/o; 64% F) walked at preferred paces while listening to 40-item word lists. In separate sessions, unique word lists were presented predictably on every fourth stride, unpredictably related to stepping, or predictably while standing. Memory tests administered 24-hr after encoding revealed that predictable word presentation led to better free-recall performance than unpredicted (p = .044); recognition memory was not impacted. Gait phase parameters during the predicted condition were more stable than the unpredicted condition or baseline assessments. Cognitive-motor entrainment may alleviate dual-task costs and enhance memory retention.

The therapeutic potential of suppressing polypyrimidine tract-binding protein 1 (Ptbp1) messenger RNA by viral transduction in a post-stroke dementia mouse model has not yet been examined. In this study, 3 days after cerebral ischemia, we injected a viral vector cocktail containing adeno-associated virus (AAV)-pGFAP-mCherry and AAV-pGFAP-CasRx (control vector) or a cocktail of AAV-pGFAP-mCherry and AAV-pGFAP-CasRx-SgRNA-(Ptbp1) (1:5, 1.0 × 1011 viral genomes) into post-stroke mice via the tail vein. We observed new mCherry/NeuN double-positive neuron-like cells in the hippocampus 56 days after cerebral ischemia. A portion of mCherry/GFAP double-positive astrocyte-like glia could have been converted into new mCherry/NeuN double-positive neuron-like cells with morphological changes. The new neuronal cells integrated into the dentate gyrus and recognition memory was significantly ameliorated. These results demonstrated that the in vivo conversion of hippocampal astrocyte-like glia into functional new neurons by the suppression of Ptbp1 might be a therapeutic strategy for post-stroke dementia.

Goal contagion, the tendency to adopt others\' goals, significantly impacts cognitive processes, which gains particular importance in the emerging field of human-robot interactions. The present study explored how observing human versus robotic actions affects preference and memory. Series of objects undergoing either human or robotic grasping actions together with static (no action) objects were presented, while participants indicated their preference for each object. After a short delay, their memory for grasped, static and new (unstudied) stimuli was tested. Human actions enhanced preference and subsequent recollection of objects, more than robotic actions. In the context of human action, static objects were also perceived as more familiar at recognition. The goal contagion\'s influence on memory was found to be independent from its impact on preference. These findings highlight the critical role of human interaction in eliciting the impact of goal contagion on cognitive evaluations, memory engagement and the creation of detailed associative memories.

OBJECTIVE: Research on cognitive and emotional functions during pregnancy challenges the prevalent perception of cognitive decline in pregnant women. This study investigates the behavioral and neural dynamics of cognitive-affective processing in third-trimester pregnant women, comparing them with non-pregnant controls.
METHODS: Using a 64-channel EEG-ERP system, we recorded brain activity as participants engaged in an emotional word recognition task. This task involved initially viewing a sequence of emotional and neutral words, followed by a recognition test where participants identified each word as \'new\' or \'previously seen\'.
RESULTS: Contrary to widespread beliefs about diminished recognition ability during late pregnancy, our results revealed no significant differences in error rates between groups. However, pregnant participants demonstrated slower reaction times. In terms of neural responses, pregnant women exhibited increased amplitudes in the N1, P2, and N400 ERP components, suggesting that they may require additional brain resources compared with non-pregnant individuals to process perceptual information. A significant interaction was observed between pregnancy status and the emotional valence of stimuli. Pregnant women showed heightened N1 and N400 responses to negative words, indicating increased sensitivity to stimuli potentially representing threat. This enhanced response was not observed for positive or neutral words. Furthermore, there was an amplified N1 response to \'new\' words, but not to \'old\' words.
CONCLUSIONS: These findings suggest that late pregnancy is characterized by heightened responsiveness to new and particularly negative stimuli, potentially leading to a more cautious behavioral approach. Heightened vigilance and sensitivity could offer evolutionary advantages, optimizing fetal development and enhancing maternal well-being.

Mathematical models explaining production effects assume that production leads to the encoding of additional features, such as phonological ones. This improves memory with a combination of encoding strength and feature distinctiveness, implementing aspects of propositional theories. However, it is not clear why production differs from other manipulations such as study time and spaced repetition, which are also thought to influence strength. Here we extend attentional subsetting theory and propose an explanation based on the dimensionality of feature spaces. Specifically, we suggest phonological features are drawn from a compact feature space. Deeper features are sparsely subselected from a larger subspace. Algebraic and numerical solutions shed light on several findings, including the dependency of production effects on how other list items are encoded (differing from other strength factors) and the production advantage even for homophones. This places production within a continuum of strength-like manipulations that differ in terms of the feature subspaces they operate upon and leads to novel predictions based on direct manipulations of feature-space properties.

The \"good is up\" metaphor, which links valence and verticality was found to influence affective judgement and to direct attention, but its effects on memory remain unclear with contradictory research findings. To provide a more accurate assessment of memory components involved in recognition, such as item memory and source-guessing biases, a standard source monitoring paradigm was applied in this research. A series of three experiments provided a conceptual replication and extension of Experiment 2 by Crawford et al., (2014) and yielded a consistent result pattern suggesting that the \"good is up\" metaphor biases participants\' guessing of source location. That is, when source memory failed, participants were more inclined to guess the \"up\" location versus \"down\" location for positive items (and vice versa for negative items). It did, however, not affect source memory or item memory for valenced stimuli learned from metaphor-congruent versus incongruent locations (i.e., no metaphor-(in)congruent effects in memory). We suggest that the \"good is up\" metaphor may affect cognitive processes in a more subtle way than originally suggested.

Parkinson\'s disease (PD), an age-associated neurodegenerative motor disorder, is associated with dementia and cognitive decline. However, the precise molecular insight into PD-induced cognitive decline is not fully understood. Here, we have investigated the possible alterations in the expression of glutamate receptor and its trafficking/scaffolding/regulatory proteins underlying the memory formation and neuroprotective effects of a specialized Bacopa monnieri extract, CDRI-08 (BME) in the hippocampus of the rotenone-induced PD mouse model. Our Western blotting and qRT-PCR data reveal that the PD-induced recognition memory decline is associated with significant upregulation of the AMPA receptor subunit GluR1 and downregulation of GluR2 subunit genes in the hippocampus of rotenone-affected mice as compared to the vehicle control. Further, expressions of the trafficking proteins are significantly upregulated in the hippocampus of rotenone-affected mice compared to the vehicle control. Our results also reveal that the above alterations in the hippocampus are associated with similar expression patterns of total CREB, pCREB, and BDNF. BME (CDRI-08, 200 mg/kg BW) reverses the expression of AMPA receptor subunits, their trafficking proteins differentially, and the transcriptional modulatory proteins depending on whether the BME treatment was given before or after the rotenone treatment. Our data suggest that expression of the above genes is significantly reversed in the BME pre-treated mice subjected to rotenone treatment towards their levels in the control mice compared to its treatment after rotenone administration. Our results provide the possible molecular basis underlying the rotenone-induced recognition memory decline, conditions mimicking the PD symptoms in mouse model and neuroprotective action of bacoside A and bacoside B (58%)-enriched Bacopa monnieri extract (BME) in the hippocampus.

OBJECTIVE: In vascular dementia (VD), memory impairment caused by the damage of synaptic plasticity is the most prominent feature that afflicts patients and their families. Treadmill exercise has proven beneficial for memory by enhancing synaptic plasticity in animal models including stroke, dementia, and mental disorders. The aim of this study was to examine the effects of treadmill exercise on recognition memory and structural synaptic plasticity in VD rat model.
METHODS: Male Sprague-Dawley rats were randomly assigned into four groups: control group (C group, n = 6), vascular dementia group (VD group, n = 6), treadmill exercise and vascular dementia group (Exe-VD group, n = 6), and treadmill exercise group (Exe group, n = 6). Four-week treadmill exercise was performed in the Exe-VD and Exe groups. Then, the common carotid arteries of rats in the VD and Exe-VD groups were identified to establish the VD model. Behavior tests (open-field test and novel recognition memory test) were adopted to evaluate anxiety-like behavior and recognition memory. Transmission electron microscopy and Golgi staining were performed to observe synaptic ultrastructure and spine density in the hippocampus.
RESULTS: Our study demonstrated that VD rat exhibited significantly anxiety-like behavior and recognition impairment (p < .01), while treadmill exercise significantly alleviated anxiety-like behavior and improved recognition memory in VD rat (p < .01). Transmission electron microscopy revealed that hippocampal synapse numbers were significantly decreased in the VD group compared to the control group (p < .05). These alterations were reversed by treadmill exercise, and the rats exhibited healthier synaptic ultrastructure, including significantly increased synapse (p < .05). Meanwhile, golgi staining revealed that the spine numbers of the hippocampus were significantly decreased in the VD group compared to the control group (p < .05). When compared with the VD group, hippocampal spine numbers were significantly increased in the Exe-VD group (p < .05).
CONCLUSIONS: The improvement of VD-associated recognition memory by treadmill exercises is associated with enhanced structural synaptic plasticity in VD rat model.

UNASSIGNED: Trisomy of human chromosome 21 (Hsa21) results in a constellation of features known as Down syndrome (DS), the most common genetic form of intellectual disability. Hsa21 is orthologous to three regions in the mouse genome on mouse chromosome 16 (Mmu16), Mmu17 and Mmu10. We investigated genotype-phenotype relationships by assessing the contribution of these three regions to memory function and age-dependent cognitive decline, using three mouse models of DS, Dp1Tyb, Dp(17)3Yey, Dp(10)2Yey, that carry an extra copy of the Hsa21-orthologues on Mmu16, Mmu17 and Mmu10, respectively.
UNASSIGNED: Prior research on cognitive function in DS mouse models has largely focused on models with an extra copy of the Mmu16 region and relatively little is known about the effects of increased copy number on Mmu17 and Mmu10 on cognition and how this interacts with the effects of aging. As aging is is a critical contributor to cognitive and psychiatric changes in DS, we hypothesised that ageing would differentially impact memory function in Dp1Tyb, Dp(17)3Yey, and Dp(10)2Yey, models of DS.
UNASSIGNED: Young (12-13 months and old (18-20 months mice Dp1Tyb, Dp(17)3Yey and Dp(10)2Yey mice were tested on a battery of object recognition memory test that assessed object novelty detection, novel location detection and associative object-in place memory. Following behavioral testing, hippocampal and frontal cortical tissue was analysed for expression of glutamatergic receptor proteins using standard immunoblot techniques.
UNASSIGNED: Young (12-13 months and old (18-20 months mice Dp1Tyb, Dp(17)3Yey and Dp(10)2Yey mice were tested on a battery of object recognition memory test that assessed object novelty detection, novel location detection and associative object-in place memory. Following behavioral testing, hippocampal and frontal cortical tissue was analysed for expression of glutamatergic receptor proteins using standard immunoblot techniques.
UNASSIGNED: Our results show that distinct Hsa21-orthologous regions contribute differentially to cognitive dysfunction in DS mouse models and that aging interacts with triplication of Hsa21-orthologous genes on Mmu10.

Serotonin is a monoamine neurotransmitter that plays a main role in regulating physiological and cognitive functions. Serotonergic system dysfunction is involved in the etiology of various psychiatric and neurological disorders. Therefore, the present study was designed to investigate the effects of early-life serotonin depletion on cognitive disorders caused by sleep deprivation. Serotonin was depleted by para-chlorophenylalanine (PCPA, 100 mg/kg, s.c.) at postnatal days 10-20, followed by sleep deprivation-induced through the multiple platform apparatus for 24 h at PND 60. After the examination of the novel object recognition and passive avoidance memories, the hippocampi and prefrontal cortex were dissected to examine the brain-derived neurotrophic factor (BDNF) mRNA expression by PCR. Our findings showed that postnatal serotonin depletion and sleep deprivation impaired the novel object recognition and passive avoidance memories and changed the BDNF levels. In the same way, the serotonin depletion in early life before sleep deprivation exacerbated the harmful effects of sleep deprivation on cognitive function and BDNF levels. It can be claimed that the serotonergic system plays a main role in the modulation of sleep and cognitive functions.