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We memorize our daily life experiences, which are often multisensory in nature, by segmenting them into distinct event models, in accordance with perceived contextual or situational changes. However, very little is known about how multisensory boundaries affect segmentation, as most studies have focused on unisensory (visual or audio) segmentation. In three experiments, we investigated the effect of multisensory boundaries on segmentation in memory and perception. In Experiment 1, participants encoded lists of pictures while audio and visual contexts changed synchronously or asynchronously. After each list, we tested recognition and temporal associative memory for pictures that were encoded in the same audio-visual context or that crossed a synchronous or an asynchronous multisensory change. We found no effect of multisensory synchrony for recognition memory: synchronous and asynchronous changes similarly impaired recognition for pictures encoded at those changes, compared to pictures encoded further away from those changes. Multisensory synchrony did affect temporal associative memory, which was worse for pictures encoded at synchronous than at asynchronous changes. Follow up experiments showed that this effect was not due to the higher dimensionality of multisensory over unisensory contexts (Experiment 2), nor that it was due to the temporal unpredictability of contextual changes inherent to Experiment 1 (Experiment 3). We argue that participants formed situational expectations through multisensory synchronicity, such that synchronous multisensory changes deviated more strongly from those expectations than asynchronous changes. We discuss our findings in light of supportive and conflicting findings of uni- and multi-sensory segmentation.

The eyewitness and fundamental memory research fields have investigated the effects of acute stress at encoding on memory performance for decades yet results often demonstrate contrasting conclusions. In this review, we first summarise findings on the effects of acute encoding stress on memory performance and discuss how these research fields often come to these diverging findings regarding the effects of encoding stress on memory performance. Next, we critically evaluate methodological choices that underpin these discrepancies, emphasising the strengths and limitations of different stress-memory experiments. Specifically, we elaborate on choice of stressors and stimuli, stress manipulation checks, stressor timing, and the interval between encoding and retrieval and discuss how methodological shortcomings in both the eyewitness and fundamental memory fields have limited our understanding of how encoding stress may affect eyewitness memory performance. Finally, we propose several recommendations for researchers interested in this topic, such as confirming stress inductions with physiological measures, implementing sufficient retrieval intervals to isolate the memory phase of interest and using ecologically valid memory paradigms. We conclude that the best progress can be made if researchers are responsive to the methodologies and findings reported in other research fields and encourage collaborations between the different disciplines.

The eyewitness and fundamental memory research fields have investigated the effects of acute stress at encoding on memory performance for decades yet results often demonstrate contrasting conclusions. In this review, we first summarise findings on the effects of acute encoding stress on memory performance and discuss how these research fields often come to these diverging findings regarding the effects of encoding stress on memory performance. Next, we critically evaluate methodological choices that underpin these discrepancies, emphasising the strengths and limitations of different stress-memory experiments. Specifically, we elaborate on choice of stressors and stimuli, stress manipulation checks, stressor timing, and the interval between encoding and retrieval and discuss how methodological shortcomings in both the eyewitness and fundamental memory fields have limited our understanding of how encoding stress may affect eyewitness memory performance. Finally, we propose several recommendations for researchers interested in this topic, such as confirming stress inductions with physiological measures, implementing sufficient retrieval intervals to isolate the memory phase of interest and using ecologically valid memory paradigms. We conclude that the best progress can be made if researchers are responsive to the methodologies and findings reported in other research fields and encourage collaborations between the different disciplines. ispartof: MEMORY vol:29 issue:8 pages:1091-1100 ispartof: location:England status: published

Background: Recent data suggest that musical practice prevents age-related cognitive decline. But experimental evidence remains sparse and no concise information on the neurophysiological bases exists, although cognitive decline represents a major impediment to healthy aging. A challenge in the field of aging is developing training regimens that stimulate neuroplasticity and delay or reverse symptoms of cognitive and cerebral decline. To be successful, these regimens should be easily integrated in daily life and intrinsically motivating. This study combines for the first-time protocolled music practice in elderly with cutting-edge neuroimaging and behavioral approaches, comparing two types of musical education. Methods: We conduct a two-site Hannover-Geneva randomized intervention study in altogether 155 retired healthy elderly (64–78) years, (63 in Geneva, 92 in Hannover), offering either piano instruction (experimental group) or musical listening awareness (control group). Over 12 months all participants receive weekly training for 1 hour, and exercise at home for ~ 30 min daily. Both groups study different music styles. Participants are tested at 4 time points (0, 6, and 12 months & post-training (18 months)) on cognitive and perceptual-motor aptitudes as well as via wide-ranging functional and structural neuroimaging and blood sampling. Discussion: We aim to demonstrate positive transfer effects for faculties traditionally described to decline with age, particularly in the piano group: executive functions, working memory, processing speed, abstract thinking and fine motor skills. Benefits in both groups may show for verbal memory, hearing in noise and subjective well-being. In association with these behavioral benefits we anticipate functional and structural brain plasticity in temporal (medial and lateral), prefrontal and parietal areas and the basal ganglia. We intend exhibiting for the first time that musical activities can provoke important societal impacts by diminishing cognitive and perceptual-motor decline supported by functional and structural brain plasticity. Trial registration: The Ethikkomission of the Leibniz Universität Hannover approved the protocol on 14.08.17 (no. 3604–2017), the neuroimaging part and blood sampling was approved by the Hannover Medical School on 07.03.18. The full protocol was approved by the Commission cantonale d’éthique de la recherche de Genève (no. 2016–02224) on 27.02.18 and registered at clinicaltrials.gov on 17.09.18 (NCT03674931, no. 81185).

Depression is theorized to be caused in part by biased cognitive processing of emotional information. Yet, prior research has adopted a reductionist approach that does not characterize how biases in cognitive processes such as attention and memory work together to confer risk for this complex multifactorial disorder. Grounded in affective and cognitive science, we highlight four mechanisms to understand how attention biases, working memory difficulties, and long-term memory biases interact and contribute to depression. We review evidence for each mechanism and highlight time- and context-dependent dynamics. We outline methodological considerations and recommendations for research in this area. We conclude with directions to advance the understanding of depression risk, cognitive training interventions, and transdiagnostic properties of cognitive biases and their interactions.

Ever since it was discovered in the monkey’s prefrontal cortex, persistent neuronal activity during the delay period of delay tasks has been considered a phenomenon of working memory. Operationally, this interpretation is correct, because during that delay those tasks require the memorization of a sensory cue, commonly visual. What is incorrect is the assumption that the persistent activity during the delay is caused exclusively by the retention of the sensory cue. In this brief review, the author takes the position that the neural substrate of working memory is an array of long-term memory networks, that is, of cognitive networks (cognits), updated and orderly activated for the attainment of a behavioral goal. In the case of a behavioral task, that activated array of cognits has been previously formed in long-term memory (throughout this text, the expression “long-term memory” refers to all experiences acquired after birth, including habits and so-called procedural memory, such as the learning of a behavioral task). The learning of a task is the forming of synaptic associations between neural representations of three cognitive components of the task: perceptual, motor, and reward-related. Thereafter, when needed, the composite cognit of the task is activated in an orderly fashion to serve working memory in the perception-action cycle. To make his points on a complex issue, which has been the focus of his work, and to delineate a frontier for future research, the author refers to several of his own publications and previously published reviews.

There is ample evidence that phosphodiesterase 4 (PDE4) inhibition can improve memory performance in animal studies. In the present study, we examined the acute effects of the PDE4 inhibitor roflumilast on memory performance in healthy individuals (60-80 years of age). We tested the effects of acute roflumilast administration (100, 250, 1000 μg) in a double-blind, placebo-controlled, 4-way crossover design. Participants were first screened for their verbal word memory performance to ensure normal memory performance (within 0.5 standard deviation from norm score; n = 20) Drug effects on memory performance were tested in a verbal memory test and a spatial memory test. Reported side effects of drug treatment were registered. Roflumilast (100 μg) improved the delayed recall performance of the participants (Cohen's d, 0.69). No effects were observed in the spatial memory task. Roflumilast was well tolerated at this low dose. Although no clear adverse side effects were reported at the low dose, mild adverse events (including headache, dizziness, insomnia, and diarrhea) were reported after the 1000 μg dose. The present study provides first evidence that the PDE4 inhibitor roflumilast improves verbal memory performance in old participants. The current data encourage further development of PDE4 inhibitors for improving memory.

Background: Recent data suggest that musical practice prevents age-related cognitive decline. But experimental evidence remains sparse and no concise information on the neurophysiological bases exists, although cognitive decline represents a major impediment to healthy aging. A challenge in the field of aging is developing training regimens that stimulate neuroplasticity and delay or reverse symptoms of cognitive and cerebral decline. To be successful, these regimens should be easily integrated in daily life and intrinsically motivating. This study combines for the first-time protocolled music practice in elderly with cutting-edge neuroimaging and behavioral approaches, comparing two types of musical education. Methods: We conduct a two-site Hannover-Geneva randomized intervention study in altogether 155 retired healthy elderly (64–78) years, (63 in Geneva, 92 in Hannover), offering either piano instruction (experimental group) or musical listening awareness (control group). Over 12 months all participants receive weekly training for 1 hour, and exercise at home for ~ 30 min daily. Both groups study different music styles. Participants are tested at 4 time points (0, 6, and 12 months & post-training (18 months)) on cognitive and perceptual-motor aptitudes as well as via wide-ranging functional and structural neuroimaging and blood sampling. Discussion: We aim to demonstrate positive transfer effects for faculties traditionally described to decline with age, particularly in the piano group: executive functions, working memory, processing speed, abstract thinking and fine motor skills. Benefits in both groups may show for verbal memory, hearing in noise and subjective well-being. In association with these behavioral benefits we anticipate functional and structural brain plasticity in temporal (medial and lateral), prefrontal and parietal areas and the basal ganglia. We intend exhibiting for the first time that musical activities can provoke important societal impacts by diminishing cognitive and perceptual-motor decline supported by functional and structural brain plasticity. Trial registration: The Ethikkomission of the Leibniz Universität Hannover approved the protocol on 14.08.17 (no. 3604–2017), the neuroimaging part and blood sampling was approved by the Hannover Medical School on 07.03.18. The full protocol was approved by the Commission cantonale d’éthique de la recherche de Genève (no. 2016–02224) on 27.02.18 and registered at clinicaltrials.gov on 17.09.18 (NCT03674931, no. 81185).

A key aspect of human cognitive flexibility concerns the ability to convert complex symbolic instructions into novel behaviors. Previous research proposes that this transformation is supported by two neurocognitive states: an initial declarative maintenance of task knowledge, and an implementation state necessary for optimal task execution. Furthermore, current models predict a crucial role of frontal and parietal brain regions in this process. However, whether declarative and procedural signals independently contribute to implementation remains unknown. We report the results of an fMRI experiment in which participants executed novel instructed stimulus-response associations. We then used a pattern-tracking procedure to quantify the contribution of format-unique signals during instruction implementation. This revealed independent procedural and declarative representations of novel S-Rs in frontoparietal areas, prior to execution. Critically, the degree of procedural activation predicted subsequent behavioral performance. Altogether, our results suggest an important contribution of frontoparietal regions to the neural architecture that regulates cognitive flexibility.

Cognitive and affective impairments are the most characterized consequences following cerebral ischemia. BAY 60-7550, a selective phosphodiesterase type 2 inhibitor (PDE2-I), presents memory-enhancing and anxiolytic-like properties. The behavioral effects of BAY 60-7550 have been associated with its ability to prevent hydrolysis of both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) thereby interfering with neuronal plasticity. Here, we hypothesize that PDE2-I treatment could promote functional recovery after brain ischemia. Mice C57Bl/6 were submitted to bilateral common carotid artery occlusion (BCCAO), an experimental model of transient brain ischemia, for 20 min. During 21 days after reperfusion, the animals were tested in a battery of behavioral tests including the elevated zero maze (EZM), object location task (OLT) and forced swim test (FST). The effects of BAY 60-7550 were evaluated on neuronal nuclei (NeuN), caspase-9, cAMP response element- binding protein (CREB), phosphorylated CREB (pCREB) and brain-derived neurotrophic factor (BDNF) expression in the hippocampus. BCCAO increased anxiety levels, impaired hippocampus-dependent cognitive function and induced despair-like behavior in mice. Hippocampal neurodegeneration was evidenced by a decrease in NeuN and increase incaspase-9 protein levels in BCCAO mice. Ischemic mice also showed low BDNF protein levels in the hippocampus. Repeated treatment with BAY 60-7550 attenuated the behavioral impairments induced by BCCAO in mice. Concomitantly, BAY 60-7550 enhanced expression of pCREB and BDNF protein levels in the hippocampus of ischemic mice. The present findings suggest that chronic inhibition of PDE2 provides functional recovery in BCCAO mice possibly by augmenting hippocampal neuronal plasticity.

Whereas the effects of attention switches occurring within perception or memory are relatively well understood, much less is known about switches of attention between them. We discuss the methodological limitations of initial research on this topic, which was never integrated with the broader cognitive literature. On the basis of this discussion, we present here a new paradigm, in which participants performed a simple probe-to-target matching task where targets were either perceived on screen or retrieved from memory. Across successive trials, repetitions or alternations (in both directions) between these 2 conditions were created, and eventually compared with each other. In line with our prediction, derived from the assumption of a top-down control mechanism, we found a cost for switching between external and internal attention in Experiment 1. Furthermore, this switch cost was asymmetric, being substantially larger when switching from (external) perception to (internal) memory than the other way around. In Experiments 2-4, we ruled out an imbalance in practice, learning, and preparation as confounds for this asymmetry. We propose that switches of attention between internal and external information are underpinned by a supervisory attention control mechanism, and that this asymmetry can be explained in terms of priming, associative interference or memory retrieval. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Attention and memory may be impaired in individuals at-risk for Alzheimer’s disease (AD), though standard cognitive assessments typically study the two in parallel. In reality, attention and memory interact to facilitate information processing, and thus a more integrative approach is required. Here, we used a novel auditory paradigm to assess how long-term memory for auditory scenes facilitates detection of an auditory target in asymptomatic carriers of Apolipoprotein E4 (APOE4), the principle risk gene for late-onset AD. We tested 60 healthy middle-aged adults with varying doses of APOE4 - 20 APOE4 homozygotes (E4/E4), 20 heterozygotes (E3/E4) and 20 non-carriers (E3/E3) - to determine effect on memory-guided attention. While explicit memory was unaffected by genotype, APOE4 dose significantly impaired memory-guided attention. A relationship between explicit memory and memory-guided attention was observed in non-carriers, but this correlation was not significant in E3/E4 and E4/E4 carriers, suggesting that APOE4 carriers rely less on explicit memory to facilitate attention. Since memory-guided attention declined with age in APOE4 homozygotes, this impairment may reflect early disease rather than being a life-long trait. In sum, asymptomatic individuals at increased genetic risk of AD show an age-dependent decline in attention-memory interaction when memory alone is not impaired.

In natural settings, the prospect of reward often influences the focus of our attention, but how cognitive and motivational systems influence sensory cortex is not well understood. Also, challenges in training nonhuman animals on cognitive tasks complicate cross-species comparisons and interpreting results on the neurobiological bases of cognition. Incentivized attention tasks could expedite training and evaluate the impact of attention on sensory cortex. Here we develop an Incentivized Attention Paradigm (IAP) and use it to show that macaque monkeys readily learn to use auditory or visual reward cues, drastically influencing their performance within a simple auditory task. Next, this paradigm was used with functional neuroimaging to measure activation modulation in the monkey auditory cortex. The results show modulation of extensive auditory cortical regions throughout primary and non-primary regions, which although a hallmark of attentional modulation in human auditory cortex, has not been studied or observed as broadly in prior data from nonhuman animals. Psycho-physiological interactions were identified between the observed auditory cortex effects and regions including basal forebrain sites along acetylcholinergic and dopaminergic pathways. The findings reveal the impact and regional interactions in the primate brain during an incentivized attention engaging auditory task.

During the last decades, there have been major advances in mapping the brain regions that underlie our ability to perceive, experience, and produce music and how musical training can shape the structure and function of the brain. This progress has fueled and renewed clinical interest towards uncovering the neural basis for the impaired or preserved processing of music in different neurological disorders and how music-based interventions can be used in their rehabilitation and care. This article reviews our contribution to and the state-of-the-art of this field. We will provide a short overview outlining the key brain networks that participate in the processing of music and singing in the healthy brain and then present recent findings on the following key music-related research topics in neurological disorders: (i) the neural architecture underlying deficient processing of music (amusia), (ii) the preservation of singing in aphasia and music-evoked emotions and memories in Alzheimer's disease, (iii) the mnemonic impact of songs as a verbal learning tool, and (iv) the cognitive, emotional, and neural efficacy of music-based interventions and activities in the rehabilitation and care of major ageing-related neurological illnesses (stroke, Alzheimer's disease, and Parkinson's disease). (C) 2018 Elsevier Ltd. All rights reserved.

Adaptation to the ever-changing world is critical for survival, and our brains are particularly tuned to remember events that differ from previous experiences. Novel experiences induce dopamine release in the hippocampus, a process which promotes memory persistence. While axons from the ventral tegmental area (VTA) were generally thought to be the exclusive source of hippocampal dopamine, recent studies have demonstrated that noradrenergic neurons in the locus coeruleus (LC) corelease noradrenaline and dopamine in the hippocampus and that their dopamine release boosts memory retention as well. In this opinion article, we propose that the projections originating from the VTA and the LC belong to two distinct systems that enhance memory of novel events. Novel experiences that share some commonality with past ones (‘common novelty’) activate the VTA and promote semantic memory formation via systems memory consolidation. By contrast, experiences that bear only a minimal relationship to past experiences (‘distinct novelty’) activate the LC to trigger strong initial memory consolidation in the hippocampus, resulting in vivid and long-lasting episodic memories., Highlights Novelty induces dopamine release in the hippocampus, triggering memory consolidation to boost memory persistence. Two dopaminergic systems (the ventral tegmental area- and locus coeruleus-hippocampus systems) can stabilise memory through novelty-induced dopamine release in the hippocampus. Novel experiences can be viewed as a spectrum, from experiences that, while clearly novel, share some commonality with past experiences (‘common novelty’), to more fundamentally distinct experiences that bear minimal relationships to past experiences (‘distinct novelty’). We propose that events characterised by ‘common novelty’ boost memory retention via activation of the ventral tegmental area-hippocampus system, resulting in initial consolidation followed by systems consolidation to create neocortical, semantic, long-term memories. We further propose that events characterised by ‘distinct novelty’ lead to the boost of detailed hippocampal, episodic, long-term memory via activation of the locus coeruleus-hippocampus system through strong upregulation of the synaptic tagging and capture mechanism.

Available online: 29 June 2016 The two-component framework of episodic memory (EM) development posits that the contributions of medial temporal lobe (MTL) and prefrontal cortex (PFC) to successful encoding differ across the lifespan. To test the framework's hypotheses, we compared subsequent memory effects (SME) of 10-12 year-old children, younger adults, and older adults using functional magnetic resonance imaging (fMRI). Memory was probed by cued recall, and SME were defined as regional activation differences during encoding between subsequently correctly recalled versus omitted items. In MTL areas, children's SME did not differ in magnitude from those of younger and older adults. In contrast, children's SME in PFC were weaker than the corresponding SME in younger and older adults, in line with the hypothesis that PFC contributes less to successful encoding in childhood. Differences in SME between younger and older adults were negligible. The present results suggest that, among individuals with high memory functioning, the neural circuitry contributing to successful episodic encoding is reorganized from middle childhood to adulthood. Successful episodic encoding in later adulthood, however, is characterized by the ability to maintain the activation patterns that emerged in young adulthood. (C) 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license.

We recently provided evidence that an intrinsic reward-related signal—triggered by successful learning in absence of any external feedback—modulated the entrance of new information into long-term memory via the activation of the dopaminergic midbrain, hippocampus, and ventral striatum (the SN/VTA-Hippocampal loop; Ripollés et al., 2016). Here, we used a double-blind, within-subject randomized pharmacological intervention to test whether this learning process is indeed dopamine-dependent. A group of healthy individuals completed three behavioral sessions of a language-learning task after the intake of different pharmacological treatments: a dopaminergic precursor, a dopamine receptor antagonist or a placebo. Results show that the pharmacological intervention modulated behavioral measures of both learning and pleasantness, inducing memory benefits after 24 hr only for those participants with a high sensitivity to reward. These results provide causal evidence for a dopamine-dependent mechanism instrumental in intrinsically regulated learning and further suggest that subject-specific reward sensitivity drastically alters learning success.

In recent decades, there has been a growing interest in investigating the effects of chronic and acute stress on cognitive processes, especially memory performance. However, research focusing on acute stress effects has reported contradictory findings, probably due to the many factors that can moderate this relationship. In addition to factors related to the individual, such as sex and age, other factors, such as the type of memory assessed, can play a critical role in the direction of these effects. This review summarizes the main findings of our research group and others about the effects of acute psychosocial stress on memory performance in young and older people of both sexes, taking into account the type and phase of memory assessed. In our opinion, an approach that addresses individual factors and other factors related to the type of stressor and temporal relationship between exposure to the stressor and performance will contribute to better understanding the mechanisms underlying the complex relationship between acute stress and memory. Finally, some new directions for future studies on this research topic are suggested.

Coupling novel verbal material with a musical melody can potentially aid in its learning and recall in healthy subjects, but this has never been systematically studied in stroke patients with cognitive deficits. In a counterbalanced design, we presented novel verbal material (short narrative stories) in both spoken and sung formats to stroke patients at the acute poststroke stage and 6 months poststroke. The task comprised three learning trials and a delayed recall trial. Memory performance on the spoken and sung tasks did not differ at the acute stage, whereas sung stories were learned and recalled significantly better compared with spoken stories at the 6 months poststroke stage. Interestingly, this pattern of results was evident especially in patients with mild aphasia, in whom the learning of sung versus spoken stories improved more from the acute to the 6-month stages compared with nonaphasic patients. Overall, these findings suggest that singing could be used as a mnemonic aid in the learning of novel verbal material in later stages of recovery after stroke.

INTRODUCTION: Phosphodiesterase (PDE) inhibitors improve signaling pathways in brain circuits by increasing intracellular cyclic adenosine monophosphate (cAMP) and/or cyclic guanosine monophosphate (cGMP). In the last decade, the first clinical studies investigating selective PDE inhibitors in Alzheimer's disease (AD) have been initiated, based on their positive effects on cognitive processes and neuroprotection in numerous animal studies. Areas covered: This article reviews the clinical studies investigating the pro-cognitive/neuroprotective effects of PDE inhibitors in patients with AD, as well as in age-associated memory impaired elderly and patients with mild cognitive impairment (MCI), the prodromal stage of AD. PDE inhibitors will also be discussed with respect to adverse effects including safety and tolerability. Expert opinion: The limited available data of clinical studies with PDE inhibitors tested in different populations of AD patients do not allow the drawing of any concrete conclusion yet. Currently, studies with a PDE3 (cilostazol) or PDE9 inhibitor (BI 409,306) are still ongoing in patients with MCI or AD, respectively. Studies with PDE4 inhibitors (HT-0712, roflumilast and BPN14770) in healthy elderly and elderly with age-associated memory impairments indicate that the optimum dose and/or inhibiting the most relevant PDE isoform hold great promise when tested in the appropriate population of patients with MCI or AD eventually.

Long-term recognition memory for some pictures is consistently better than for others (Isola, Xiao, Parikh, Torralba, & Oliva, IEEE Transaction on Pattern Analysis and Machine Intelligence (PAMI), 36(7), 1469–1482, 2014). Here, we investigated whether pictures found to be memorable in a long-term memory test are also perceived more easily when presented in ultra-rapid RSVP. Participants viewed 6 pictures they had never seen before that were presented for 13 to 360 ms per picture in a rapid serial visual presentation (RSVP) sequence. In half the trials, one of the pictures was a memorable or a nonmemorable picture and perception of this picture was probed by a visual recognition test at the end of the sequence. Recognition for pictures from the memorable set was higher than for those from the nonmemorable set, and this difference increased with increasing duration. Nonmemorable picture recognition was low initially, did not increase until 120 ms, and never caught up with memorable picture recognition performance. Thus, the long-term memorability of an image is associated with initial perceptibility: A picture that is hard to grasp quickly is hard to remember later.

Various types of long-term stable relationships that individuals uphold, including cooperation and competition between group members, define social complexity in vertebrates. Numerous life history, physiological and cognitive traits have been shown to affect, or to be affected by, such social relationships. As such, differences in developmental modes, i.e. the 'altricial-precocial' spectrum, may play an important role in understanding the interspecific variation in occurrence of social interactions, but to what extent this is the case is unclear because the role of the developmental mode has not been studied directly in across-species studies of sociality. In other words, although there are studies on the effects of developmental mode on brain size, on the effects of brain size on cognition, and on the effects of cognition on social complexity, there are no studies directly investigating the link between developmental mode and social complexity. This is surprising because developmental differences play a significant role in the evolution of, for example, brain size, which is in turn considered an essential building block with respect to social complexity. Here, we compiled an overview of studies on various aspects of the complexity of social systems in altricial and precocial mammals and birds. Although systematic studies are scarce and do not allow for a quantitative comparison, we show that several forms of social relationships and cognitive abilities occur in species along the entire developmental spectrum. Based on the existing evidence it seems that differences in developmental modes play a minor role in whether or not individuals or species are able to meet the cognitive capabilities and requirements for maintaining complex social relationships. Given the scarcity of comparative studies and potential subtle differences, however, we suggest that future studies should consider developmental differences to determine whether our finding is general or whether some of the vast variation in social complexity across species can be explained by developmental mode. This would allow a more detailed assessment of the relative importance of developmental mode in the evolution of vertebrate social systems.

Various types of long-term stable relationships that individuals uphold, including cooperation and competition between group members, define social complexity in vertebrates. Numerous life history, physiological and cognitive traits have been shown to affect, or to be affected by, such social relationships. As such, differences in developmental modes, i.e. the ‘altricial-precocial’ spectrum, may play an important role in understanding the interspecific variation in occurrence of social interactions, but to what extent this is the case is unclear because the role of the developmental mode has not been studied directly in across-species studies of sociality. In other words, although there are studies on the effects of developmental mode on brain size, on the effects of brain size on cognition, and on the effects of cognition on social complexity, there are no studies directly investigating the link between developmental mode and social complexity. This is surprising because developmental differences play a significant role in the evolution of, for example, brain size, which is in turn considered an essential building block with respect to social complexity. Here, we compiled an overview of studies on various aspects of the complexity of social systems in altricial and precocial mammals and birds. Although systematic studies are scarce and do not allow for a quantitative comparison, we show that several forms of social relationships and cognitive abilities occur in species along the entire developmental spectrum. Based on the existing evidence it seems that differences in developmental modes play a minor role in whether or not individuals or species are able to meet the cognitive capabilities and requirements for maintaining complex social relationships. Given the scarcity of comparative studies and potential subtle differences, however, we suggest that future studies should consider developmental differences to determine whether our finding is general or whether some of the vast variation in social complexity across species can be explained by developmental mode. This would allow a more detailed assessment of the relative importance of developmental mode in the evolution of vertebrate social systems.

Huntington’s disease (HD) is a neurodegenerative disorder whose major symptoms include progressive motor and cognitive dysfunction. Cognitive decline is a critical quality of life concern for HD patients and families. The enzyme histone deacetylase 3 (HDAC3) appears to be important in HD pathology by negatively regulating genes involved in cognitive functions. Furthermore, HDAC3 has been implicated in the aberrant transcriptional patterns that help cause disease symptoms in HD mice. HDAC3 also helps fuel CAG repeat expansions in human cells, suggesting that HDAC3 may power striatal expansions in the HTT gene thought to drive disease progression. This multifaceted role suggests that early HDAC3 inhibition offers an attractive mechanism to prevent HD cognitive decline and to suppress striatal expansions. This hypothesis was investigated by treating HdhQ111 knock-in mice with the HDAC3-selective inhibitor RGFP966. Chronic early treatment prevented long-term memory impairments and normalized specific memory-related gene expression in hippocampus. Additionally, RGFP966 prevented corticostriatal-dependent motor learning deficits, significantly suppressed striatal CAG repeat expansions, partially rescued striatal protein marker expression and reduced accumulation of mutant huntingtin oligomeric forms. These novel results highlight RGFP966 as an appealing multiple-benefit therapy in HD that concurrently prevents cognitive decline and suppresses striatal CAG repeat expansions.

The current experiment was designed to assess the mnemonic consequences of false denials and forced confabulations. Children (aged 6-8 and 10-12 years) and adults viewed a video and then their memory and belief about the event were tested. Participants were then divided into three groups. In the cued recall condition, participants were asked to answer true- and false-event questions, but could choose not to respond if they did not know the answer. In the forced confabulation group, participants received the same set of questions, but were forced to answer all of them. In the false denial group, participants were instructed to falsely deny in response to each question. One week later, participants received a source memory test, and they had to provide memory and belief ratings once more. Forced confabulations resulted in false memories in the youngest group. Moreover, our analyses showed that repeated false denials led children and adults to be highly inclined to falsely deny that they had talked to the experimenter about certain presented details, when in fact they had done so. Furthermore, false denial and non-believed memory rates were more pronounced in younger than in older children and adults. Our results imply that denying experienced events is not a good strategy in an interviewing setting, as it adversely affects memory statements about the interview. Copyright (c) 2014 John Wiley & Sons, Ltd.

Animals can adjust their behaviour according to previous experience gained during foraging. In parasitoids, experience plays a key role in host location, a hierarchical process in which air-borne and substrate-borne semiochemicals are used to find hosts. In nature, chemical traces deposited by herbivore hosts when walking on the plant are adsorbed by leaf surfaces and perceived as substrate-borne semiochemicals by parasitoids. Chemical traces left on cabbage leaves by adults of the harlequin bug (Murgantia histrionica) induce an innate arrestment response in the egg parasitoid Trissolcus brochymenae characterized by an intense searching behaviour on host-contaminated areas. Here we investigated whether the T. brochymenae response to host walking traces left on leaf surfaces is affected by previous experience in the context of parasitoid foraging behaviour. We found that: 1) an unrewarded experience (successive encounters with host-contaminated areas without successful oviposition) decreased the intensity of the parasitoid response; 2) a rewarded experience (successful oviposition) acted as a reinforcing stimulus; 3) the elapsed time between two consecutive unrewarded events affected the parasitoid response in a host-gender specific manner. The ecological role of these results to the host location process of egg parasitoids is discussed.

The delay associated with cerebral processing time implies a lack of real-time representation of changes in the observed environment. To bridge this gap for motor actions in a dynamical environment, the brain uses predictions of the most plausible future reality based on previously provided information. To optimise these predictions, adjustments to actual experiences are necessary. This requires a perceptual memory buffer. In our study we gained more insight how the brain treats (real-time) information by comparing cerebral activations related to judging past-, present- and future locations of a moving ball, respectively. Eighteen healthy subjects made these estimations while fMRI data was obtained. All three conditions evoked bilateral dorsal-parietal and premotor activations, while judgment of the location of the ball at the moment of judgment showed increased bilateral posterior hippocampus activation relative to making both future and past judgments at the one-second time-sale. Since the condition of such 'real-time' judgments implied undistracted observation of the ball's actual movements, the associated hippocampal activation is consistent with the concept that the hippocampus participates in a top-down exerted sensory gating mechanism. In this way, it may play a role in novelty (saliency) detection.

We study universal quantum codes for entanglement-assisted quantum communication over compound quantum channels. In this setting, sender and receiver do not know the specific channel that will be used for communication, but only know the set that the channel is selected from. We investigate different variations of the problem: uninformed users, informed receiver, informed sender, and feedback assistance. We derive single-letter formulas for all corresponding channel capacities. Our proofs are based on one-shot decoupling bounds and properties of smooth entropies., 16 pages

D1 and D2 dopamine receptors (D1DRs and D2DRs) may contribute differently to various aspects of memory and cognition. The D1DR system has been linked to functions supported by the prefrontal cortex. By contrast, the role of the D2DR system is less clear, although it has been hypothesized that D2DRs make a specific contribution to hippocampus-based cognitive functions. Here we present results from 181 healthy adults between 64 and 68 y of age who underwent comprehensive assessment of episodic memory, working memory, and processing speed, along with MRI and D2DR assessment with [(11)C]raclopride and PET. Caudate D2DR availability was positively associated with episodic memory but not with working memory or speed. Whole-brain analyses further revealed a relation between hippocampal D2DR availability and episodic memory. Hippocampal and caudate D2DR availability were interrelated, and functional MRI-based resting-state functional connectivity between the ventral caudate and medial temporal cortex increased as a function of caudate D2DR availability. Collectively, these findings indicate that D2DRs make a specific contribution to hippocampus-based cognition by influencing striatal and hippocampal regions, and their interactions.

It is well established that the activity of chromatin-modifying enzymes is crucial for regulating gene expression associated with hippocampal-dependent memories. However, very little is known about how these epigenetic mechanisms influence the formation of cortically dependent memory, particularly when there is competition between opposing memory traces, such as that which occurs during the acquisition and extinction of conditioned fear. Here we demonstrate, in C57BL/6 mice, that the activity of p300/CBP-associated factor (PCAF) within the infralimbic prefrontal cortex is required for long-term potentiation and is necessary for the formation of memory associated with fear extinction, but not for fear acquisition. Further, systemic administration of the PCAF activator SPV106 enhances memory for fear extinction and prevents fear renewal. The selective influence of PCAF on fear extinction is mediated, in part, by a transient recruitment of the repressive transcription factor ATF4 to the promoter of the immediate early genezif268, which competitively inhibits its expression. Thus, within the context of fear extinction, PCAF functions as a transcriptional coactivator, which may facilitate the formation of memory for fear extinction by interfering with reconsolidation of the original memory trace.

Although many genetic association studies have been carried out, it remains unclear which genes contribute to depression. This may be due to heterogeneity of the DSM-IV category of depression. Specific symptom-dimensions provide a more homogenous phenotype. Furthermore, as effects of individual genes are small, analysis of genetic data at the pathway-level provides more power to detect associations and yield valuable biological insight. In 1,398 individuals with a Major Depressive Disorder, the symptom dimensions of the tripartite model of anxiety and depression, General Distress, Anhedonic Depression, and Anxious Arousal, were measured with the Mood and Anxiety Symptoms Questionnaire (30-item Dutch adaptation; MASQ-D30). Association of these symptom dimensions with candidate gene sets and gene sets from two public pathway databases was tested using the Global test. One pathway was associated with General Distress, and concerned molecules expressed in the endoplasmatic reticulum lumen. Seven pathways were associated with Anhedonic Depression. Important themes were neurodevelopment, neurodegeneration, and cytoskeleton. Furthermore, three gene sets associated with Anxious Arousal regarded development, morphology, and genetic recombination. The individual pathways explained up to 1.7% of the variance. These data demonstrate mechanisms that influence the specific dimensions. Moreover, they show the value of using dimensional phenotypes on one hand and gene sets on the other hand. (C) 2012 Wiley Periodicals, Inc.

This article reports on a study on learning new and relearning forgotten words of French as a foreign language in young (mean age 22.4), middle-aged (mean age 50.3), and elderly speakers (mean age 76.0). The three age groups performed similarly on relearning old words, but the younger learners were significantly better at learning new words. Data from a questionnaire on contact with French and a working-memory test showed that neither diminished language contact nor age-related decline in working memory can be seen as single factors explaining differences between learning and relearning. The decline in older adults ability to learn new lexical information is discussed in terms of theories explaining age-related memory deficits and conceived of as an age-related deficiency to form associations between unrelated concepts.

In the present study, we investigated the functional characteristics of task sets that were never applied before and were formed only on the basis of instructions. We tested if such task sets could elicit a task-rule congruency effect, which implies the automatic activation of responses in the context of another task. To this end, a novel procedure was developed that revealed instruction-based task-rule congruency effects in 2 experiments. Although the effect seems quite general (Experiment 1), it still necessitates the formation of a task set, as it cannot be induced by the mere maintenance of instructions in declarative working memory (Experiment 2). We conclude that a task set representing only key features of an upcoming task can be formed on the basis of instructions alone to such a degree that it can automatically trigger a response tendency in another task. Implications of our results for the impact of instructions on performance in general and for the occurrence of task-rule congruency effects in particular are discussed.

Deficits in memory function are an incapacitating aspect of various psychiatric and neurological disorders. Animal studies have recently provided strong evidence for involvement of the endocannabinoid (eCB) system in memory function. Neuropsychological studies in humans have shown less convincing evidence but suggest that administration of cannabinoid substances affects encoding rather than recall of information. In this study, we examined the effects of perturbation of the eCB system on memory function during both encoding and recall. We performed a pharmacological MRI study with a placebo-controlled, crossover design, investigating the effects of Δ9-tetrahydrocannabinol (THC) inhalation on associative memory-related brain function in 13 healthy volunteers. Performance and brain activation during associative memory were assessed using a pictorial memory task, consisting of separate encoding and recall conditions. Administration of THC caused reductions in activity during encoding in the right insula, the right inferior frontal gyrus, and the left middle occipital gyrus and a network-wide increase in activity during recall, which was most prominent in bilateral cuneus and precuneus. THC administration did not affect task performance, but while during placebo recall activity significantly explained variance in performance, this effect disappeared after THC. These findings suggest eCB involvement in encoding of pictorial information. Increased precuneus activity could reflect impaired recall function, but the absence of THC effects on task performance suggests a compensatory mechanism. These results further emphasize the eCB system as a potential novel target for treatment of memory disorders and a promising target for development of new therapies to reduce memory deficits in humans.

Our memories are not all created equally strong: Some experiences are well remembered while others are remembered poorly, if at all. Research on memory modulation investigates the neurobiological processes and systems that contribute to such differences in the strength of our memories. Extensive evidence from both animal and human research indicates that emotionally significant experiences activate hormonal and brain systems that regulate the consolidation of newly acquired memories. These effects are integrated through noradrenergic activation of the basolateral amygdala that regulates memory consolidation via interactions with many other brain regions involved in consolidating memories of recent experiences. Modulatory systems not only influence neurobiological processes underlying the consolidation of new information, but also affect other mnemonic processes, including memory extinction, memory recall, and working memory. In contrast to their enhancing effects on consolidation, adrenal stress hormones impair memory retrieval and working memory. Such effects, as with memory consolidation, require noradrenergic activation of the basolateral amygdala and interactions with other brain regions.

For some cancer survivors chemotherapy treatment is associated with lasting cognitive impairment, long after treatment cessation. Several candidate mechanisms have been suggested, yet clinical research has been unable to clearly tease apart these hypotheses. Rodent research has allowed a systematic study of these underlying mechanisms in the absence of potential patient confounds. Herein, this research is reviewed with emphasis on the role of the blood-brain barrier, neurogenesis, oxidative stress, white matter, immune system/(neuro) inflammation, HPA axis, blood flow, and cancer in chemotherapy-induced cognitive impairment. Furthermore, potential pharmacotherapy and behavioral intervention strategies are reviewed. This paper ends with methodological considerations in study of chemotherapy and cognition. (C) 2010 Elsevier Ltd. All rights reserved.