Associative Memory Deficit Research Articles

Age-related changes in overcoming proactive interference in associative memory: The role of PFC-mediated executive control processes at retrieval

Behavioral evidence has shown age-related impairments in overcoming proactive interference in memory, but it is unclear what underlies this deficit. Imaging studies in the young suggest overcoming interference may require several executive control processes supported by the ventrolateral prefrontal cortex (VLPFC) and dorsolateral PFC (DLPFC). The present functional magnetic resonance imaging (fMRI) study investigated whether age-related changes in dissociable executive control processes underlie deficits in overcoming proactive interference in associative memory during retrieval. Participants were tasked with remembering which associate (face or scene) objects were paired with most recently during study, under conditions of high or low proactive interference. Behavioral results demonstrated that, as interference increased, memory performance decreased similarly across groups, with slight associative memory deficits in older adults. Imaging results demonstrated that, across groups, left mid-VLPFC showed increasing activity with increasing interference, though activity did not distinguish correct from incorrect associative memory responses, suggesting this region may not directly serve in successful resolution of proactive interference, per se. Under conditions of high interference, older adults showed reduced associative memory accuracy effects in the DLPFC and anterior PFC. These results suggest that age-related PFC dysfunction may not be ubiquitous. Executive processes supported by ventral regions that detect mnemonic interference may be less affected than processes supported by dorsal and anterior regions that directly resolve interference.

Beneficial effects of semantic memory support on older adults' episodic memory: Differential patterns of support of item and associative information.

The effects of two types of semantic memory support-meaningfulness of an item and relatedness between items-in mitigating age-related deficits in item and associative, memory are examined in a marketing context. In Experiment 1, participants studied less (vs. more) meaningful brand logo graphics (pictures) paired with meaningful brand names (words) and later were assessed by item (old/new) and associative (intact/recombined) memory recognition tests. Results showed that meaningfulness of items eliminated age deficits in item memory, while equivalently boosting associative memory for older and younger adults. Experiment 2, in which related and unrelated brand logo graphics and brand name pairs served as stimuli, revealed that relatedness between items eliminated age deficits in associative memory, while improving to the same degree item memory in older and younger adults. Experiment 2 also provided evidence for a probable boundary condition that could reconcile seemingly contradictory extant results. Overall, these experiments provided evidence that although the two types of semantic memory support can improve both item and associative memory in older and younger adults, older adults' memory deficits can be eliminated when the type of support provided is compatible with the type of information required to perform well on the test.

DRYAD and ADH: Further comments on explaining age-related differences in memory.

Recently, Smyth and Naveh-Benjamin (2016) questioned some of the main assumptions/hypotheses of DRYAD (or density of representations yields age-related deficits), a global-deficit model of aging and memory judgments (Benjamin, 2010; Benjamin et al., 2012). Smyth and Naveh-Benjamin (2016) provided empirical evidence that seems incompatible with DRYAD, but that fits the associative deficit hypothesis (ADH; Naveh-Benjamin, 2000), 1 specific-deficit theoretical view. In response, Aaron Benjamin (2016) offered a discussion of the complementary strengths and weaknesses of the DRYAD and the ADH, and the potential ways they might work together. We agree with many of his comments, but are not convinced that DRYAD is able to explain basic replicable empirical evidence of the type mentioned in Smyth and Naveh-Benjamin (2016). We discuss the reasons why we are not fully convinced by the demonstration of DRYAD's simulation of results presented in Benjamin (2016) and then present an implementation of ADH in a computationally based age-related impaired neuromodulation approach that was shown to simulate the basic empirical results of age-related associative memory deficits. We also discuss the issues of parsimony of theories and the appropriate type of representation, in the context of global versus specific deficits theoretical views. Finally, we show that the ADH's take on the distinction between items and associations has been adopted by some global computational models of memory. We believe that considerations of the above issues and others raised by Benjamin (2016) can lead to fruitful discussions that will benefit both theory development and existing knowledge of aging and memory.

Can DRYAD explain age-related associative memory deficits?

A recent interesting theoretical account of aging and memory judgments, the DRYAD (density of representations yields age-related deficits; Benjamin, 2010; Benjamin, Diaz, Matzen, & Johnson, 2012), attributes the extensive findings of disproportional age-related deficits in memory for source, context, and associations, to a global decline in memory fidelity. It is suggested that this global deficit, possibly due to a decline in attentional processes, is moderated by weak representation of contextual information to result in disproportional age-related declines. In the current article, we evaluate the DRYAD model, comparing it to specific age-related deficits theories, in particular, the ADH (associative deficit hypothesis, Naveh-Benjamin, 2000). We question some of the main assumptions/hypotheses of DRYAD in light of data reported in the literature, and we directly assess the role of attention in age-related deficits by manipulations of divided attention and of the instructions regarding what to pay attention to in 2 experiments (one from the literature and a new one). The results of these experiments fit the predictions of the ADH and do not support the main assumption/hypotheses of DRYAD.

Age-related associative memory deficits in value-based remembering: The contribution of agenda-based regulation and strategy use.

Value-based remembering in free-recall tasks may be spared from the typical age-related cognitive decline observed for episodic memory. However, it is unclear whether value-based remembering for associative information is also spared from age-related cognitive decline. The current experiments evaluated the contribution of agenda-based based regulation and strategy use during study to age differences and similarities in value-based remembering of associative information. Participants studied word pairs (Experiments 1-2) or single words (Experiment 2) slated with different point values by moving a mouse controlled cursor to different spatial locations to reveal either items for study or the point value associated with remembering each item. Some participants also provided strategy reports for each item. Younger and older adults allocated greater time to studying high- than low-valued information, reported using normatively effective encoding strategies to learn high-valued pairs, and avoided study of low-valued pairs. As a consequence, both age groups selectively remembered more high- than low-valued items. Despite nearly identical regulatory behavior, an associative memory deficit for older adults was present for high-valued pairs. Age differences in value-based remembering did not occur when the materials were word lists. Fluid intelligence also moderated the effectiveness of older adults' strategy use for high-valued pairs (Experiment 2). These results suggest that age differences in associative value-based remembering may be due to some older adults' gleaning less benefit from using normatively effective encoding strategies rather than age differences in metacognitive self-regulation per se.

The Interaction Between Memory Trace and Memory Judgment in Age-Related Decline

Background/Study Context: Associative memory deficit and executive functioning deficit are two alternative—but nonexclusive—accounts of the episodic memory deficit observed in aging. The first explain the episodic memory decline generally observed in aging by an associative memory deficit (memory decline per se), whereas the second explains it by an executive functioning deficit. This distinction could be critical in early discrimination between healthy aging and very mild Alzheimer’s-type dementia.Methods: Memory performance was measured in older adults (n = 20) and paired younger participants (n = 20), whereas the facial expression and auditory context (spoken voice) associated with the face were manipulated between study and test. Recollection and familiarity were estimated using a remember/know judgment, and source memory performance was obtained depending on the information to retrieve.Results: Although no between-group difference was observed for correctly recognized old faces, older participants made more false alarms than younger ones, thus revealing lower discriminability (d’). Facial expression change decreased recognition for all participants, whereas auditory context change decreased recognition only for younger participants. Remember/know judgments revealed age-related deficits in both recollection and familiarity, the relative decrease in familiarity reported by older adults was particularly large in the expression change conditions, and a disadvantage in source memory performance was particularly pronounced when the task was to retrieve auditory context associated with the face at study.Conclusions: The present findings show that age-related associative memory differences occur with familiarity as well as recollection and are observed in situations that do not necessarily require conscious retrieval. This age-related decline is more prominent for multimodal (face–auditory context) than for intraitem (face-expression) associations. The value of exploring both memory trace and memory judgment was discussed, and potential applications for the development of neuropsychological tools for memory assessment in aging were highlighted.

Proactive interference and concurrent inhibitory processes do not differentially affect item and associative recognition: Implication for the age-related associative memory deficit

ABSTRACTPrevious studies have suggested an associative deficit hypothesis [Naveh-Benjamin, M. (2000). Adult age differences in memory performance: Tests of an associative deficit hypothesis. Journal of Experimental Psychology: Learning, Memory, and Cognition, 26, 1170–1187] to explain age-related episodic memory declines. The hypothesis attributes part of the deficient episodic memory performance in older adults to a difficulty in creating and retrieving cohesive episodes. In this article, we further evaluate this hypothesis by testing two alternative processes that potentially mediate associative memory deficits in older adults. Four experiments are presented that assess whether failure of inhibitory processes (proactive interference in Experiments 1 and 2), and concurrent inhibition (in Experiments 3 and 4) are mediating factors in age-related associative deficits. The results suggest that creating conditions that require the operation of inhibitory processes, or that interfere with such processes, cannot simulate associative memory deficit in older adults. Instead, such results support the idea that associative memory deficits reflect a unique binding failure in older adults. This failure seems to be independent of other cognitive processes, including inhibitory and other resource-demanding processes.

Negative Emotional Arousal Impairs Associative Memory Performance for Emotionally Neutral Content in Healthy Participants.

The effect of emotional arousal on memory presents a complex pattern with previous studies reporting conflicting results of both improved and reduced memory performance following arousal manipulations. In this study we further tested the effect of negative emotional arousal (NEA) on individual-item recognition and associative recognition of neutral stimuli in healthy participants, and hypothesized that NEA will particularly impair associative memory performance. The current study consists of two experiments; in both, participants studied a list of word-pairs and were then tested for items (items recognition test), and for associations (associative recognition test). In the first experiment, the arousal manipulation was induced by flashing emotionally-negative or neutral pictures between study-pairs while in the second experiment arousal was induced by presenting emotionally-negative or neutral pictures between lists. The results of the two experiments converged and supported an associative memory deficit observed under NEA conditions. We suggest that NEA is associated with an altered ability to bind one stimulus to another as a result of impaired recollection, resulting in poorer associative memory performance. The current study findings may contribute to the understanding of the mechanism underlying memory impairments reported in disorders associated with traumatic stress.

Neuritin reverses deficits in murine novel object associative recognition memory caused by exposure to extremely low-frequency (50 Hz) electromagnetic fields.

Animal studies have shown that electromagnetic field exposure may interfere with the activity of brain cells, thereby generating behavioral and cognitive disturbances. However, the underlying mechanisms and possible preventions are still unknown. In this study, we used a mouse model to examine the effects of exposure to extremely low-frequency (50 Hz) electromagnetic fields (ELF MFs) on a recognition memory task and morphological changes of hippocampal neurons. The data showed that ELF MFs exposure (1 mT, 12 h/day) induced a time-dependent deficit in novel object associative recognition memory and also decreased hippocampal dendritic spine density. This effect was observed without corresponding changes in spontaneous locomotor activity and was transient, which has only been seen after exposing mice to ELF MFs for 7-10 days. The over-expression of hippocampal neuritin, an activity-dependent neurotrophic factor, using an adeno-associated virus (AAV) vector significantly increased the neuritin level and dendritic spine density. This increase was paralleled with ELF MFs exposure-induced deficits in recognition memory and reductions of dendritic spine density. Collectively, our study provides evidence for the association between ELF MFs exposure, impairment of recognition memory, and resulting changes in hippocampal dendritic spine density. Neuritin prevented this ELF MFs-exposure-induced effect by increasing the hippocampal spine density.

Electrophysiological evidence for the effects of unitization on associative recognition memory in older adults

Normal aging is associated with greater decline in associative memory relative to item memory due to impaired recollection. Familiarity may also contribute to associative recognition when stimuli are perceived as a ‘unitized’ representation. Given that familiarity is relatively preserved in older adults, we explored whether age-related associative memory deficits could be attenuated when associations were unitized (i.e., compounds) compared with those non-unitized (i.e., unrelated word pairs). Young and older adults performed an associative recognition task while electroencephalogram (EEG) was recorded. Behavioral results showed that age differences were smaller for recognition of compounds than for unrelated word pairs. ERP results indicated that only compounds evoked an early frontal old/new effect in older adults. Moreover, the early frontal old/new effect was positively correlated with associative discrimination accuracy. These findings suggest that reduced age-related associative deficits under unitized condition may be associated with the presence of familiarity-based retrieval of compounds in older adults.

Targeting human central nervous system protein kinases: An isoform selective p38αMAPK inhibitor that attenuates disease progression in Alzheimer's disease mouse models.

The first kinase inhibitor drug approval in 2001 initiated a remarkable decade of tyrosine kinase inhibitor drugs for oncology indications, but a void exists for serine/threonine protein kinase inhibitor drugs and central nervous system indications. Stress kinases are of special interest in neurological and neuropsychiatric disorders due to their involvement in synaptic dysfunction and complex disease susceptibility. Clinical and preclinical evidence implicates the stress related kinase p38αMAPK as a potential neurotherapeutic target, but isoform selective p38αMAPK inhibitor candidates are lacking and the mixed kinase inhibitor drugs that are promising in peripheral tissue disease indications have limitations for neurologic indications. Therefore, pursuit of the neurotherapeutic hypothesis requires kinase isoform selective inhibitors with appropriate neuropharmacology features. Synaptic dysfunction disorders offer a potential for enhanced pharmacological efficacy due to stress-induced activation of p38αMAPK in both neurons and glia, the interacting cellular components of the synaptic pathophysiological axis, to be modulated. We report a novel isoform selective p38αMAPK inhibitor, MW01-18-150SRM (=MW150), that is efficacious in suppression of hippocampal-dependent associative and spatial memory deficits in two distinct synaptic dysfunction mouse models. A synthetic scheme for biocompatible product and positive outcomes from pharmacological screens are presented. The high-resolution crystallographic structure of the p38αMAPK/MW150 complex documents active site binding, reveals a potential low energy conformation of the bound inhibitor, and suggests a structural explanation for MW150’s exquisite target selectivity. As far as we are aware, MW150 is without precedent as an isoform selective p38MAPK inhibitor or as a kinase inhibitor capable of modulating in vivo stress related behavior.

Frontal-parietal alpha networks reflect a compensatory mechanism to overcome the associative deficit in mild cognitive impairment

Event Abstract Back to Event Frontal-parietal alpha networks reflect a compensatory mechanism to overcome the associative deficit in mild cognitive impairment Laura Prieto Del Val1*, José Luis Cantero Lorente1 and Mercedes Atienza Ruiz1 1 University Pablo de Olavide, Department of Physiology, Anatomy, and Cellular Biology, Spain People with amnestic mild cognitive impairment (aMCI), like healthy older adults (HO), present a disproportionate deficit in associative memory; but unlike HO, they do not benefit from semantic congruence. The presence of the e4 allele of the apolipoprotein E gene (APOE) makes this memory loss worse. Here, we show that encoding of face-location associations are accompanied by different patterns of large-scale EEG oscillatory dynamics under semantically congruent and incongruent conditions. These differences were reflected by theta power increases and alpha/beta power decreases in both HO and aMCI. However, after localizing the brain sources of these oscillations, enhanced theta and decreased beta revealed higher activation of temporal regions in HO, and of frontal regions in aMCI. Source analysis of EEG oscillations yielded two further important results. On the one hand, dynamics of beta oscillations indicated that aMCI, mainly APOE-e4 carriers, have problems to activate an extensive neural network related to associative memory in the right hemisphere. And on the other, the better memory performance shown by aMCI e4 non-carriers relative to e4 carriers not only was similar to that of HO, but was also related to alpha power decreases in left frontal and parietal regions. All together, these findings suggest that associative memory deficits in aMCI are linked to abnormal beta oscillatory dynamics in the right hemisphere, whereas impaired semantic memory might be related to activation deficits of left temporal regions. Most important, these results suggest that associative memory in aMCI can be improved through activation of an alpha oscillatory network comprising frontal and parietal regions, and that recruitment of such a compensatory mechanism depends on the APOE genotype. Keywords: Associative Memory, brain oscillations, compensatory mechanisms, amnestic mild cognitive impairment, APOE e4 Conference: XII International Conference on Cognitive Neuroscience (ICON-XII), Brisbane, Queensland, Australia, 27 Jul - 31 Jul, 2014. Presentation Type: Poster Topic: Memory and Learning Citation: Prieto Del Val L, Cantero Lorente J and Atienza Ruiz M (2015). Frontal-parietal alpha networks reflect a compensatory mechanism to overcome the associative deficit in mild cognitive impairment. Conference Abstract: XII International Conference on Cognitive Neuroscience (ICON-XII). doi: 10.3389/conf.fnhum.2015.217.00360 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Feb 2015; Published Online: 24 Apr 2015. * Correspondence: Mrs. Laura Prieto Del Val, University Pablo de Olavide, Department of Physiology, Anatomy, and Cellular Biology, Seville, Spain, lpridel@upo.es Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Laura Prieto Del Val José Luis Cantero Lorente Mercedes Atienza Ruiz Google Laura Prieto Del Val José Luis Cantero Lorente Mercedes Atienza Ruiz Google Scholar Laura Prieto Del Val José Luis Cantero Lorente Mercedes Atienza Ruiz PubMed Laura Prieto Del Val José Luis Cantero Lorente Mercedes Atienza Ruiz Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Urtica dioica leaves modulates muscarinic cholinergic system in the hippocampus of streptozotocin-induced diabetic mice.

Diabetes mellitus is a chronic metabolic disorder and has been associated with cognitive dysfunction. In our earlier study, chronic Urtica dioica (UD) treatment significantly ameliorated diabetes induced associative and spatial memory deficit in mice. The present study was designed to explore the effect of UD leaves extract on muscarinic cholinergic system, which has long been known to be involved in cognition. Streptozotocin (STZ) (50 mg/kg, i.p., consecutively for 5 days) was used to induce diabetes followed by treatment with UD extract (50 mg/kg, oral) or rosiglitazone (5 mg/kg, oral) for 8 weeks. STZ-induced diabetic mice showed significant reduction in hippocampal muscarinic acetylcholine receptor-1 and choline acetyltransferase expressions. Chronic diabetes significantly up-regulated the protein expression of acetylcholinesterase associated with oxidative stress in hippocampus. Besides, STZ-induced diabetic mice showed hypolocomotion with up-regulation of muscarinic acetylcholine receptor-4 expression in striatum. Chronic UD treatment significantly attenuated the cholinergic dysfunction and oxidative stress in the hippocampus of diabetic mice. UD had no effect on locomotor activity and muscarinic acetylcholine receptor-4 expression in striatum. In conclusion, UD leaves extract has potential to reverse diabetes mediated alteration in muscarinic cholinergic system in hippocampus and thereby improve memory functions.

Age-related differences in associative memory: the role of sensory decline.

Numerous studies show age-related decline in episodic memory. One of the explanations for this decline points to older adults' deficit in associative memory, reflecting the difficulties they have in binding features of episodes into cohesive entities and retrieving these bindings. Here, we evaluate the degree to which this deficit may be mediated by sensory loss associated with increased age. In 2 experiments, young adults studied word pairs that were degraded at encoding either visually (Experiment 1) or auditorily (Experiment 2). We then tested their memory for both the component words and the associations with recognition tests. For both experiments, young adults under nondegraded conditions showed an advantage in associative over item memory, relative to a group of older adults. In contrast, under perceptually degraded conditions younger adults performed similarly to the older adults who were tested under nondegraded conditions. More specifically, under perceptual degradation, young adults' associative memory declined and their component memory improved somewhat, resulting in an associative deficit, similar to that shown by older adults. This evidence is consistent with a sensory acuity decline in old age being one mediator in the associative deficit of older adults. These results broaden our understanding of age-related memory changes and how sensory and cognitive processes interact to shape these changes. The theoretical implications of these results are discussed with respect to mechanisms underlying age-related changes in episodic memory and resource tradeoffs in the encoding of component and associative memory.

Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice

Methamphetamine abuse is common among individuals infected by human immunodeficiency virus (HIV). Neurocognitive outcomes tend to be worse in methamphetamine users with HIV. However, it is unclear whether discrete cognitive domains are susceptible to impairment after combined HIV infection and methamphetamine abuse. The expression of HIV/gp120 protein induces neuropathology in mice similar to HIV-induced pathology in humans. We investigated the separate and combined effects of methamphetamine exposure and gp120 expression on cognitive function in transgenic (gp120-tg) and control mice. The mice underwent an escalating methamphetamine binge regimen and were tested in novel object/location recognition, object-in-place recognition, and Barnes maze tests. gp120 expression disrupted performance in the object-in-place test (i.e. similar time spent with all objects, regardless of location), indicating deficits in associative recognition memory. gp120 expression also altered reversal learning in the Barnes maze, suggesting impairments in executive function. Methamphetamine exposure impaired spatial strategy in the Barnes maze, indicating deficits in spatial learning. Methamphetamine-exposed gp120-tg mice had the lowest spatial strategy scores in the final acquisition trials in the Barnes maze, suggesting greater deficits in spatial learning than all of the other groups. Although HIV infection involves interactions between multiple proteins and processes, in addition to gp120, our findings in gp120-tg mice suggest that humans with the dual insult of HIV infection and methamphetamine abuse may exhibit a broader spectrum of cognitive deficits than those with either factor alone. Depending on the cognitive domain, the combination of both insults may exacerbate deficits in cognitive performance compared with each individual insult.

Sarm1 deficiency impairs synaptic function and leads to behavioral deficits, which can be ameliorated by an mGluR allosteric modulator.

Innate immune responses have been shown to influence brain development and function. Dysregulation of innate immunity is significantly associated with psychiatric disorders such as autism spectrum disorders and schizophrenia, which are well-known neurodevelopmental disorders. Recent studies have revealed that critical players of the innate immune response are expressed in neuronal tissues and regulate neuronal function and activity. For example, Sarm1, a negative regulator that acts downstream of Toll-like receptor (TLR) 3 and 4, is predominantly expressed in neurons. We have previously shown that Sarm1 regulates neuronal morphogenesis and the expression of inflammatory cytokines in the brain, which then affects learning ability, cognitive flexibility, and social interaction. Because impaired neuronal morphogenesis and dysregulation of cytokine expression may disrupt neuronal activity, we investigated whether Sarm1 knockdown affects the synaptic responses of neurons. We here show that reduced Sarm1 expression impairs metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) formation but enhances N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation production in hippocampal CA1 neurons. The expression levels of post-synaptic proteins, including NR2a, NR1, Shank1 and Shank3, are also altered in Sarm1 knockdown mice, suggesting a role for Sarm1 in the maintenance of synaptic homeostasis. The addition of a positive allosteric modulator of mGluR5, CDPPB, ameliorates the LTD defects in slice recording and the behavioral deficits in social interaction and associative memory. These results suggest an important role for mGluR5 signaling in the function of Sarm1. In conclusion, our study demonstrates a role for Sarm1 in the regulation of synaptic plasticity. Through these mechanisms, Sarm1 knockdown results in the impairment of associative memory and social interactions in mice.

The role of reduced working memory storage and processing resources in the associative memory deficit of older adults: simulation studies with younger adults

Previous research indicates that relative to younger adults, older adults show a larger decline in long-term memory (LTM) for associations than for the components that make up these associations. The purpose of the present study was to investigate whether we can impair associative memory performance in young adults by reducing their working memory (WM) resources, hence providing potential clues regarding the underlying causes of the associative memory deficit in older adults. With two experiments, we investigated whether we can reduce younger adults’ long-term associative memory using secondary tasks in which either storage or processing WM loads were manipulated, while participants learned name–face pairs and then remembered the names, the faces, and the name–face associations. Results show that reducing either the storage or the processing resources of WM produced performance patterns of an associative long-term memory deficit in young adults. Furthermore, younger adults’ associative memory deficit was a function of their performance on a working memory span task. These results indicate that one potential reason older adults have an associative deficit is a reduction in their WM resources but further research is needed to assess the mechanisms involved in age-related associative memory deficits.

Reduced Corpus‐Callosum Volume in Posttraumatic Stress Disorder Highlights the Importance of Interhemispheric Connectivity for Associative Memory

Memory deficits are a common complaint of patients with posttraumatic stress disorder (PTSD). Despite vivid trauma-related memory, previous studies report memory impairment for nontrauma-related stimuli when compared to controls, specifically in associative memory (Guez etal., 2011). Healthy individuals show hemispheric memory asymmetry with left-prefrontal lateralization of encoding and right-prefrontal lateralization of episodic retrieval, suggesting a role for interhemispheric communication in memory-related tasks (Gazzaniga, ; Ringo, Doty, Demeter, & Simard, ). Because brain magnetic resonance imaging (bMRI) studies in PTSD patients report volume changes in various regions, including white matter and corpus callosum (CC), we aimed to test the relationship between memory deficits and CC volume in PTSD patients. We probed for specific alterations in associative memory in PTSD and measured the volume of subportions within the CC employing bMRI. Ourmain finding was a reduction in CC white-matter volume in PTSD patients, as compared to controls, t(35) = -2.7, p = .010, that was correlated with lower associative performance (r = .76, p = .003). We propose that CC volume reduction is a substrate for the associative memory deficits found in PTSD.

Back to the future: past and future era-based schematic support and associative memory for prices in younger and older adults.

Older adults typically display various associative memory deficits, but these deficits can be reduced when conditions allow for the use of prior knowledge or schematic support. To determine how era-specific schematic support and future simulation might influence associative memory, we examined how younger and older adults remember prices from the past as well as the future. Younger and older adults were asked to imagine the past or future, and then studied items and prices from approximately 40 years ago (market value prices from the 1970s) or 40 years in the future. In Experiment 1, all items were common items (e.g., movie ticket, coffee) and the associated prices reflected the era in question, whereas in Experiment 2, some item-price pairs were specific to the time period (e.g., typewriter, robot maid), to test different degrees of schematic support. After studying the pairs, participants were shown each item and asked to recall the associated price. In both experiments, older adults showed similar performance as younger adults in the past condition for the common items, whereas age-related differences were greater in the future condition and for the era-specific items. The findings suggest that in order for schematic support to be effective, recent (and not simply remote) experience is needed in order to enhance memory. Thus, whereas older adults can benefit from "turning back the clock," younger adults better remember future-oriented information compared with older adults, outlining age-related similarities and differences in associative memory and the efficient use of past and future-based schematic support.

Reversal learning and associative memory impairments in a BACHD rat model for Huntington disease.

Chorea and psychiatric symptoms are hallmarks of Huntington disease (HD), a neurodegenerative disorder, genetically characterized by the presence of expanded CAG repeats (>35) in the HUNTINGTIN (HTT) gene. HD patients present psychiatric symptoms prior to the onset of motor symptoms and we recently found a similar emergence of non motor and motor deficits in BACHD rats carrying the human full length mutated HTT (97 CAG-CAA repeats). We evaluated cognitive performance in reversal learning and associative memory tests in different age cohorts of BACHD rats. Male wild type (WT) and transgenic (TG) rats between 2 and 12 months of age were tested. Learning and strategy shifting were assessed in a cross-maze test. Associative memory was evaluated in different fear conditioning paradigms (context, delay and trace). The possible confound of a fear conditioning phenotype by altered sensitivity to a ‘painful’ stimulus was assessed in a flinch-jump test. In the cross maze, 6 months old TG rats showed a mild impairment in reversal learning. In the fear conditioning tasks, 4, 6 and 12 months old TG rats showed a marked reduction in contextual fear conditioning. In addition, TG rats showed impaired delay conditioning (9 months) and trace fear conditioning (3 months). This phenotype was unlikely to be affected by a change in ‘pain’ sensitivity as WT and TG rats showed no difference in their threshold response in the flinch-jump test. Our results suggest that BACHD rats have a profound associative memory deficit and, possibly, a deficit in reversal learning as assessed in a cross maze task. The time course for the emergence of these symptoms (i.e., before the occurrence of motor symptoms) in this rat model for HD appears similar to the time course in patients. These data suggest that BACHD rats may be a useful model for preclinical drug discovery.