Aging Predicts Decline in Explicit and Implicit Memory: A Life-Span Study.

Explicit memory declines with age, but age effects on implicit memory are debated. This issue is important because if implicit memory is age invariant, it may support effective interventions in individuals experiencing memory decline. In this study, we overcame several methodological issues in past research to clarify age effects on implicit memory (priming) and their relationship to explicit memory (recognition, source memory). We (a) recruited a large life-span sample of participants (N = 1,072) during a residency at the Science Museum in London, (b) employed an implicit task that was unaffected by explicit contamination, and (c) systematically manipulated attention and depth of processing to assess their contribution to age effects. Participants witnessed a succession of overlapping colored objects, attending to one color stream and ignoring the other, and identified masked objects at test before judging whether they were previously attended, unattended, or new. Age significantly predicted decline in both explicit and implicit memory for attended items.

A single system account of enhanced recognition memory in synaesthesia.

Researchers often adjudicate between models of memory according to the models' ability to explain impaired patterns of performance (e.g., in amnesia). In contrast, evidence from special groups with enhanced memory is very rarely considered. Here, we explored how people with unusual perceptual experiences (synaesthesia) perform on various measures of memory and test how computational models of memory may account for their enhanced performance. We contrasted direct and indirect measures of memory (i.e., recognition memory, repetition priming, and fluency) in grapheme-colour synaesthetes and controls using a continuous identification with recognition (CID-R) paradigm. Synaesthetes outperformed controls on recognition memory and showed a different reaction-time pattern for identification. The data were most parsimoniously accounted for by a single-system computational model of the relationship between recognition and identification. Overall, the findings speak in favour of enhanced processing as an explanation for the memory advantage in synaesthesia. In general, our results show how synaesthesia can be used as an effective tool to study how individual differences in perception affect cognitive functions.

A single-system model predicts recognition memory and repetition priming in amnesia.

We challenge the claim that there are distinct neural systems for explicit and implicit memory by demonstrating that a formal single-system model predicts the pattern of recognition memory (explicit) and repetition priming (implicit) in amnesia. In the current investigation, human participants with amnesia categorized pictures of objects at study and then, at test, identified fragmented versions of studied (old) and nonstudied (new) objects (providing a measure of priming), and made a recognition memory judgment (old vs new) for each object. Numerous results in the amnesic patients were predicted in advance by the single-system model, as follows: (1) deficits in recognition memory and priming were evident relative to a control group; (2) items judged as old were identified at greater levels of fragmentation than items judged new, regardless of whether the items were actually old or new; and (3) the magnitude of the priming effect (the identification advantage for old vs new items) overall was greater than that of items judged new. Model evidence measures also favored the single-system model over two formal multiple-systems models. The findings support the single-system model, which explains the pattern of recognition and priming in amnesia primarily as a reduction in the strength of a single dimension of memory strength, rather than a selective explicit memory system deficit.

Everyday amnesia: Residual memory for high confidence misses and implications for decision models of recognition.

Despite studying a list of items only minutes earlier, when reencountered in a recognition memory test, undergraduate participants often say with total confidence that they have not studied some of the items before. Such high confidence miss (HCM) responses have been taken as evidence of rapid and complete forgetting and of everyday amnesia (Roediger & Tekin, 2020). We investigated (a) if memory for HCMs is completely lost or whether a residual memory effect exists and (b) whether dominant decision models predict the effect. Participants studied faces (Experiments 1a, 2, and 3) or words (Experiment 1b), then completed a single-item recognition memory task, followed by either (a) a two-alternative forced-choice recognition task, in which the studied and nonstudied alternatives on each trial were matched for their previous old/new decision and confidence rating (Experiments 1 and 2) or (b) a second single-item recognition task in which the targets and foils were HCMs and high confidence correct rejections, respectively (Experiment 3). In each experiment, participants reliably distinguished HCMs from high-confidence correct rejections. The unequal variance signal detection and dual-process signal detection models were fit to the single-item recognition data, and the parameter estimates were used to predict the memory effect for HCMs. The dual-process signal detection model predicted the residual memory effect (as did another popular model, the mixture signal detection theory model). However, the unequal variance signal detection model incorrectly predicted a negative, or no, effect, invalidating this model. The residual memory effect for HCMs demonstrates that everyday amnesia is not associated with complete memory loss and distinguishes between decision models. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Does variability in recognition memory scale with mean memory strength or encoding variability in the UVSD model?

The unequal variance signal detection (UVSD) model of recognition memory assumes that the variance of old item memory strength (σo) is typically greater than that of new items. It has been suggested that this old item variance effect can be explained by the encoding variability hypothesis. However, Spanton and Berry (2020) failed to find evidence for this account, suggesting that σo may simply scale with mean memory strength (d) in the UVSD model. Experiments 1 and 2 examined the effects of encoding variability and strength scaling on old item variance by creating conditions in which mean memory strength and variability in item characteristics was either low or high in 2 × 2 factorial designs. In Experiment 1, overall strength determined estimates of σo, with no effect of item characteristic variability. The same effect of overall strength was found in Experiment 2; there was also a significant effect of item characteristic variability, although this manipulation also had some effect on d and was therefore partially confounded. Experiment 3 similarly found a simultaneous increase in old item variance and memory strength in a design using mixed item characteristic variability conditions in a single-study/test block. We conclude that old item variance increases with mean memory strength in the UVSD model, with uncertainty about the effects of encoding variability, and that future explanations of the old item variance effect should bear this in mind.

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome.

Bardet-Biedl syndrome (BBS) is a heterogeneous genetic disorder characterized by many features, including obesity and cardiovascular disease. We previously developed knockout mouse models of 3 BBS genes: BBS2, BBS4, and BBS6. To dissect the mechanisms involved in the metabolic disorders associated with BBS, we assessed the development of obesity in these mouse models and found that BBS-null mice were hyperphagic, had low locomotor activity, and had elevated circulating levels of the hormone leptin. The effect of exogenous leptin on body weight and food intake was attenuated in BBS mice, which suggests that leptin resistance may contribute to hyperleptinemia. In other mouse models of obesity, leptin resistance may be selective rather than systemic; although mice became resistant to leptin's anorectic effects, the ability to increase renal sympathetic nerve activity (SNA) was preserved. Although all 3 of the BBS mouse models were similarly resistant to leptin, the sensitivity of renal SNA to leptin was maintained in Bbs4 -/- and Bbs6 -/- mice, but not in Bbs2 -/- mice. Consequently, Bbs4 -/- and Bbs6 -/- mice had higher baseline renal SNA and arterial pressure and a greater reduction in arterial pressure in response to ganglionic blockade. Furthermore, we found that BBS mice had a decreased hypothalamic expression of proopiomelanocortin, which suggests that BBS genes play an important role in maintaining leptin sensitivity in proopiomelanocortin neurons.

Explaining the association between repetition priming and source memory: No evidence for a contribution of recognition or fluency.

In a conjoint memory task (measuring repetition priming, recognition memory, and source memory), items recognised as previously studied and receiving correct source decisions also tend to show a greater magnitude of the repetition priming effect. These associations have been explained as arising from a single memory system or signal, rather than multiple distinct ones. In the present work, we examine whether the association between priming and source memory can alternatively be explained as being driven by recognition or fluency. We first reproduced the basic priming-source association (Experiment 1). In Experiments 2 and 3, we found that the association persisted even when the task was modified so that overt and covert recognition judgements were precluded. In Experiment 4, the association was again present even though fluency (as measured by identification response time) could not influence the source decision, although the association was notably weaker. These findings suggest that the association between priming and source memory is not attributable to a contribution of recognition or fluency; instead, the findings are consistent with a single-system account in which a common memory signal drives responding.

Lowering plasma cholesterol levels halts progression of aortic valve disease in mice.

BACKGROUND: Treatment of hyperlipidemia produces functional and structural improvements in atherosclerotic vessels. However, the effects of treating hyperlipidemia on the structure and function of the aortic valve have been controversial, and any effects could be confounded by pleiotropic effects of hypolipidemic treatment. The goal of this study was to determine whether reducing elevated plasma lipid levels with a "genetic switch" in Reversa mice (Ldlr-/-/Apob(100/100)/Mttp(fl/fl)/Mx1-Cre+/+) reduces oxidative stress, reduces pro-osteogenic signaling, and retards the progression of aortic valve disease. METHODS AND RESULTS: After 6 months of hypercholesterolemia, Reversa mice exhibited increases in superoxide, lipid deposition, myofibroblast activation, calcium deposition, and pro-osteogenic protein expression in the aortic valve. Maximum aortic valve cusp separation, as judged by echocardiography, was not altered. During an additional 6 months of hypercholesterolemia, superoxide levels, valvular lipid deposition, and myofibroblast activation remained elevated. Furthermore, calcium deposition and pro-osteogenic gene expression became more pronounced, and the aortic cusp separation decreased from 0.85+/-0.04 to 0.70+/-0.04 mm (mean+/-SE; P<0.05). Rapid normalization of cholesterol levels at 6 months of age (by inducing expression of Cre recombinase) normalized aortic valve superoxide levels, decreased myofibroblast activation, reduced valvular calcium burden, suppressed pro-osteogenic signaling cascades, and prevented reductions in aortic valve cusp separation. CONCLUSIONS: Collectively, these data indicate that reducing plasma lipid levels by genetic inactivation of the mttp gene in hypercholesterolemic mice with early aortic valve disease normalizes oxidative stress, reduces pro-osteogenic signaling, and halts the progression of aortic valve stenosis.

A knockin mouse model of the Bardet-Biedl syndrome 1 M390R mutation has cilia defects, ventriculomegaly, retinopathy, and obesity.

Bardet-Biedl syndrome (BBS) is a genetically heterogeneous disorder that results in retinal degeneration, obesity, cognitive impairment, polydactyly, renal abnormalities, and hypogenitalism. Of the 12 known BBS genes, BBS1 is the most commonly mutated, and a single missense mutation (M390R) accounts for approximately 80% of BBS1 cases. To gain insight into the function of BBS1, we generated a Bbs1(M390R/M390R) knockin mouse model. Mice homozygous for the M390R mutation recapitulated aspects of the human phenotype, including retinal degeneration, male infertility, and obesity. The obese mutant mice were hyperphagic and hyperleptinemic and exhibited reduced locomotor activity but no elevation in mean arterial blood pressure. Morphological evaluation of Bbs1 mutant brain neuroanatomy revealed ventriculomegaly of the lateral and third ventricles, thinning of the cerebral cortex, and reduced volume of the corpus striatum and hippocampus. Similar abnormalities were also observed in the brains of Bbs2(-/-), Bbs4(-/-), and Bbs6(-/-) mice, establishing these neuroanatomical defects as a previously undescribed BBS mouse model phenotype. Ultrastructural examination of the ependymal cell cilia that line the enlarged third ventricle of the Bbs1 mutant brains showed that, whereas the 9 + 2 arrangement of axonemal microtubules was intact, elongated cilia and cilia with abnormally swollen distal ends were present. Together with data from transmission electron microscopy analysis of photoreceptor cell connecting cilia, the Bbs1 M390R mutation does not affect axonemal structure, but it may play a role in the regulation of cilia assembly and/or function.

The unequal variance signal-detection model of recognition memory: Investigating the encoding variability hypothesis.

Despite the unequal variance signal-detection (UVSD) model's prominence as a model of recognition memory, a psychological explanation for the unequal variance assumption has yet to be verified. According to the encoding variability hypothesis, old item memory strength variance (σo) is greater than that of new items because items are incremented by variable, rather than fixed, amounts of strength at encoding. Conditions that increase encoding variability should therefore result in greater estimates of σo. We conducted three experiments to test this prediction. In Experiment 1, encoding variability was manipulated by presenting items for a fixed or variable (normally distributed) duration at study. In Experiment 2, we used an attentional manipulation whereby participants studied items while performing an auditory one-back task in which distractors were presented at fixed or variable intervals. In Experiment 3, participants studied stimuli with either high or low variance in word frequency. Across experiments, estimates of σo were unaffected by our attempts to manipulate encoding variability, even though the manipulations weakly affected subsequent recognition. Instead, estimates of σo tended to be positively correlated with estimates of the mean difference in strength between new and studied items (d), as might be expected if σo generally scales with d. Our results show that it is surprisingly hard to successfully manipulate encoding variability, and they provide a signpost for others seeking to test the encoding variability hypothesis.

A unitary signal-detection model of implicit and explicit memory.

Do dissociations imply independent systems? In the memory field, the view that there are independent implicit and explicit memory systems has been predominantly supported by dissociation evidence. Here, we argue that many of these dissociations do not necessarily imply distinct memory systems. We review recent work with a single-system computational model that extends signal-detection theory (SDT) to implicit memory. SDT has had a major influence on research in a variety of domains. The current work shows that it can be broadened even further in its range of application. Indeed, the single-system model that we present does surprisingly well in accounting for some key dissociations that have been taken as evidence for independent implicit and explicit memory systems.

Biventricular adaptation to volume overload in mice with aortic regurgitation.

BACKGROUND: Aortic valve regurgitation is usually caused by impaired coaptation of the aortic valve cusps during diastole. Hypercholesterolemia produces aortic valve lipid deposition, fibrosis, and calcification in both mice and humans, which could impair coaptation of cusps. However, a link between hypercholesterolemia and aortic regurgitation has not been established in either species. The purpose of this study was to ascertain the prevalence of aortic regurgitation in hypercholesterolemic mice and to determine its impact on the left and right ventricles. METHODS AND RESULTS: Eighty Ldlr-/-/Apob100/100/Mttpfl/fl/Mx1Cre+/+ ("Reversa") hypercholesterolemic mice and 40 control mice were screened for aortic regurgitation (AR) with magnetic resonance imaging at age 7.5 months. The prevalence of AR was 40% in Reversa mice, with moderate or severe regurgitation (AR+) in 19% of mice. In control mice, AR prevalence was 13% (p = 0.004 vs. Reversa), and was invariably trace or mild in severity. In-depth evaluation of cardiac response to volume overload was performed in 12 AR-positive and 12 AR-negative Reversa mice. Regurgitant fraction was 0.34 +/- 0.04 in AR-positive vs. 0.02 +/- 0.01 in AR-negative (mean +/- SE; p < 0.001). AR-positive mice had significantly increased left ventricular end-diastolic volume and mass and reduced ejection fraction in both ventricles. When left ventricular ejection fraction fell below 0.60 in AR-positive (n = 7) mice, remodeling occurred and right ventricular systolic function progressively worsened. CONCLUSION: Hypercholesterolemia causes aortic valve regurgitation with moderate prevalence in mice. When present, aortic valve regurgitation causes volume overload and pathological remodeling of both ventricles.

Effects of deep sedation or general anesthesia on cardiac function in mice undergoing cardiovascular magnetic resonance.

BACKGROUND: Genetically engineered mouse models of human cardiovascular disease provide an opportunity to understand critical pathophysiological mechanisms. Cardiovascular magnetic resonance (CMR) provides precise reproducible assessment of cardiac structure and function, but, in contrast to echocardiography, requires that the animal be immobilized during image acquisition. General anesthetic regimens yield satisfactory images, but have the potential to significantly perturb cardiac function. The purpose of this study was to assess the effects of general anesthesia and a new deep sedation regimen, respectively, on cardiac function in mice as determined by CMR, and to compare them to results obtained in mildly sedated conscious mice by echocardiography. RESULTS: In 6 mildly sedated normal conscious mice assessed by echo, heart rate was 615 +/- 25 min-1 (mean +/- SE) and left ventricular ejection fraction (LVEF) was 0.94 +/- 0.01. In the CMR studies of normal mice, heart rate was slightly lower during deep sedation with morphine/midazolam (583 +/- 30 min-1), but the difference was not statistically significant. General anesthesia with 1% inhaled isoflurane significantly depressed heart rate (468 +/- 7 min-1, p < 0.05 vs. conscious sedation). In 6 additional mice with ischemic LV failure, trends in heart rate were similar, but not statistically significant. In normal mice, deep sedation depressed LVEF (0.79 +/- 0.04, p < 0.05 compared to light sedation), but to a significantly lesser extent than general anesthesia (0.60 +/- 0.04, p < 0.05 vs. deep sedation). In mice with ischemic LV failure, ejection fraction measurements were comparable when performed during light sedation, deep sedation, and general anesthesia, respectively. Contrast-to-noise ratios were similar during deep sedation and during general anesthesia, indicating comparable image quality. Left ventricular mass measurements made by CMR during deep sedation were nearly identical to those made during general anesthesia (r2 = 0.99, mean absolute difference < 4%), indicating equivalent quantitative accuracy obtained with the two methods. The imaging procedures were well-tolerated in all mice. CONCLUSION: In mice with normal cardiac function, CMR during deep sedation causes significantly less depression of heart rate and ejection fraction than imaging during general anesthesia with isoflurane. In mice with heart failure, the sedation/anesthesia regimen had no clear impact on cardiac function. Deep sedation and general anesthesia produced CMR with comparable image quality and quantitative accuracy.

A single-system account of the relationship between priming, recognition, and fluency.

A single-system computational model of priming and recognition was applied to studies that have looked at the relationship between priming, recognition, and fluency in continuous identification paradigms. The model was applied to 3 findings that have been interpreted as evidence for a multiple-systems account: (a) priming can occur for items not recognized; (b) the pattern of identification reaction times (RTs) to hits, misses, correct rejections, and false alarms can change as a function of recognition performance; and (c) fluency effects (shorter RTs to words judged old vs. judged new) and priming effects (shorter RTs to old vs. new words) can be observed in amnesic patients at levels comparable with healthy adults despite impaired or near-chance recognition. The authors' simulations suggest, contrary to previous interpretations, that these results are consistent with a single-system account.

On the status of unconscious memory: Merikle and Reingold (1991) revisited.

Four experiments are reported that reevaluate P. M. Merikle and E. M. Reingold's (1991) demonstration of unconscious memory: the greater sensitivity to familiarity (repetition) of an indirect (implicit) memory task than of a comparable direct (explicit) task. At study, participants named the cued member of a pair of visually presented words. At test, new and uncued study words were presented against a background mask. Participants judged whether each word was old or new (direct task) or whether the contrast between the word and the background was high or low (indirect task). Contrary to the original findings, the sensitivity of the indirect task to familiarity never exceeded that of the direct task. These findings pose a challenge to a key pillar of evidence for unconscious influences of memory.

Review of concrete biodeterioration in relation to nuclear waste.

Storage of radioactive waste in concrete structures is a means of containing wastes and related radionuclides generated from nuclear operations in many countries. Previous efforts related to microbial impacts on concrete structures that are used to contain radioactive waste showed that microbial activity can play a significant role in the process of concrete degradation and ultimately structural deterioration. This literature review examines the research in this field and is focused on specific parameters that are applicable to modeling and prediction of the fate of concrete structures used to store or dispose of radioactive waste. Rates of concrete biodegradation vary with the environmental conditions, illustrating a need to understand the bioavailability of key compounds involved in microbial activity. Specific parameters require pH and osmotic pressure to be within a certain range to allow for microbial growth as well as the availability and abundance of energy sources such as components involved in sulfur, iron and nitrogen oxidation. Carbon flow and availability are also factors to consider in predicting concrete biodegradation. The microbial contribution to degradation of the concrete structures containing radioactive waste is a constant possibility. The rate and degree of concrete biodegradation is dependent on numerous physical, chemical and biological parameters. Parameters to focus on for modeling activities and possible options for mitigation that would minimize concrete biodegradation are discussed and include key conditions that drive microbial activity on concrete surfaces.

Good Liars Are Neither 'Dark' Nor Self-Deceptive.

Deception is a central component of the personality 'Dark Triad' (Machiavellianism, Psychopathy and Narcissism). However, whether individuals exhibiting high scores on Dark Triad measures have a heightened deceptive ability has received little experimental attention. The present study tested whether the ability to lie effectively, and to detect lies told by others, was related to Dark Triad, Lie Acceptability, or Self-Deceptive measures of personality using an interactive group-based deception task. At a group level, lie detection accuracy was correlated with the ability to deceive others-replicating previous work. No evidence was found to suggest that Dark Triad traits confer any advantage either to deceive others, or to detect deception in others. Participants who considered lying to be more acceptable were more skilled at lying, while self-deceptive individuals were generally less credible and less confident when lying. Results are interpreted within a framework in which repeated practice results in enhanced deceptive ability.

An effect of age on implicit memory that is not due to explicit contamination: implications for single and multiple-systems theories.

Recognition memory is typically weaker in healthy older relative to young adults, while performance on implicit tests (e.g., repetition priming) is often comparable between groups. Such observations are commonly taken as evidence for independent explicit and implicit memory systems. On a picture version of the continuous identification with recognition (CID-R) task, we found a reliable age-related reduction in recognition memory, while the age effect on priming did not reach statistical significance (Experiment 1). This pattern was consistent with the predictions of a formal single-system model. Experiment 2 replicated these observations using separate priming (continuous identification; CID) and recognition phases, while a combined data analysis revealed a significant effect of age on priming. In Experiment 3, we provide evidence that priming in this task is unaffected by explicit processing, and we conclude that the age difference in priming is unlikely to have been driven by differences in explicit processing between groups of young and older adults ("explicit contamination"). The results support the view that explicit and implicit expressions of memory are driven by a single underlying memory system.

Deceptively simple The "deception-general" ability and the need to put the liar under the spotlight.

This Focused Review expands upon our original paper (You can't kid a kidder": Interaction between production and detection of deception in an interactive deception task. Frontiers in Human Neuroscience, 6:87). In that paper we introduced a new socially interactive, laboratory-based task, the Deceptive Interaction Task (DeceIT), and used it to measure individuals' ability to lie, their ability to detect the lies of others, and potential individual difference measures contributing to these abilities. We showed that the two skills were correlated; better liars made better lie detectors (a "deception general" ability) and this ability seemed to be independent of cognitive (IQ) and emotional (EQ) intelligence. Here, following the Focused Review format, we outline the method and results of the original paper and comment more on the value of lab-based experimental studies of deception, which have attracted criticism in recent years. While acknowledging that experimental paradigms may fail to recreate the full complexity and potential seriousness of real-world deceptive behavior, we suggest that lab-based deception paradigms can offer valuable insight into ecologically-valid deceptive behavior. The use of the DeceIT procedure enabled deception to be studied in an interactive setting, with motivated participants, and importantly allowed the study of both the liar and the lie detector within the same deceptive interaction. It is our thesis that by addressing deception more holistically-by bringing the liar into the "spotlight" which is typically trained exclusively on the lie detector-we may further enhance our understanding of deception.