Exposure to and recall of violence reduce short-term memory and cognitive control

From Bogliacino et al.:

Significance

Research on violence has mainly focused on its consequences on individuals’ health and behavior. This study establishes the effects of exposure to violence on individuals’ short-term memory and cognitive control. These are key factors affecting individual well-being and societal development. We sampled Colombian civilians who were exposed either to urban violence or to warfare. We found that higher exposure to violence significantly reduces short-term memory and cognitive control only in the group actively recalling emotional states linked with such experiences. This finding demonstrates and characterizes the long-lasting effects of violence. Existing studies have found effects of poverty on cognitive control similar to those that we found for violence. This set of findings supports the validity of the cognitive theory underpinning these studies.

Abstract

Previous research has investigated the effects of violence and warfare on individuals' well-being, mental health, and individual prosociality and risk aversion. This study establishes the short- and long-term effects of exposure to violence on short-term memory and aspects of cognitive control. Short-term memory is the ability to store information. Cognitive control is the capacity to exert inhibition, working memory, and cognitive flexibility. Both have been shown to affect positively individual well-being and societal development. We sampled Colombian civilians who were exposed either to urban violence or to warfare more than a decade earlier. We assessed exposure to violence through either the urban district-level homicide rate or self-reported measures. Before undertaking cognitive tests, a randomly selected subset of our sample was asked to recall emotions of anxiety and fear connected to experiences of violence, whereas the rest recalled joyful or emotionally neutral experiences. We found that higher exposure to violence was associated with lower short-term memory abilities and lower cognitive control in the group recalling experiences of violence, whereas it had no effect in the other group. This finding demonstrates that exposure to violence, even if a decade earlier, can hamper cognitive functions, but only among individuals actively recalling emotional states linked with such experiences. A laboratory experiment conducted in Germany aimed to separate the effect of recalling violent events from the effect of emotions of fear and anxiety. Both factors had significant negative effects on cognitive functions and appeared to be independent from each other.

Suppressing memory of trauma causes forgetting of other memories.

An interesting article from Hulbert et.al. on how suppressing memory of a trauma also causes forgetting of unrelated experiences in the period surrounding the trauma.:

Hippocampal damage profoundly disrupts the ability to store new memories of life events. Amnesic windows might also occur in healthy people due to disturbed hippocampal function arising during mental processes that systemically reduce hippocampal activity. Intentionally suppressing memory retrieval (retrieval stopping) reduces hippocampal activity via control mechanisms mediated by the lateral prefrontal cortex. Here we show that when people suppress retrieval given a reminder of an unwanted memory, they are considerably more likely to forget unrelated experiences from periods surrounding suppression. This amnesic shadow follows a dose-response function, becomes more pronounced after practice suppressing retrieval, exhibits characteristics indicating disturbed hippocampal function, and is predicted by reduced hippocampal activity. These findings indicate that stopping retrieval engages a suppression mechanism that broadly compromises hippocampal processes and that hippocampal stabilization processes can be interrupted strategically. Cognitively triggered amnesia constitutes an unrecognized forgetting process that may account for otherwise unexplained memory lapses following trauma.

Savoring happy memories - value representations in the striatum

Speer et al. observe responses in the corticostriatal circuits that respond to monetary reward when positive autobiographical memories are recalled. These response "may be adaptive for regulating positive emotion and promoting better well-being."

Highlights 

•The act of recalling positive life events enhances emotion and has tangible value
•Corticostriatal fMRI signals index emotion evoked by recalling positive life events
•Striatal activity relates to positive mood enhancing effects of reminiscing
•Striatal responses to positive memories may relate to individual resilience 

Summary 

Reminders of happy memories can bring back pleasant feelings tied to the original experience, suggesting an intrinsic value in reminiscing about the positive past. However, the neural circuitry underlying the rewarding aspects of autobiographical memory is poorly understood. Using fMRI, we observed enhanced activity during the recall of positive relative to neutral autobiographical memories in corticostriatal circuits that also responded to monetary reward. Enhanced activity in the striatum and medial prefrontal cortex was associated with increases in positive emotion during recall, and striatal engagement further correlated with individual measures of resiliency. Striatal response to the recall of positive memories was greater in individuals whose mood improved after the task. Notably, participants were willing to sacrifice a more tangible reward, money, in order to reminisce about positive past experiences. Our findings suggest that recalling positive autobiographical memories is intrinsically valuable, which may be adaptive for regulating positive emotion and promoting better well-being.

The power of positivity.

Ramirez et al. make the fascinating observation that depressive-like stress responses in mice can be acutely suppressed through artificial reactivation of a small population of neurons that had previously been activated by a positive experience - these cells apparently being the physical substrate, or engram, of the positive memory. This suggests a fundamental explanation for why eliciting the recall of pleasant memories can sometimes be an effective psychotherapeutic technique for relieving stress, lack of motivation, or anhedonia in humans.

Stress is considered a potent environmental risk factor for many behavioural abnormalities, including anxiety and mood disorders. Animal models can exhibit limited but quantifiable behavioural impairments resulting from chronic stress, including deficits in motivation, abnormal responses to behavioural challenges, and anhedonia. The hippocampus is thought to negatively regulate the stress response and to mediate various cognitive and mnemonic aspects of stress-induced impairments, although the neuronal underpinnings sufficient to support behavioural improvements are largely unknown. Here we acutely rescue stress-induced depression-related behaviours in mice by optogenetically reactivating dentate gyrus cells that were previously active during a positive experience. A brain-wide histological investigation, coupled with pharmacological and projection-specific optogenetic blockade experiments, identified glutamatergic activity in the hippocampus–amygdala–nucleus-accumbens pathway as a candidate circuit supporting the acute rescue. Finally, chronically reactivating hippocampal cells associated with a positive memory resulted in the rescue of stress-induced behavioural impairments and neurogenesis at time points beyond the light stimulation. Together, our data suggest that activating positive memories artificially is sufficient to suppress depression-like behaviours and point to dentate gyrus engram cells as potential therapeutic nodes for intervening with maladaptive behavioural states.

A bit of amphetamine turns older brains into younger brains.

Fascinating. Garrett et al. show that raising dopamine levels with amphetamine (sold as the prescription drug Adderall, for ADHD), increases the brain wave variability that enhances working memory, so that seniors perform as well as younger people on the n-back working memory test. (Common prescription doses of 5-30 mg act as a cognitive enhancer.

Higher doses can be aphrodisiac, euphoriant, addictive, and have many bad side effects.) I pass on both their statement of significance and abstract. Also, a figure that tempts me to try to get an adderall prescription and do a self experiment.

Significance

Younger, better performing adults typically show greater brain signal variability than older, poorer performers, but the mechanisms underlying this observation remain elusive. We attempt to restore deficient functional-MRI–based blood oxygen level-dependent (BOLD) signal variability (SDBOLD) levels in older adults by boosting dopamine via d-amphetamine (AMPH). Notably, older adults met or exceeded young adult SDBOLD levels under AMPH. AMPH-driven changes in SDSDBOLD also predicted AMPH-driven changes in reaction time speed and variability on a working memory task, but depended greatly on age and drug administration order. These findings (i) suggest that dopamine may account for adult age differences in brain signal variability and (ii) highlight the importance of considering practice effects and state dependencies when evaluating the neurochemical basis of age- and cognition-related brain dynamics. 

Abstract

Better-performing younger adults typically express greater brain signal variability relative to older, poorer performers. Mechanisms for age and performance-graded differences in brain dynamics have, however, not yet been uncovered. Given the age-related decline of the dopamine (DA) system in normal cognitive aging, DA neuromodulation is one plausible mechanism. Hence, agents that boost systemic DA [such as d-amphetamine (AMPH)] may help to restore deficient signal variability levels. Furthermore, despite the standard practice of counterbalancing drug session order (AMPH first vs. placebo first), it remains understudied how AMPH may interact with practice effects, possibly influencing whether DA up-regulation is functional. We examined the effects of AMPH on functional-MRI–based blood oxygen level-dependent (BOLD) signal variability (SDBOLD) in younger and older adults during a working memory task (letter n-back). Older adults expressed lower brain signal variability at placebo, but met or exceeded young adult SDBOLD levels in the presence of AMPH. Drug session order greatly moderated change–change relations between AMPH-driven SDBOLD and reaction time means (RTmean) and SDs (RTSD). Older adults who received AMPH in the first session tended to improve in RTmean and RTSD when SDBOLD was boosted on AMPH, whereas younger and older adults who received AMPH in the second session showed either a performance improvement when SDBOLD decreased (for RTmean) or no effect at all (for RTSD). The present findings support the hypothesis that age differences in brain signal variability reflect aging-induced changes in dopaminergic neuromodulation. The observed interactions among AMPH, age, and session order highlight the state- and practice-dependent neurochemical basis of human brain dynamics.

Figure. Increased BOLD variability and improved cognitive performance under AMPH. Multivariate partial least-squares model of relation between SDBOLD, Age Group, AMPH, and Task Condition. Higher brain scores reflect higher BOLD signal variability. Error bars represent bootstrapped 95% confidence intervals (1,000× with replacement). Brain images are plotted in neurological orientation (left is Left). AMPH, amphetamine; BSR, bootstrap ratio.

In older people, moderate alcohol intake improves memory.

Articles like this work from Downer et al. make me worry less about the possible deleterious effects of the happy hour cocktail that is part of my daily ritual. Several studies have shown that light and moderate alcohol consumption during late life is associated with higher cognitive functioning among older adults and a decreased risk of dementia, and they now document relevant correlations with the volume of the hippocampus, which is important in memory. Their abstract, slightly edited:

This study utilized data from the Framingham Heart Study Offspring Cohort to examine the relationship between midlife and late-life alcohol consumption, cognitive functioning, and regional brain volumes among older adults without dementia or a history of abusing alcohol. The results from multiple linear regression models indicate that late life, but not midlife, alcohol consumption status is associated with episodic memory and hippocampal volume. Compared to late life abstainers, moderate consumers had larger hippocampal volume, and light consumers had higher episodic memory. The differences in episodic memory according to late life alcohol consumption status were no longer significant when hippocampal volume was included in the regression model (This suggests that the observed relationship between alcohol consumption and episodic memory and alcohol consumption during old age may be due to larger hippocampal volume.) The findings from this study provide new evidence that hippocampal volume may contribute to the observed differences in episodic memory among older adults and late life alcohol consumption status.

The authors note that findings from animal studies suggest that moderate alcohol consumption may contribute to preserved hippocampal volume by promoting the generation of new neurons in the hippocampus. In addition, exposing the brain to moderate amounts of alcohol may increase the release of acetylcholine and other neurotransmitters that are involved in cognitive functioning.

Mind wandering that makes effort more efficient.

MindBlog has done numerous posts on our brains' default mode and executive control networks, with the idea usually being that activating the default network or mind wandering during an attention demanding task can impair performance. Spreng et al. now do a study showing that it also can improve performance if the mind wandering is congruent with the task itself. In this case the default and executive control networks appear to relate external goals and internal meaning:

Substantial neuroimaging evidence suggests that spontaneous engagement of the default network impairs performance on tasks requiring executive control. We investigated whether this impairment depends on the congruence between executive control demands and internal mentation. We hypothesized that activation of the default network might enhance performance on an executive control task if control processes engage long-term memory representations that are supported by the default network. Using fMRI, we scanned 36 healthy young adult humans on a novel two-back task requiring working memory for famous and anonymous faces. In this task, participants (1) matched anonymous faces interleaved with anonymous face, (2) matched anonymous faces interleaved with a famous face, or (3) matched a famous faces interleaved with an anonymous face. As predicted, we observed a facilitation effect when matching famous faces, compared with anonymous faces. We also observed greater activation of the default network during these famous face-matching trials. The results suggest that activation of the default network can contribute to task performance during an externally directed executive control task. Our findings provide evidence that successful activation of the default network in a contextually relevant manner facilitates goal-directed cognition.

Associative memory enhanced by brain stimulation.

Wang et al. do a proof that the hippocampus facilitates associative memory formation in humans by interacting with distributed brain regions. Here is a description of their approach (sufficiently sophisticated that one will probably not be seeing DIY self help kits on the internet anytime soon!):

We ...developed methods to modulate cortical-hippocampal brain networks in healthy adults (n = 16 subjects) in order to test their role in associative memory. We focused modulatory stimulation on the lateral parietal cortex component of a well-characterized cortical-hippocampal network on the basis of hypothesized interactions between hippocampus and lateral parietal cortex in memory as well as robust functional connectivity between these regions, which is likely mediated by lateral parietal projections to retrosplenial and parahippocampal cortex. We defined a target within the left hippocampus for each subject and used resting-state fMRI to identify a subject-specific left lateral parietal location that demonstrated high functional connectivity with the hippocampal target. Noninvasive high-frequency repetitive transcranial magnetic stimulation (rTMS) was delivered to the parietal location for 5 consecutive days on the basis of evidence that rTMS can induce changes in connectivity within stimulated networks and that such effects can increase over multiple-day stimulation sessions.

Here is their abstract:

The influential notion that the hippocampus supports associative memory by interacting with functionally distinct and distributed brain regions has not been directly tested in humans. We therefore used targeted noninvasive electromagnetic stimulation to modulate human cortical-hippocampal networks and tested effects of this manipulation on memory. Multiple-session stimulation increased functional connectivity among distributed cortical-hippocampal network regions and concomitantly improved associative memory performance. These alterations involved localized long-term plasticity because increases were highly selective to the targeted brain regions, and enhancements of connectivity and associative memory persisted for ~24 hours after stimulation. Targeted cortical-hippocampal networks can thus be enhanced noninvasively, demonstrating their role in associative memory.

The myth of cognitive decline with aging? Yes and No....

Offering something of an antidote to the drumbeat of articles measuring cognitive declines on again, Ramscar et al. (open source) suggest that changing performance patterns that are typically taken as evidence for (and measures of) cognitive decline arise out of basic principles of learning and emerge naturally in learning models as they acquire more knowledge, with patterns of performance reflect the information-processing costs that must inevitably be incurred as knowledge is acquired. Their arguments seem relevant to lexical tasks such as recalling words, but are not germane to declines in visual or auditory attention and processing speed (usually described as 'cognitive' declines) for which underlying brain structural and functional correlates have been observed. They also do not address the issue of noise, or competition from competing memories, as influencing lexical retrieval tasks. The second abstract below, work of Healey et al., notes this possibility. So, first the Ramscar et al. abstract:

As adults age, their performance on many psychometric tests changes systematically, a finding that is widely taken to reveal that cognitive information-processing capacities decline across adulthood. Contrary to this, we suggest that older adults'; changing performance reflects memory search demands, which escalate as experience grows. A series of simulations show how the performance patterns observed across adulthood emerge naturally in learning models as they acquire knowledge. The simulations correctly identify greater variation in the cognitive performance of older adults, and successfully predict that older adults will show greater sensitivity to fine-grained differences in the properties of test stimuli than younger adults. Our results indicate that older adults'; performance on cognitive tests reflects the predictable consequences of learning on information-processing, and not cognitive decline. We consider the implications of this for our scientific and cultural understanding of aging.

And now the Healey et al. abstract on noise or interference resolution by younger but not older adults:

Resolving interference from competing memories is a critical factor in efficient memory retrieval, and several accounts of cognitive aging suggest that difficulty resolving interference may underlie memory deficits such as those seen in the elderly. Although many researchers have suggested that the ability to suppress competitors is a key factor in resolving interference, the evidence supporting this claim has been the subject of debate. Here, we present a new paradigm and results demonstrating that for younger adults, a single retrieval attempt is sufficient to suppress competitors to below-baseline levels of accessibility even though the competitors are never explicitly presented. The extent to which individual younger adults suppressed competitors predicted their performance on a memory span task. In a second experiment, older adults showed no evidence of suppression, which supports the theory that older adults’ memory deficits are related to impaired suppression.

ADDED NOTE:

After I composed the above post Benedict Carey's mention of the Ramscar et al. article appeared in the NYTimes and became a 'most emailed article' for several days. He makes the same points that I do as a counter to over-interpreting Ramscar et al.'s data.