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Enhancing Human Cognitive Capital by Harnessing the Brain’s Inherent Neuroplasticity

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Abstract

This chapter addresses the capability to enhance human cognitive performance (i.e., cognitive capital) through training, with the down-range goal of improving functionality in contexts of great complexity, including military/political operations, corporate directions, and educational preparation. It highlights a multidimensional framework to measure gains in cognitive capital on brain, cognitive, psychological, life-functionality, and emotional-cognition factors. To illustrate the potential to harness neuroplasticity, the chapter summarizes evidence showing improved agility and focus from a specific cognitive training that targets strategic thinking (e.g., filter/focus, big picture thinking, innovation). This chapter also adds to the notion of increasing peak performance utilizing moderate stress levels to boost responses. Optimizing performance in continually changing and stressful environments relies on strengthening human cognitive capital in the healthy brain across the life span—similar to that achieved for physical fitness.

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The most powerful, most staggeringly complex machine ever created is all in your head. Our brain is the most adaptable, modifiable organ in our body, and yet it is the organ we most likely give the least attention. Many individuals who are concerned with having a physically fit body stop their “workout” at the neck. In the past five years brain scientists have discovered much more about how the brain works, including that it can be trained to perform better than ever before. You are never too young or too old to adopt healthy brain habits that strengthen the brain’s capacity to think smarter.
Article
A recent study shows that the fronto-parietal network (FPN), and subregions therein, alters its functional connectivity with nodes of other networks based on task goals. Moreover, FPN patterns of connectivity not only reflect engagement of specific tasks, but also serve as a code that can be transferred to facilitate learning novel tasks.
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ABSTRACT Goal-setting theory is summarized regarding the effectiveness of specific, difficult goals; the relationship of goals to affect; the mediators of goal effects; the relation of goals to self-efficacy; the moderators of goal effects; and the generality of goal effects across people, tasks, countries, time spans, experimental designs, goal sources (i.e., self-set, set jointly with others, or assigned), and dependent variables. Recent studies concerned with goal choice and the factors that influence it, the function of learning goals, the effect of goal framing, goals and affect (well-being), group goal setting, goals and traits, macro-level goal setting, and conscious versus subconscious goals are described. Suggestions are given for future research.
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Data from preclinical and clinical studies have implicated the norepinephrine system in the development and maintenance of post-traumatic stress disorder. The primary source of norepinephrine in the forebrain is the locus coeruleus (LC); however, LC activity cannot be directly measured in humans, and previous research has often relied upon peripheral measures of norepinephrine to infer changes in central LC-norepinephrine function. To directly assess LC-norepinephrine function, we measured single-unit activity of LC neurons in a validated rat model of post-traumatic stress disorder - single prolonged stress (SPS). We also examined tyrosine hydroxylase mRNA levels in the LC of SPS and control rats as an index of norepinephrine utilisation. For electrophysiological recordings, 92 LC neurons were identified from 19 rats (SPS, 12; control, 7), and spontaneous and evoked responses to a noxious event (paw compression) were recorded. Baseline and restraint stress-evoked tyrosine hydroxylase mRNA expression levels were measured in SPS and control rats (n = 16 per group) in a separate experiment. SPS rats showed lower spontaneous activity but higher evoked responses, leading to an enhanced signal-to-noise ratio of LC neurons, accompanied by impaired recovery from post-stimulus inhibition. In concert, tyrosine hydroxylase mRNA expression in the LC of SPS rats tended to be lower at baseline, but was exaggerated following restraint stress. These data demonstrate persistent changes in LC function following stress/trauma in a rat model of post-traumatic stress, as measured by differences in both the electrophysiological properties of LC neurons and tyrosine hydroxylase mRNA transcription.
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Working memory (WM) training (WMT) alters the task-related brain activity and structure of the external attention system (EAS). We investigated whether WMT also alters resting-state brain mechanisms, which are assumed to reflect intrinsic brain activity and connectivity. Our study subjects were subjected to a 4-week WMT program and brain scans before and after the intervention for determining changes of functional connectivity and regional cerebral blood flow during rest (resting-FC/resting-rCBF). Compared with no-intervention, WMT (a) increased resting-FC between the medial prefrontal cortex (mPFC) and precuneus, which are key nodes of the default mode network (DMN), (b) decreased resting-FC between mPFC and the right posterior parietal cortex/right lateral prefrontal cortex (LPFC), which are key nodes of the EAS, and (c) increased resting-rCBF in the right LPFC. However, the training-related decreases in resting-FC between the key DMN node and the nodes of EAS were only observed when the whole brain signal was regressed out in individual analyses, and these changes were not observed when the whole brain signal was not regressed out in individual analyses. Further analyses indicated that these differences may be mediated by a weak but a widespread increase in resting-FC between the nodes of EAS and activity of multiple bilateral areas across the brain. These results showed that WMT induces plasticity in neural mechanisms involving DMN and the EAS during rest and indicated that intrinsic brain activity and connectivity can be affected by cognitive training.
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Chronic stress could trigger maladaptive changes associated with stress-related mental disorders; however, the underlying mechanisms remain elusive. In this study, we found that exposing juvenile male rats to repeated stress significantly impaired the temporal order recognition memory, a cognitive process controlled by the prefrontal cortex (PFC). Concomitantly, significantly reduced AMPAR- and NMDAR-mediated synaptic transmission and glutamate receptor expression were found in PFC pyramidal neurons from repeatedly stressed animals. All these effects relied on activation of glucocorticoid receptors and the subsequent enhancement of ubiquitin/proteasome-mediated degradation of GluR1 and NR1 subunits, which was controlled by the E3 ubiquitin ligase Nedd4-1 and Fbx2, respectively. Inhibition of proteasomes or knockdown of Nedd4-1 and Fbx2 in PFC prevented the loss of glutamatergic responses and recognition memory in stressed animals. Our results suggest that repeated stress dampens PFC glutamatergic transmission by facilitating glutamate receptor turnover, which causes the detrimental effect on PFC-dependent cognitive processes.
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The study examined the accumulated as well as the differential influence of negative life events on cognitive decline in older persons, and whether this association was different for persons with normal and poor cognitive functioning, and for ApoE ε4 carriers and noncarriers. We used data from the Longitudinal Aging Study Amsterdam (N = 1,356). Data were analyzed using linear mixed models. We found differential associations for different negative life events with cognitive decline none of which were mediated by depressive symptoms. The death of a child or grandchild, which may be considered a highly stressful event, was associated to a higher rate of cognitive decline, whereas more chronic stressors, such as the illness of a partner or relative, or serious conflicts, were associated with better cognitive function. The associations between life events and cognitive function were stronger in ApoE ε4 carriers compared with noncarriers, suggesting that this gene plays a role in the association between stress and cognitive function. Highly stressful events seem to be associated with a higher rate of cognitive decline, whereas mild chronic stressors may have an arousing function that stimulates cognitive performance.
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To test the effects of cognitive training on subsequent motor vehicle collision (MVC) involvement of older drivers. Randomized, controlled, multisite, single-blind clinical trial. Community-dwelling seniors at four U.S. sites: Birmingham, Alabama; Baltimore, Maryland; Indianapolis, Indiana; and State College, Pennsylvania. Nine hundred eight older drivers (mean age 73.1; 18.6% African American) who were randomized to one of three cognitive interventions or a control condition. Up to 10 sessions of cognitive training for memory, reasoning, or speed of processing. State-recorded MVC involvement up to 6 years after study enrollment. Speed-of-processing and reasoning training resulted in lower rates of at-fault collision involvement over the subsequent approximately 6-year period than controls. After adjusting for age, sex, race, education, mental status, health, vision, depressive symptoms, and testing site, participants randomized to the speed-of-processing and reasoning interventions had an approximately 50% lower rate (per person-mile) of at-fault MVCs than the control group (rate ratio (RR) = 0.57, 95% confidence interval (CI) = 0.34-0.96 for speed of processing), and (RR = 0.50, 95% CI = 0.27-0.92 for reasoning). There was no significant difference observed for the memory group. Cognitive speed-of-processing and reasoning training resulted in a lower at-fault MVC rate in older drivers than in controls. Considering the importance of driving mobility, the costs of crashes, and the benefits of cognitive training, these interventions have great potential to sustain independence and quality of life of older adults. More research is needed to understand the effects of different types and quantities of training.
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Cognitive impairment is a key factor that threatens functionality and quality of life in seniors. Given the projection that the population of individuals 65 years of age and older will double within the next 25 years, a critical need exists to identify and test effectiveness of protocols that target higher-order cognitive skills such as gist reasoning to maximize cognitive capacity in later life. This study examined the effects of eight hours of gist reasoning training in 26 cognitively normal seniors between the ages of 64-85 years (M = 74.23, SD = 6.67). Findings suggest that top-down strategy-based gist reasoning training significantly improved abstraction ability, a skill relevant to everyday life, as well as generalized to untrained measures of executive function including concept abstraction, cognitive switching, and verbal fluency. Individuals with lower baseline ability to abstract gist showed the greatest gain in the target domain trained. These findings highlight the potential value of engaging in cognitively challenging activities that involve gist reasoning, to strengthen and preserve cognitive capacity with aging.
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Trauma to the brain can change the core of a person's being—their thinking, memory, personality, and behavior. Although individuals who have suffered traumatic brain injury (TBI) may feel alone in their struggle to deal with the aftermath of injury, they actually join the ranks of those affected by one of the most common neurological diagnoses in the United States (Rutland-Brown et al., 2006). TBI affects every age group and segment of society. Recent combat-related activities have increased the incidence of TBI as well as piqued the attention of the public and elected representatives. Concussions suffered during sports activities have been a major issue for years and are only now receiving widespread coverage in the news media with high-profile cases. Undoubtedly, many more individuals have suffered brain injury than are diagnosed. Changes in society and advances in neuroscience make it worthwhile to re-examine the scope of the problem, neural mechanisms underlying the cognitive and behavioral deficits of this disorder, and approaches that can be taken to help individuals that have suffered from TBI heal. We highlight several major paradigm shifts that must occur for the field to advance.
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To describe the most recent estimates of the incidence and prevalence of traumatic brain injury (TBI) and review current issues related to measurement and use of these data. State of the science literature for the United States and abroad was analyzed and issues were identified for (1) incidence of TBI, (2) prevalence of lifetime history of TBI, and (3) incidence and prevalence of disability associated with TBI. The most recent estimates indicate that each year 235 000 Americans are hospitalized for nonfatal TBI, 1.1 million are treated in emergency departments, and 50 000 die. The northern Finland birth cohort found that 3.8% of the population had experienced at least 1 hospitalization due to TBI by 35 years of age. The Christchurch New Zealand birth cohort found that by 25 years of age 31.6% of the population had experienced at least 1 TBI, requiring medical attention (hospitalization, emergency department, or physician office). An estimated 43.3% of Americans have residual disability 1 year after hospitalization with TBI. [corrected] The most recent estimate of the prevalence of US civilian residents living with disability following hospitalization with TBI is 3.2 million. Estimates of the incidence and prevalence of TBI are based on varying sources of data, methods of calculation, and assumptions. Informed users should be cognizant of the limitations of these estimates when determining their applicability.
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To investigate the efficacy of a novel brain plasticity-based computerized cognitive training program in older adults and to evaluate the effect on untrained measures of memory and attention and participant-reported outcomes. Multisite randomized controlled double-blind trial with two treatment groups. Communities in northern and southern California and Minnesota. Community-dwelling adults aged 65 and older (N=487) without a diagnosis of clinically significant cognitive impairment. Participants were randomized to receive a broadly-available brain plasticity-based computerized cognitive training program (intervention) or a novelty- and intensity-matched general cognitive stimulation program modeling treatment as usual (active control). Duration of training was 1 hour per day, 5 days per week, for 8 weeks, for a total of 40 hours. The primary outcome was a composite score calculated from six subtests of the Repeatable Battery for the Assessment of Neuropsychological Status that use the auditory modality (RBANS Auditory Memory/Attention). Secondary measures were derived from performance on the experimental program, standardized neuropsychological assessments of memory and attention, and participant-reported outcomes. RBANS Auditory Memory/Attention improvement was significantly greater (P=.02) in the experimental group (3.9 points, 95% confidence interval (CI)=2.7-5.1) than in the control group (1.8 points, 95% CI=0.6-3.0). Multiple secondary measures of memory and attention showed significantly greater improvements in the experimental group (word list total score, word list delayed recall, digits backwards, letter-number sequencing; P<.05), as did the participant-reported outcome measure (P=.001). No advantage for the experimental group was seen in narrative memory. The experimental program improved generalized measures of memory and attention more than an active control program.
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Traumatic brain injury (TBI) is a common occurrence, with a rate of nearly 400,000 new injuries per year. Cognitive and emotional disturbances may become persistent and disabling for many injured persons, and frequently involve symptomatic impairment in attention and memory. Impairments in attention and memory have been well characterized in TBI, and are likely related to disruption of cholinergic functioning in the hippocampus. Additionally, disturbances in this neurotransmitter system may also account for disturbances in sensory gating and discriminative attention in this population. The electroencephalographic P50 waveform of the evoked response to paired auditory stimuli may provide a physiologic market of impaired sensory gating among TBI survivors. The first application of this recording assessment to the TBI population is reported. Preliminary findings in three cases are presented, and the interpretation of impaired sensory gating in this population is discussed. Given the impact of TBI on cholinergic systems, the effects of cholinergic augmentation on attention and memory impairment, and the availability of an electrophysiologic marker of cholinergic dysfunction responsive to cholinergic agents, a testable cholinergic hypothesis for investigation and treatment of these patients is proposed.