Brain plasticity (Amsterdam, Netherlands)最新文献

Self-control has been defined as the mental capacity of an individual to alter, modify, change or override their impulses, desires, and habitual responses. In this review, we will discuss the bi-directional nature of the relationship between self-control and exercise. In brief, higher levels of trait self-control have been associated with greater exercise performance and adherence; whilst the depletion of state self-control has been shown to decrease performance and persistence on subsequent exercise tasks requiring self-control. In the opposite direction, long-term participation in exercise (and improved physical fitness) has been demonstrated to enhance self-control. Furthermore, an acute bout of exercise has been shown to enhance subsequent self-control, particularly when the exercise is of a moderate intensity and requires some degree of cognitive engagement. Throughout, when discussing each of these relationships, evidence will be drawn from other aspects of the review, where appropriate, to enhance our understanding of the observed effects. Finally, recommendations for future research will be made; including the importance of considering the bi-directional nature of the relationship, given that this has implications for our understanding of both self-control and exercise performance and adherence.

Yoga is the most popular complementary health approach practiced by adults in the United States. It is an ancient mind and body practice with origins in Indian philosophy. Yoga combines physical postures, rhythmic breathing and meditative exercise to offer the practitioners a unique holistic mind-body experience. While the health benefits of physical exercise are well established, in recent years, the active attentional component of breathing and meditation practice has garnered interest among exercise neuroscientists. As the scientific evidence for the physical and mental health benefits of yoga continues to grow, this article aims to summarize the current knowledge of yoga practice and its documented positive effects for brain structure and function, as assessed with MRI, fMRI, and SPECT. We reviewed 11 studies examining the effects of yoga practice on the brain structures, function and cerebral blood flow. Collectively, the studies demonstrate a positive effect of yoga practice on the structure and/or function of the hippocampus, amygdala, prefrontal cortex, cingulate cortex and brain networks including the default mode network (DMN). The studies offer promising early evidence that behavioral interventions like yoga may hold promise to mitigate age-related and neurodegenerative declines as many of the regions identified are known to demonstrate significant age-related atrophy.

Background: Although higher cardiorespiratory fitness (CRF) has been linked to better executive function, the mechanisms by which this occurs remain a matter of speculation. One hypothesis is that higher CRF is associated with elevated top-down control in which brain regions processing task-relevant information are up-regulated and brain regions processing task-irrelevant information are down-regulated.

Methods: We tested this top-down hypothesis in 50 young adults (μ age = 25.22 ± 5.17 years) by measuring CRF via a graded maximal exercise test and performing functional Magnetic Resonance Imaging (fMRI) during a color-word Stroop task. We used task-evoked functional connectivity, quantified from a psychophysiological interaction analysis (PPI), to test our hypotheses that (a) higher CRF would be associated with greater connectivity between control centers (i.e., prefrontal and parietal areas) and visual feature centers (i.e., occipital areas) that are involved with processing task-relevant stimulus dimensions (i.e., color), and (b) higher CRF would be associated with lower connectivity between control centers and visual feature centers that are involved with processing task-irrelevant dimensions of the stimuli (i.e., word processing areas).

Results: Controlling for sex and BMI, we found, consistent with our second hypothesis, that higher CRF was associated with reduced functional connectivity between parietal and occipital areas involved in the task-irrelevant dimension of the task (i.e., word form areas). There were no associations between CRF and functional connectivity with the prefrontal cortex or evidence of heightened connectivity between attentional control and visual feature centers.

Conclusions: These results suggest that CRF associations with executive functioning might be explained by CRF-mediated differences between brain regions involved with attentional control (parietal regions) and the down-regulation of regions involved with processing task-irrelevant stimulus features (occipital regions).

Although both exercise and sleep are significant lifestyle factors in cognitive aging, the interaction of these two factors with respect to cognition remains to be determined. Also, little is known regarding the role of the basal ganglia (BG) in cognitive aging despite its involvement in both sleep and executive function. The primary objective of this study was to investigate the interaction between sleep and acute exercise on executive function performance, and secondarily, to assess if BG volume mediates this interaction. Thirty healthy older adults (65.8±7.3 years) completed 30 minutes of seated rest or moderate-intensity cycling exercise on different days. Structural MRI was used to assess the volumes of BG components including caudate, putamen, and globus pallidus shortly after the experimental conditions. Approximately 90 minutes after each condition, the Stroop task was administered to measure executive function. To examine sleep, participants wore a wrist actigraph for 8.0±3.6 days prior to the first experimental session. Results revealed that while longer total sleep time (TST) was associated with shorter Stroop response time (RT), shorter TST was associated with longer RT after exercise, compared to rest, for both congruent (p = 0.029) and incongruent (p = 0.022) trials. Longer TST was correlated with greater caudate volume, and greater caudate volume was associated with exercise-related improvement in Stroop incongruent RT. Ultimately, we found that the association between longer sleep duration and faster processing speed after acute exercise was mediated by greater caudate volume. These findings suggest that TST is an important factor for acute exercise-induced cognitive improvements in older adults, and that our study is a first step in understanding the interactive effects of these important lifestyle factors in cognitive aging that might simultaneously be addressed to promote healthy cognitive aging. Future studies should examine the interactive effects of sleep and chronic exercise on cognitive function, and whether BG volume might also mediate this interaction.

Acute exercise bouts alter resting state functional connectivity (rs-FC) within cognitive, sensorimotor, and affective networks, but it remains unknown how these effects are influenced by exercise intensity. Twenty-five male athletes underwent individual fitness assessments using an incremental treadmill test. On separate days, they performed 'low' (35% below lactate threshold) and 'high' (20% above lactate threshold) intensity exercise bouts of 30 min. Rs-fMRI and Positive and Negative Affect Scale (PANAS) were acquired before and after each exercise bout. Networks of interest were extracted from twenty-two participants (3 dropouts). Pre-to-post changes and between conditions effects were evaluated using FSL's randomise by applying repeated measures ANOVA. Results were reported at p < 0.05, corrected for multiple comparisons using threshold free cluster enhancement. PANAS revealed a significant increase in positive mood after both exercise conditions. Significant effects were observed between conditions in the right affective and reward network (ARN), the right fronto parietal network (FPN) and the sensorimotor network (SMN). Pre-to-post comparisons after 'low' exercise intensity revealed a significant increase in rs-FC in the left and right FPN, while after 'high'-intensity exercise rs-FC decreased in the SMN and the dorsal attention network (DAN) and increased in the left ARN. Supporting recent findings, this study is the first to report distinct rs-FC alterations driven by exercise intensity: (i) Increased rs-FC in FPN may indicate beneficial functional plasticity for cognitive/attentional processing, (ii) increased rs-FC in ARN may be linked to endogenous opioid-mediated internal affective states. Finally, (iii) decreased rs-FC in the SMN may signify persistent motor fatigue. The distinct effects on rs-FC fit with theories of transient persistent network alterations after acute exercise bouts that are mediated by different exercise intensities and impact differentially on cognitive/attentional or affective responses.

Alzheimer's disease and related dementias (ADRD) represent an increasingly urgent public health concern, with an increasing number of baby boomers now at risk. Due to a lack of efficacious therapies among symptomatic older adults, an increasing emphasis has been placed on preventive measures that can curb or even prevent ADRD development among middle-aged adults. Lifestyle modification using aerobic exercise and dietary modification represents one of the primary treatment modalities used to mitigate ADRD risk, with an increasing number of trials demonstrating that exercise and dietary change, individually and together, improve neurocognitive performance among middle-aged and older adults. Despite several optimistic findings, examination of treatment changes across lifestyle interventions reveals a variable pattern of improvements, with large individual differences across trials. The present review attempts to synthesize available literature linking lifestyle modification to neurocognitive changes, outline putative mechanisms of treatment improvement, and discuss discrepant trial findings. In addition, previous mechanistic assumptions linking lifestyle to neurocognition are discussed, with a focus on potential solutions to improve our understanding of individual neurocognitive differences in response to lifestyle modification. Specific recommendations include integration of contemporary causal inference approaches for analyzing parallel mechanistic pathways and treatment-exposure interactions. Methodological recommendations include trial multiphase optimization strategy (MOST) design approaches that leverage individual differences for improved treatment outcomes.

Fragile X syndrome (FXS) is the most common cause of inherited intellectual disability that can be traced to a single gene mutation. This disorder is caused by the hypermethylation of the Fmr1 gene, which impairs translation of Fragile X Mental Retardation Protein (FMRP). In Fmr1 knockout (KO) mice, the loss of FMRP has been shown to negatively impact adult hippocampal neurogenesis, and to contribute to learning, memory, and emotional deficits. Conversely, physical exercise has been shown to enhance cognitive performance, emotional state, and increase adult hippocampal neurogenesis. In the current experiments, we used two different voluntary running paradigms to examine how exercise impacts adult neurogenesis in the dorsal and ventral hippocampal dentate gyrus (DG) of Fmr1 KO mice. Immunohistochemical analyses showed that short-term (7 day) voluntary running enhanced cell proliferation in both wild-type (WT) and Fmr1 KO mice. In contrast, long-term (28 day) running only enhanced cell proliferation in the whole DG of WT mice, but not in Fmr1 KO mice. Interestingly, cell survival was enhanced in both WT and Fmr1 KO mice following exercise. Interestingly we found that running promoted cell proliferation and survival in the ventral DG of WTs, but promoted cell survival in the dorsal DG of Fmr1 KOs. Our data indicate that long-term exercise has differential effects on adult neurogenesis in ventral and dorsal hippocampi in Fmr1 KO mice. These results suggest that physical training can enhance hippocampal neurogenesis in the absence of FMRP, may be a potential intervention to enhance learning and memory and emotional regulation in FXS.

Aerobic exercise (AE) interventions represent promising therapeutic approaches in disorders that compromise hippocampal integrity, but a more comprehensive account of the neural mechanisms stimulated by AE in the human brain is needed. We conducted a longitudinal pilot-study to assess the impact of a 12-week AE intervention on hippocampal structure and function in 10 healthy, human participants (50% females; 25-59 years). Using a novel combination of multimodal MRI techniques, we found significant increases in left hippocampal volume, Cornu Ammonis subfield area 1, NAA concentration and immediate verbal recall performance. Our preliminary findings highlight the utility of a multimodal approach in assessing hippocampal integrity.

Glypican 4 (Gpc4) is a heparan sulfate proteoglycan that regulates glutamatergic synapse formation and function in the developing brain. Gpc4 KO mice have been shown to have decreased excitatory synapse number and less synaptic GluA1 AMPA receptors, leading to decreased synaptic transmission. Further, decreased expression of Gpc4 has been linked to autism spectrum disorder (ASD). Gpc4 is expressed by both astrocytes and neurons during postnatal development, with astrocyte expression higher in juvenile stages, and neuronal expression increasing with maturation. We therefore asked if mice lacking Gpc4 display behavioral alterations that are consistent with loss of GluA1 or ASD, and if so if they occur at juvenile ages when astrocyte Gpc4 is high, or at adult ages when both astrocytes and neurons express Gpc4. We found that juvenile (P14) Gpc4 KO mice display hyperactivity in the open field, which is corrected in adult mice (3 month). Adult Gpc4 KO mice show deficient behavior in social novelty, whilst non-social behaviors such as working memory and anxiety are unaffected. Thus, Gpc4 KO mice show age-specific behavioral alterations that are consistent with altered synaptic levels of GluA1 and behaviors associated with ASD.