Brain plasticity (Amsterdam, Netherlands)最新文献

Objectives: In this pilot study, we evaluated the use of electrophysiological measures at rest as paradigm-independent predictors of second language (L2) development for the first time in older adult learners. We then assessed EEG correlates of the learning outcome in a language-switching paradigm after the training, which to date has only been done in younger adults and at intermediate to advanced L2 proficiency.

Methods: Ten (Swiss) German-speaking adults between 65-74 years of age participated in an intensive 3-week English training for beginners. A resting-state EEG was recorded before the training to predict the ensuing L2 development (Experiment 1). A language-switching ERP experiment was conducted after the training to assess the learning outcome (Experiment 2).

Results: All participants improved their L2 skills but differed noticeably in their individual development. Experiment 1 showed that beta1 oscillations at rest (13-14.5 Hz) predicted these individual differences. We interpret resting-state beta1 oscillations as correlates of attentional capacities and semantic working memory that facilitate the extraction and processing of novel forms and meanings from the L2 input.In Experiment 2, we found that language switching from the L2 into the native language (L1) elicited an N400 component, which was reduced in the more advanced learners. Thus, for learners beginning the acquisition of an L2 in third age, language switching appears to become less effortful with increasing proficiency, suggesting that the lexicons of the L1 and L2 become more closely linked.

Conclusions: In sum, our findings extend the available evidence of neurological processes in L2 learning from younger to older adults, suggesting that electrophysiological mechanisms are similar across the lifespan.

Background: Cognitive impairment is common among adolescent and young adult (AYA) cancer survivors. Physical activity (PA) may help mitigate cognitive impairment post-treatment by positively impacting two indicators of general brain health: fractional anisotropy (FA) and functional connectivity (FC). As part of a two-arm, mixed-methods pilot randomized controlled trial (RCT), this sub-study was designed to provide preliminary proof-of-concept evidence for the effects of PA on FA and FC among AYA cancer survivors post-treatment to help inform decisions about proceeding to larger trials.

Methods: AYA cancer survivors who had completed cancer treatment and who were enrolled in a larger pilot RCT comparing a 12-week PA intervention to a waitlist control group, were invited to participate in this sub-study. Sub-study participants completed diffusion tensor imaging and resting-state functional magnetic resonance imaging prior to randomization and post-intervention. Data were analyzed with descriptive statistics, independent component analysis, and paired sample t-tests.

Results: Post-intervention, participants showed increases in FA of the bilateral hippocampal cingulum, left anterior corona radiata, middle cingulum, left anterior thalamic radiation, and left cerebellum. A decrease in overall FC of the default mode network and increases in the cerebellar and visual networks were also noted post-intervention (p < .05).

Conclusion: Results provide preliminary evidence for the possible positive effects of PA on FA and FC among AYA cancer survivors post-treatment. On the basis of these results, larger trials assessing the effects of PA on specific brain health indicators, as captured by FA and FC, among AYA cancer survivors are appropriate and warranted.

Background: Previous studies found traditional Chinese mind-body exercise Baduanjin could modulate cognition of community older adults.

Objective: This study aims to investigate the effect of 6 months of Baduanjin exercise on brain structure and cognitive function in older adults with mild cognitive impairment (MCI).

Methods: The MCI older adults were randomly assigned into either Baduanjin training, brisk walking training or usual physical activity control group. Magnetic Resonance Imaging (MRI), Montreal Cognitive Assessment (MoCA) and Wechsler Memory Scale-Chinese Revised (WMS-CR) were applied to measure gray matter volume (GMV), global cognitive ability and memory at baseline and end of intervention.

Results: Compared to usual physical activity, Baduanjin exercise significantly improved MoCA, WMS-CR scores, WMS-MQ, and mental control and comprehension memory subscores of the WMS-CR; significantly increased the GMV in the temporal gyrus, frontal gyrus, parietal gyrus, medial occipital gyrus, cingulate gyrus and angular gyrus after 6 months of intervention. Compared to brisk walking, Baduanjin significantly improved MoCA scores and picture reproduction subscores of memory, and significantly increased the GMV in the right frontal gyrus, precentral gyrus, occipital gyrus. Furthermore, the increased GMV in the right medial temporal gyrus was significantly associated with improvement in the MoCA scores.

Conclusion: The present study suggested that regular Baduanjin training could have a positive effect in increasing brain gray matter and improving cognitive function in older adults with MCI.

Tyro3, Axl and Mertk are members of the TAM family of tyrosine kinase receptors. TAMs are activated by two structurally homologous ligands GAS6 and PROS1. TAM receptors and ligands are widely distributed and often co-expressed in the same cells allowing diverse functions across many systems including the immune, reproductive, vascular, and the developing as well as adult nervous systems. This review will focus specifically on TAM signaling in the nervous system, highlighting the essential roles this pathway fulfills in maintaining cell survival and homeostasis, cellular functions such as phagocytosis, immunity and tissue repair. Dysfunctional TAM signaling can cause complications in development, disruptions in homeostasis which can rouse autoimmunity, neuroinflammation and neurodegeneration. The development of therapeutics modulating TAM activities in the nervous system has great prospects, however, foremost we need a complete understanding of TAM signaling pathways.

Background: MERTK encodes a receptor tyrosine kinase that regulates immune homeostasis via phagocytosis of apoptotic cells and cytokine-mediated immunosuppression. MERTK is highly expressed in the central nervous system (CNS), specifically in myeloid derived innate immune cells and its dysregulation is implicated in CNS pathologies including the autoimmune disease multiple sclerosis (MS).

Objective: While the cell types and tissues that express MERTK have been well described, the genetic elements that define the gene's promoter and regulate specific transcription domains remain unknown. The primary objective of this study was to define and characterise the human MERTK promoter region.

Methods: We cloned and characterized the 5' upstream region of MERTK to identify cis-acting DNA elements that promote gene transcription in luciferase reporter assays. In addition, promoter regions were tested for sensitivity to the anti-inflammatory glucocorticoid dexamethasone.

Results: This study identified identified both proximal and distal-acting DNA elements that promote transcription. The strongest promoter activity was identified in an ∼850 bp region situated 3 kb upstream of the MERTK transcription start site. Serial deletions of this putative enhancer revealed that the entire region is essential for expression activity. Using in silico analysis, we identified several candidate transcription factor binding sites. Despite a well-established upregulation of MERTK in response to anti-inflammatory glucocorticoids, no DNA region within the 5 kb putative promoter was found to directly respond to dexamethasone treatment.

Conclusions: Elucidating the genetic mechanisms that regulate MERTK expression gives insights into gene regulation during homeostasis and disease, providing potential targets for therapeutic modulation of MERTK transcription.

Interleukin-1 (IL-1) is an inflammatory cytokine that has been shown to modulate neuronal signaling in homeostasis and diseases. In homeostasis, IL-1 regulates sleep and memory formation, whereas in diseases, IL-1 impairs memory and alters affect. Interestingly, IL-1 can cause long-lasting changes in behavior, suggesting IL-1 can alter neuroplasticity. The neuroplastic effects of IL-1 are mediated via its cognate receptor, Interleukin-1 Type 1 Receptor (IL-1R1), and are dependent on the distribution and cell type(s) of IL-1R1 expression. Recent reports found that IL-1R1 expression is restricted to discrete subpopulations of neurons, astrocytes, and endothelial cells and suggest IL-1 can influence neural circuits directly through neuronal IL-1R1 or indirectly via non-neuronal IL-1R1. In this review, we analyzed multiple mechanisms by which IL-1/IL-1R1 signaling might impact neuroplasticity based upon the most up-to-date literature and provided potential explanations to clarify discrepant and confusing findings reported in the past.

Precipitous declines in cognitive function can occur in older individuals following a variety of peripheral immune insults, such as surgery, infection, injury, and unhealthy diet. Aging is associated with numerous changes to the immune system that shed some light on why this abrupt cognitive deterioration may occur. Normally, peripheral-to-brain immune signaling is tightly regulated and advantageous; communication between the two systems is bi-directional, via either humoral or neural routes. Following an immune challenge, production, secretion, and translocation of cytokines into the brain is critical to the development of adaptive sickness behaviors. However, aging is normally associated with neuroinflammatory priming, notably microglial sensitization. Microglia are the brain's innate immune cells and become sensitized with advanced age, such that upon immune stimulation they will mount more exaggerated neuroimmune responses. The resultant elevation of pro-inflammatory cytokine expression, namely IL-1β, has profound effects on synaptic plasticity and, consequentially, cognition. In this review, we (1) investigate the processes which lead to aberrantly elevated inflammatory cytokine expression in the aged brain and (2) examine the impact of the pro-inflammatory cytokine IL-1β on brain plasticity mechanisms, including its effects on BDNF, AMPA and NMDA receptor-mediated long-term potentiation.