Brain plasticity (Amsterdam, Netherlands)最新文献

Physical activity is a powerful lifestyle factor capable of improving cognitive function, modifying the risk for dementia associated with neurodegeneration and possibly slowing neurodegenerative disease progression in both men and women. However, men and women show differences in the biological responses to physical activity and in the vulnerabilities to the onset, progression and outcome of neurodegenerative diseases, prompting the question of whether sex-specific regulatory mechanisms might differentially modulate the benefits of exercise on the brain. Mechanistic studies aimed to better understand how physical activity improves brain health and function suggest that the brain responds to physical exercise by overall reducing neuroinflammation and increasing neuroplasticity. Here, we review the emerging literature considering sex-specific differences in the immune system response to exercise as a potential mechanism by which physical activity affects the brain. Although the literature addressing sex differences in this light is limited, the initial findings suggest a potential influence of biological sex in the brain benefits of exercise, and lay out a scientific foundation to support very much needed studies investigating the potential effects of sex-differences on exercise neurobiology. Considering biological sex and sex-differences in the neurobiological hallmarks of exercise will help to enhance our understanding of the mechanisms by which physical activity benefits the brain and also improve the development of treatments and interventions for diseases of the central nervous system.

Skeletal muscle health and function are important determinants of systemic metabolic homeostasis and organism-wide responses, including disease outcome. While it is well known that exercise protects the central nervous system (CNS) from aging and disease, only recently this has been found to depend on the endocrine capacity of skeletal muscle. Here, we review muscle-secreted growth factors and cytokines (myokines), metabolites (myometabolites), and other unconventional signals (e.g. bioactive lipid species, enzymes, and exosomes) that mediate muscle-brain and muscle-retina communication and neuroprotection in response to exercise and associated processes, such as the muscle unfolded protein response and metabolic stress. In addition to impacting proteostasis, neurogenesis, and cognitive functions, muscle-brain signaling influences complex brain-dependent behaviors, such as depression, sleeping patterns, and biosynthesis of neurotransmitters. Moreover, myokine signaling adapts feeding behavior to meet the energy demands of skeletal muscle. Contrary to protective myokines induced by exercise and associated signaling pathways, inactivity and muscle wasting may derange myokine expression and secretion and in turn compromise CNS function. We propose that tailoring muscle-to-CNS signaling by modulating myokines and myometabolites may combat age-related neurodegeneration and brain diseases that are influenced by systemic signals.

The term "neural plasticity" was first used to describe non-pathological changes in neuronal structure. Today, it is generally accepted that the brain is a dynamic system whose morphology and function is influenced by a variety of factors including stress, diet, and exercise. Neural plasticity involves learning and memory, the synthesis of new neurons, the repair of damaged connections, and several other compensatory mechanisms. It is altered in neurodegenerative disorders and following damage to the central or peripheral nervous system. Understanding the mechanisms that regulate neural plasticity in both healthy and diseased states is of significant importance to promote cognition and develop rehabilitation techniques for functional recovery after injury. In this minireview, we will discuss the mechanisms by which environmental factors promote neural plasticity with a focus on exercise- and diet-induced factors. We will highlight the known circulatory factors that are released in response to exercise and discuss how all factors activate pathways that converge in part on the activation of BDNF signaling. We propose to harness the therapeutic potential of exercise by using BDNF as a biomarker to identify novel endogenous factors that promote neural plasticity. We also discuss the importance of combining exercise factors with dietary factors to develop a lifestyle pill for patients afflicted by CNS disorders.

Objectives: The objectives of the study were to determine the effect of moderate-intensity exercise (MIE) and high-intensity interval exercise (HIIE) on serum brain-derived neurotrophic factor (BDNF) levels and working memory (WM) in young adult females.

Methodology: This study was conducted in the Physiology Department, Khyber Girls Medical College Peshawar. Young adult females (n = 22), with a mean age of 20±2 years were recruited for two experimental sessions of MIE and HIIE, respectively. Baseline and post exercise blood samples were taken for determination of serum BDNF level and backward digit span test (BDST) for assessment of working memory in both sessions.

Results: Serum BDNF levels pre and post MIE were 707±448 pg/ml and 829±476 pg/ml (p = 0.006) respectively while pre and post HIIE were 785±329 pg /ml and 1116±379 pg/ml (p < 0.001) respectively. BDST scores were significantly high at post intervention for both MIE (p = 0.05) and HIIE (p 0.001).

Conclusions: Altogether our findings showed that both MIE and HIIE significantly increased serum BDNF levels and working memory in young adult females.

 This is a summary of the 2022 Nansen Neuroscience Lectures. On 10 October 2022, Professors Henriette van Praag and David Gems gave the 2022 Nansen Neuroscience Lectures on the theme "Is ageing inevitable?" in the Norwegian Academy of Science and Letters, Oslo, Norway. While van Praag gave a lecture entitled "The benefits of exercise for brain function", Gems gave the 2^nd lecture discussing "What causes ageing? Lessons from The Worm". Understanding the fundamental mechanisms of ageing will pave the way to the development of future interventions to pre-empt the development of the diseases, including Alzheimer's disease and other dementias, of later life.

[This corrects the article DOI: 10.3233/BPL210126.].

Understanding the brain is not only intrinsically fascinating to apprehend life's complexity or to further progress in fundamental biosciences, but it is also highly relevant to increase our well-being since the brain exhibits a power over the body that makes it capable both of triggering illness or facilitating the healing process. Considering the dual role at play by the brain, using ascending and descending pathways to combine information issued from the external world and the internal environment, this review challenges the cerebro-centered vision of the brain. In our daily life, we construct a representation of the outside world by transforming chemical, pressure changes, and light waves into tastes, smells, touches, sounds and sights. In doing so, we create our experience of the external world by interpreting our senses through a process called exteroception. But to be compelling, this Descartes' vision of the brain has to be completed by integration of events from inside our body. The way the brain constructs our inner sensations called interoception, is now starting to be unrevealed. As such, brain sciences have undergone, and will undergo, an important revolution, redefining its boundaries beyond the skull to prefer a more holistic vision carried out by the notion of an embodied brain acting as a coincidence detector to combine sensory experiences with corporeal homeostasis. The goal of this review is to highlight some mechanisms by which the brain activity is controlled by internal cues for better prediction. The gut-brain axis is here taken as a canonical example to discuss about the communication between the milieu intérieur and brain functions that shapes how we feel, and how we think.

Background: Cathepsin B (CTSB) and brain derived neurotrophic factor (BDNF) are increased with aerobic exercise (AE) and skeletal muscle has been identified as a potential source of secretion. However, the intensity of AE and the potential for skeletal muscle contributions to circulating CTSB and BDNF have not been fully studied in humans.

Objective: Determine the effects of AE intensity on circulating and skeletal muscle CTSB and BDNF expression profiles.

Methods: Young healthy subjects (n = 16) completed treadmill-based AE consisting of VO₂max and calorie-matched acute AE sessions at 40%, 65% and 80% VO₂max. Fasting serum was obtained before and 30-minutes after each bout of exercise. Skeletal muscle biopsies (vastus lateralis) were taken before, 30-minutes and 3-hours after the 80% bout. Circulating CTSB and BDNF were assayed in serum. CTSB protein, BDNF protein and mRNA expression were measured in skeletal muscle tissue.

Results: Serum CTSB increased by 20±7% (p = 0.02) and 30±18% (p = 0.04) after 80% and VO₂max AE bouts, respectively. Serum BDNF showed a small non-significant increase (6±3%; p = 0.09) after VO₂max. In skeletal muscle tissue, proCTSB increased 3 h-post AE (87±26%; p < 0.01) with no change in CTSB gene expression. Mature BDNF protein decreased (31±35%; p = 0.03) while mRNA expression increased (131±41%; p < 0.01) 3 h-post AE. Skeletal muscle fiber typing revealed that type IIa and IIx fibers display greater BDNF expression compared to type I (p = 0.02 and p < 0.01, respectively).

Conclusions: High intensity AE elicits greater increases in circulating CTSB compared with lower intensities. Skeletal muscle protein and gene expression corroborate the potential role of skeletal muscle in generating and releasing neuroprotective exerkines into the circulation.NEW AND NOTEWORTHY: 1) CTSB is enriched in the circulation in an aerobic exercise intensity dependent manner. 2) Skeletal muscle tissue expresses both message and protein of CTSB and BDNF. 3) BDNF is highly expressed in glycolytic skeletal muscle fibers.

Background: Aerobic exercise and environmental enrichment have been shown to enhance brain function. Virtual reality (VR) is a promising method for combining these activities in a meaningful and ecologically valid way.

Objective: The purpose of this Phase 2 pilot study was to calculate relative change and effect sizes to assess the impact of simultaneous exercise and cognitive training in VR on brain health and cognition in older adults.

Methods: Twelve cognitively normal older adults (64.7±8.8 years old, 8 female) participated in a 12-week intervention, 3 sessions/week for 25-50 minutes/session at 50-80% HR_max. Participants cycled on a custom-built stationary exercise bike while wearing a VR head-mounted display and navigating novel virtual environments to train spatial memory. Brain and cognitive changes were assessed using MRI imaging and a cognitive battery.

Results: Medium effect size (ES) improvements in cerebral flow and brain structure were observed. Pulsatility, a measure of peripheral vascular resistance, decreased 10.5% (ES(d) = 0.47). Total grey matter volume increased 0.73% (ES(r) = 0.38), while thickness of the superior parietal lobule, a region associated with spatial orientation, increased 0.44% (ES(r) = 0.30). Visual memory discrimination related to pattern separation showed a large improvement of 68% (ES(η _p ²) = 0.43). Cognitive flexibility (Trail Making Test B) (ES(r) = 0.42) and response inhibition (ES(W) = 0.54) showed medium improvements of 14% and 34%, respectively.

Conclusions: Twelve weeks of simultaneous exercise and cognitive training in VR elicits positive changes in brain volume, vascular resistance, memory, and executive function with moderate-to-large effect sizes in our pilot study.