Brain Plasticity - Volume 8, issue 1

Authors: van Praag, Henriette | Wrann, Christiane D.

Article Type: Editorial

DOI: 10.3233/BPL-229001

Citation: Brain Plasticity, vol. 8, no. 1, pp. 1-3, 2022

Authors: Mazo, Corey E. | Miranda, Edwin R. | Shadiow, James | Vesia, Michael | Haus, Jacob M.

Article Type: Research Article

Abstract: 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 VO2 max and calorie-matched acute AE sessions at 40%, 65% and 80% VO2 max. 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 VO2 max AE bouts, respectively. Serum BDNF showed a small non-significant increase (6±3%; p  = 0.09) after VO2 max. 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. Show more

Keywords: Human, cathepsin B, brain derived neurotrophic factor

DOI: 10.3233/BPL-220137

Citation: Brain Plasticity, vol. 8, no. 1, pp. 5-18, 2022

Authors: Kim, Jeongwoon | McKenna, Colleen F. | Salvador, Amadeo F. | Scaroni, Susannah E. | Askow, Andrew T. | Cerna, Jonathan | Cannavale, Corinne N. | Paluska, Scott A. | De Lisio, Michael | Petruzzello, Steven J. | Burd, Nicholas A. | Khan, Naiman A.

Article Type: Research Article

Abstract: Although muscular strength has been linked to greater cognitive function across different cognitive domains, the mechanism(s) through which this occurs remain(s) poorly understood. Indeed, while an emerging body of literature suggests peripheral myokines released from muscular contractions may play a role in this relationship, additional research is needed to understand this link. Accordingly, this study sought to compare the influences of a particular myokine, Cathepsin B (CTSB), and muscular strength on hippocampal-dependent relational memory and cognitive control in 40 adults (age = 50.0±7.3 yrs). Overnight fasted venous blood draws were taken to assess plasma CTSB and muscular strength was assessed as maximal …isokinetic strength testing using a Biodex dynamometer. Cognitive performance was assessed using a Spatial Reconstruction Task to assess relational memory and a modified Flanker task to assess cognitive control. Neuroelectric function for cognitive control was assessed using event-related potentials (ERPs) recorded during the Flanker task. Initial bivariate correlational analyses revealed that neither sex, age, lean body mass, or muscular strength was associated with CTSB. However, CTSB was inversely associated with reaction time and fractional peak latency of the P3 component of the Flanker task. Muscular strength was also inversely associated with reaction time and positively associated with relational memory performance. However, the influence of muscular strength on relational memory did not persist following adjustment for covariates. Greater circulating CTSB was selectively associated with greater cognitive control as well as faster information processing speed. These findings are the first to link circulating CTSB to both cognitive control and neuroelectric function. Future intervention studies are needed to examine the effects of changes in muscular strength, circulating myokines, and different domains of cognitive function. Show more

Keywords: Cathepsin B, attentional control, electroencephalography, cognition, physical fitness, muscle strength

DOI: 10.3233/BPL-210136

Citation: Brain Plasticity, vol. 8, no. 1, pp. 19-33, 2022

Authors: Shah, Zubia | Ahmad, Farida | Zahra, Musarrat | Zulfiqar, Fatma | Aziz, Sabeena | Mahmood, Afsheen

Article Type: Research Article

Abstract: 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. Show more

Keywords: Brain-derived neurotrophic factor, females, high intensity interval exercise, moderate intensity exercise, working memory

DOI: 10.3233/BPL-210130

Citation: Brain Plasticity, vol. 8, no. 1, pp. 35-42, 2022

Authors: Rai, Mamta | Demontis, Fabio

Article Type: Review Article

Abstract: 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. Show more

Keywords: Skeletal muscle, central nervous system, myokine, myometabolite, aging, neurodegeneration, feeding behavior, stress signaling, retina, brain

DOI: 10.3233/BPL-210133

Citation: Brain Plasticity, vol. 8, no. 1, pp. 43-63, 2022

Authors: Cortes, Constanza J. | De Miguel, Zurine

Article Type: Review Article

Abstract: 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. Show more

DOI: 10.3233/BPL-220139

Citation: Brain Plasticity, vol. 8, no. 1, pp. 65-77, 2022

Authors: Formolo, Douglas A. | Cheng, Tong | Yu, Jiasui | Kranz, Georg S. | Yau, Suk-Yu

Article Type: Review Article

Abstract: Brain plasticity and metabolism are tightly connected by a constant influx of peripheral glucose to the central nervous system in order to meet the high metabolic demands imposed by neuronal activity. Metabolic disturbances highly affect neuronal plasticity, which underlies the prevalent comorbidity between metabolic disorders, cognitive impairment, and mood dysfunction. Effective pro-cognitive and neuropsychiatric interventions, therefore, should consider the metabolic aspect of brain plasticity to achieve high effectiveness. The adipocyte-secreted hormone, adiponectin, is a metabolic regulator that crosses the blood-brain barrier and modulates neuronal activity in several brain regions, where it exerts neurotrophic and neuroprotective properties. Moreover, adiponectin has been …shown to improve neuronal metabolism in different animal models, including obesity, diabetes, and Alzheimer’s disease. Here, we aim at linking the adiponectin’s neurotrophic and neuroprotective properties with its main role as a metabolic regulator and to summarize the possible mechanisms of action on improving brain plasticity via its role in regulating the intracellular energetic activity. Such properties suggest adiponectin signaling as a potential target to counteract the central metabolic disturbances and impaired neuronal plasticity underlying many neuropsychiatric disorders. Show more

Keywords: Adiponectin, metabolism, stress, brain plasticity, cognition, depression

DOI: 10.3233/BPL-220138

Citation: Brain Plasticity, vol. 8, no. 1, pp. 79-96, 2022

Authors: Guzzetta, Katherine E. | Cryan, John F. | O’Leary, Olivia F.

Article Type: Review Article

Abstract: The birth, maturation, and integration of new neurons in the adult hippocampus regulates specific learning and memory processes, responses to stress, and antidepressant treatment efficacy. This process of adult hippocampal neurogenesis is sensitive to environmental stimuli, including peripheral signals from certain cytokines, hormones, and metabolites, which can promote or hinder the production and survival of new hippocampal neurons. The trillions of microorganisms resident to the gastrointestinal tract, collectively known as the gut microbiota, also demonstrate the ability to modulate adult hippocampal neurogenesis. In doing so, the microbiota-gut-brain axis can influence brain functions regulated by adult hippocampal neurogenesis. Unlike the hippocampus, …the gut microbiota is highly accessible to direct interventions, such as prebiotics, probiotics, and antibiotics, and can be manipulated by lifestyle choices including diet. Therefore, understanding the pathways by which the gut microbiota shapes hippocampal neurogenesis may reveal novel targets for non-invasive therapeutics to treat disorders in which alterations in hippocampal neurogenesis have been implicated. This review first outlines the factors which influence both the gut microbiome and adult hippocampal neurogenesis, with cognizance that these effects might happen either independently or due to microbiota-driven mechanisms. We then highlight approaches for investigating the regulation of adult hippocampal neurogenesis by the microbiota-gut-brain axis. Finally, we summarize the current evidence demonstrating the gut microbiota’s ability to influence adult hippocampal neurogenesis, including mechanisms driven through immune pathways, microbial metabolites, endocrine signalling, and the nervous system, and postulate implications for these effects in disease onset and treatment. Show more

Keywords: Gut microbiome, gut microbiota, hippocampal neurogenesis, hippocampus, neurogenesis, microbiota-gut-brain axis, immune, vagus nerve, short-chain fatty acid, antidepressant, stress, cognition, diet, probiotic

DOI: 10.3233/BPL-220141

Citation: Brain Plasticity, vol. 8, no. 1, pp. 97-119, 2022

Authors: Fakhoury, Marc | Eid, Fady | El Ahmad, Perla | Khoury, Reine | Mezher, Amar | El Masri, Diala | Haddad, Zena | Zoghbi, Yara | Ghayad, Litsa Maria | Sleiman, Sama F. | Stephan, Joseph S.

Article Type: Review Article

Abstract: 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. Show more

Keywords: BDNF, diet, exercise, neural plasticity, beta-hydroxybutyrate, irisin, lactate, osteocalcin

DOI: 10.3233/BPL-220140

Citation: Brain Plasticity, vol. 8, no. 1, pp. 121-128, 2022