Brain plasticity (Amsterdam, Netherlands)最新文献

{"title":"Maintaining a Dynamic Brain: A Review of Empirical Findings Describing the Roles of Exercise, Learning, and Environmental Enrichment in Neuroplasticity from 2017-2023.","authors":"Katrina A Milbocker, Ian F Smith, Anna Y Klintsova","doi":"10.3233/BPL-230151","DOIUrl":"10.3233/BPL-230151","url":null,"abstract":"<p><p>Brain plasticity, also termed neuroplasticity, refers to the brain's life-long ability to reorganize itself in response to various changes in the environment, experiences, and learning. The brain is a dynamic organ capable of responding to stimulating or depriving environments, activities, and circumstances from changes in gene expression, release of neurotransmitters and neurotrophic factors, to cellular reorganization and reprogrammed functional connectivity. The rate of neuroplastic alteration varies across the lifespan, creating further challenges for understanding and manipulating these processes to benefit motor control, learning, memory, and neural remodeling after injury. Neuroplasticity-related research spans several decades, and hundreds of reviews have been written and published since its inception. Here we present an overview of the empirical papers published between 2017 and 2023 that address the unique effects of exercise, plasticity-stimulating activities, and the depriving effect of social isolation on brain plasticity and behavior.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11234674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141592257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to: Flavonoids as an Intervention for Alzheimer's Disease: Progress and Hurdles Towards Defining a Mechanism of Action.","authors":"","doi":"10.3233/BPL-239000","DOIUrl":"https://doi.org/10.3233/BPL-239000","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3233/BPL-200098.].</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11234686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141592256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Multifaceted Effects of Flavonoids on Neuroplasticity","authors":"Veronica Rivi, Anuradha Batabyal, Ken Lukowiak","doi":"10.3233/bpl-230150","DOIUrl":"https://doi.org/10.3233/bpl-230150","url":null,"abstract":"There has been a significant increase in the incidence of multiple neurodegenerative and terminal diseases in the human population with life expectancy increasing in the current times. This highlights the urgent need for a more comprehensive understanding of how different aspects of lifestyle, in particular diet, may affect neural functioning and consequently cognitive performance as well as in enhancing overall health. Flavonoids, found in a variety of fruits, vegetables, and derived beverages, provide a new avenue of research that shows a promising influence on different aspects of brain function. However, despite the promising evidence, most bioactive compounds lack strong clinical research efficacy. In the current scoping review, we highlight the effects of Flavonoids on cognition and neural plasticity across vertebrates and invertebrates with special emphasis on the studies conducted in the pond snail, Lymnaea stagnalis, which has emerged to be a functionally dynamic model for studies on learning and memory. In conclusion, we suggest future research directions and discuss the social, cultural, and ethnic dependencies of bioactive compounds that influence how these compounds are used and accepted globally. Bridging the gap between preclinical and clinical studies about the effects of bioactive natural compounds on brain health will surely lead to lifestyle choices such as dietary Flavonoids being used complementarily rather than as replacements to classical drugs bringing about a healthier future.","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136023021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The <i>BDNF</i> Val66Met Polymorphism is a Relevant, But not Determinant, Risk Factor in the Etiology of Neuropsychiatric Disorders - Current Advances in Human Studies: A Systematic Review.","authors":"Gilmara Gomes de Assis, Jay R Hoffman","doi":"10.3233/BPL-210132","DOIUrl":"10.3233/BPL-210132","url":null,"abstract":"<p><p>Brain-derived neurotrophic factor (BDNF) is the brain's most-produced neurotrophin during the lifespan, essentially involved in multiple mechanisms of nervous system development and function. The production/release of BDNF requires multi-stage processing that appears to be regulated at various stages in which the presence of a polymorphism \"Val66Met\" can exert a critical influence.</p><p><strong>Aim: </strong>To synthesize the knowledge on the BDNF Val66Met polymorphism on intracellular processing and function of BDNF.</p><p><strong>Methods: </strong>We performed a systematic review and collected all available studies on the post-translation processes of BDNF, regarding the Val66Met polymorphism. Searches were performed up to 21st March 2021.</p><p><strong>Results: </strong>Out of 129 eligible papers, 18 studies addressed or had findings relating to BDNF post-translation processes and were included in this review.</p><p><strong>Discussion: </strong>Compilation of experimental findings reveals that the Val66Met polymorphism affects BDNF function by slightly altering the processing, distribution, and regulated release of BDNF. Regarding the critical role of pro-BDNF as a pro-apoptotic factor, such alteration might represent a risk for the development of neuropsychiatric disorders.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/89/db/bpl-8-bpl210132.PMC9837733.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10592942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotinamide Mononucleotide Prevents Cisplatin-Induced Mitochondrial Defects in Cortical Neurons Derived from Human Induced Pluripotent Stem Cells.","authors":"Mohammad Abdur Rashid, Alfredo Oliveros, Yu Shin Kim, Mi-Hyeon Jang","doi":"10.3233/BPL-220143","DOIUrl":"10.3233/BPL-220143","url":null,"abstract":"<p><strong>Background: </strong>Chemotherapy-induced cognitive impairment (CICI) is a neurotoxic side effect of chemotherapy that has yet to have an effective treatment.</p><p><strong>Objective: </strong>Using cisplatin, a platinum-based chemotherapy together with excitatory cortical neurons derived from human induced pluripotent cells (iPSCs) to model of CICI, our recent study demonstrated that dysregulation of brain NAD⁺ metabolism contributes to cisplatin-induced impairments in neurogenesis and cognitive function, which was prevented by administration of the NAD⁺ precursor, nicotinamide mononucleotide (NMN). However, it remains unclear how cisplatin causes neurogenic dysfunction and the mechanism by which NMN prevents cisplatin-induced cognitive impairment. Given that mitochondrial dysfunction is thought to play a prominent role in age-related neurodegenerative disease and chemotherapy-induced neurotoxicity, we sought to explore if NMN prevents chemotherapy-related neurotoxicity by attenuating cisplatin-induced mitochondrial damage.</p><p><strong>Results: </strong>We demonstrate that cisplatin induces neuronal DNA damage, increases generation of mitochondrial reactive oxygen species (ROS) and decreases ATP production, all of which are indicative of oxidative DNA damage and mitochondrial functional defects. Ultrastructural analysis revealed that cisplatin caused loss of cristae membrane integrity and matrix swelling in human cortical neurons. Notably, pretreatment with NMN prevents cisplatin-induced defects in mitochondria of human cortical neurons.</p><p><strong>Conclusion: </strong>Our results suggest that increased mitochondrial oxidative stress and functional defects play key roles in cisplatin-induced neurotoxicity. Thus, NMN may be an effective therapeutic strategy to prevent cisplatin-induced deleterious effects on mitochondria, making this organelle a key factor in amelioration of cisplatin-induced cognitive impairments.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b9/ba/bpl-8-bpl220143.PMC9837732.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9336005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proceedings from the Albert Charitable Trust Inaugural Workshop on 'Understanding the Acute Effects of Exercise on the Brain'.","authors":"Jill N Barnes, Jeffrey M Burns, Marcas M Bamman, Sandra A Billinger, Sue C Bodine, Frank W Booth, Patrice Brassard, Tameka A Clemons, Paul J Fadel, Paige C Geiger, Swathi Gujral, Jacob M Haus, Scott E Kanoski, Benjamin F Miller, Jill K Morris, Kristin M S O'Connell, David C Poole, Darleen A Sandoval, J Carson Smith, Russell H Swerdlow, Shawn N Whitehead, Eric D Vidoni, Henriette van Praag","doi":"10.3233/BPL-220146","DOIUrl":"10.3233/BPL-220146","url":null,"abstract":"<p><p>An inaugural workshop supported by \"The Leo and Anne Albert Charitable Trust,\" was held October 4-7, 2019 in Scottsdale, Arizona, to focus on the effects of exercise on the brain and to discuss how physical activity may prevent or delay the onset of aging-related neurodegenerative conditions. The Scientific Program Committee (led by Dr. Jeff Burns) assembled translational, clinical, and basic scientists who research various aspects of the effects of exercise on the body and brain, with the overall goal of gaining a better understanding as to how to delay or prevent neurodegenerative diseases. In particular, research topics included the links between cardiorespiratory fitness, the cerebrovasculature, energy metabolism, peripheral organs, and cognitive function, which are all highly relevant to understanding the effects of acute and chronic exercise on the brain. The Albert Trust workshop participants addressed these and related topics, as well as how other lifestyle interventions, such as diet, affect age-related cognitive decline associated with Alzheimer's and other neurodegenerative diseases. This report provides a synopsis of the presentations and discussions by the participants, and a delineation of the next steps towards advancing our understanding of the effects of exercise on the aging brain.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/93/1a/bpl-8-bpl220146.PMC9837736.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9969539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota-Gut-Brain Axis Regulation of Adult Hippocampal Neurogenesis.","authors":"Katherine E Guzzetta, John F Cryan, Olivia F O'Leary","doi":"10.3233/BPL-220141","DOIUrl":"10.3233/BPL-220141","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6c/f7/bpl-8-bpl220141.PMC9661352.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40517278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Central Adiponectin Signaling - A Metabolic Regulator in Support of Brain Plasticity.","authors":"Douglas A Formolo,&nbsp;Tong Cheng,&nbsp;Jiasui Yu,&nbsp;Georg S Kranz,&nbsp;Suk-Yu Yau","doi":"10.3233/BPL-220138","DOIUrl":"https://doi.org/10.3233/BPL-220138","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a6/65/bpl-8-bpl220138.PMC9661362.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40517280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cathepsin B and Muscular Strength are Independently Associated with Cognitive Control.","authors":"Jeongwoon Kim,&nbsp;Colleen F McKenna,&nbsp;Amadeo F Salvador,&nbsp;Susannah E Scaroni,&nbsp;Andrew T Askow,&nbsp;Jonathan Cerna,&nbsp;Corinne N Cannavale,&nbsp;Scott A Paluska,&nbsp;Michael De Lisio,&nbsp;Steven J Petruzzello,&nbsp;Nicholas A Burd,&nbsp;Naiman A Khan","doi":"10.3233/BPL-210136","DOIUrl":"https://doi.org/10.3233/BPL-210136","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/47/9a/bpl-8-bpl210136.PMC9661349.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40517277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Special Issue: Peripheral Factors and Neural Plasticity.","authors":"Henriette van Praag, Christiane D Wrann","doi":"10.3233/BPL-229001","DOIUrl":"10.3233/BPL-229001","url":null,"abstract":"","PeriodicalId":72451,"journal":{"name":"Brain plasticity (Amsterdam, Netherlands)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ac/64/bpl-8-bpl229001.PMC9661356.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40517275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}