Abstract The increasing availability of ultra-processed, energy dense food is contributing to the spread of the obesity pandemic, which is a serious health threat in today’s world. One possible cause for this association arises from the fact that the brain is wired to derive pleasure from eating. Specifically, food intake activates reward pathways involving dopamine receptor signalling. The reinforcing value of specific food items results from the interplay between taste and nutritional properties. Increasing evidence suggests that nutritional value is sensed in the gut by chemoreceptors in the intestinal tract and the hepatic portal vein, and conveyed to the brain through neuronal and endocrine pathways to guide food selection behaviour. Ultra-processed food is designed to potentiate the reward response through a combination of high fat and high sugar, therebye seeming highly appetizing. There is increasing evidence that overconsumption of processed food distorts normal reward signalling, leading to compulsive eating behaviour and obesity. Hence, it is essential to understand food reward and gut-brain signalling to find an effective strategy to combat the obesity pandemic.
{"title":"Food reward and gut-brain signalling","authors":"Sharmili Edwin Thanarajah, M. Tittgemeyer","doi":"10.1515/nf-2019-0020","DOIUrl":"https://doi.org/10.1515/nf-2019-0020","url":null,"abstract":"Abstract The increasing availability of ultra-processed, energy dense food is contributing to the spread of the obesity pandemic, which is a serious health threat in today’s world. One possible cause for this association arises from the fact that the brain is wired to derive pleasure from eating. Specifically, food intake activates reward pathways involving dopamine receptor signalling. The reinforcing value of specific food items results from the interplay between taste and nutritional properties. Increasing evidence suggests that nutritional value is sensed in the gut by chemoreceptors in the intestinal tract and the hepatic portal vein, and conveyed to the brain through neuronal and endocrine pathways to guide food selection behaviour. Ultra-processed food is designed to potentiate the reward response through a combination of high fat and high sugar, therebye seeming highly appetizing. There is increasing evidence that overconsumption of processed food distorts normal reward signalling, leading to compulsive eating behaviour and obesity. Hence, it is essential to understand food reward and gut-brain signalling to find an effective strategy to combat the obesity pandemic.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"26 1","pages":"1 - 9"},"PeriodicalIF":0.0,"publicationDate":"2020-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45513726","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":"Prof. Dr. med. Dr. med. h.c. Georg W. Kreutzberg","authors":"W. Streit, M. Graeber","doi":"10.1515/nf-2019-0033","DOIUrl":"https://doi.org/10.1515/nf-2019-0033","url":null,"abstract":"","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"26 1","pages":"55 - 56"},"PeriodicalIF":0.0,"publicationDate":"2020-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/nf-2019-0033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44974325","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}
Abstract The gut’s own autonomous nervous system, the enteric nervous system (ENS), has fascinated scientists for more than 100 years. It functions, in the true sense of the word, autonomously, by performing complex tasks and controlling vital functions independently of extrinsic inputs. At the same time, the ENS is bombarded with signals from other cells in the gut wall and lumen and has to integrate all of these inputs. We describe the main functions of the ENS under physiological conditions and give a few examples of its role in gut diseases. The ENS has received increasing attention recently as scientists outside the field of Neurogastroenterology realize its important role in the pathogenesis of Parkinson’s, autism and multiple sclerosis.
{"title":"The enteric nervous system: “A little brain in the gut”","authors":"A. Annaházi, M. Schemann","doi":"10.1515/nf-2019-0027","DOIUrl":"https://doi.org/10.1515/nf-2019-0027","url":null,"abstract":"Abstract The gut’s own autonomous nervous system, the enteric nervous system (ENS), has fascinated scientists for more than 100 years. It functions, in the true sense of the word, autonomously, by performing complex tasks and controlling vital functions independently of extrinsic inputs. At the same time, the ENS is bombarded with signals from other cells in the gut wall and lumen and has to integrate all of these inputs. We describe the main functions of the ENS under physiological conditions and give a few examples of its role in gut diseases. The ENS has received increasing attention recently as scientists outside the field of Neurogastroenterology realize its important role in the pathogenesis of Parkinson’s, autism and multiple sclerosis.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"26 1","pages":"31 - 42"},"PeriodicalIF":0.0,"publicationDate":"2020-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/nf-2019-0027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41614748","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}
Abstract Lysosomes are cellular organelles that are important for the degradation and recycling of various biomolecules. Specialized lysosomal membrane proteins, as well as soluble enzymes, are important for the efficient turn-over of lysosomal substrates. A deficiency in the degradative capacity of lysosomes leads to severe pathologies referred to as lysosomal storage disorders. There is increasing evidence for the importance of lysosomal function in neurodegenerative disorders, including Parkinson’s disease. One reason for this might be the vulnerability of neuronal cells. Since neurons do not undergo further cell division, non-degraded substrates accumulate in aging cells, causing a buildup of toxicity. Recent genomic screenings identified a number of lysosome-associated genes as potential risk factors for Parkinson’s disease, which are discussed in this review. Moreover, it is outlined how targeting lysosomal function might help in developing novel therapeutic strategies.
{"title":"The function of lysosomes and their role in Parkinson’s disease","authors":"Friederike Zunke","doi":"10.1515/nf-2019-0035","DOIUrl":"https://doi.org/10.1515/nf-2019-0035","url":null,"abstract":"Abstract Lysosomes are cellular organelles that are important for the degradation and recycling of various biomolecules. Specialized lysosomal membrane proteins, as well as soluble enzymes, are important for the efficient turn-over of lysosomal substrates. A deficiency in the degradative capacity of lysosomes leads to severe pathologies referred to as lysosomal storage disorders. There is increasing evidence for the importance of lysosomal function in neurodegenerative disorders, including Parkinson’s disease. One reason for this might be the vulnerability of neuronal cells. Since neurons do not undergo further cell division, non-degraded substrates accumulate in aging cells, causing a buildup of toxicity. Recent genomic screenings identified a number of lysosome-associated genes as potential risk factors for Parkinson’s disease, which are discussed in this review. Moreover, it is outlined how targeting lysosomal function might help in developing novel therapeutic strategies.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"26 1","pages":"43 - 51"},"PeriodicalIF":0.0,"publicationDate":"2020-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/nf-2019-0035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45710652","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}
Abstract Age is the greatest risk factor for Alzheimer’s disease (AD). Today, due to an increase in global life expectancy, AD-related deaths are ranked as the sixth most common cause of death. The allele isoform ɛ4 of apolipoprotein E (ApoE4) is the most important genetic risk factor for AD. Three ApoE isoforms are common in humans: ApoE2, ApoE3, and ApoE4. ApoE3 is the most frequent isoform and considered neutral with regards to AD, whereas the isoform ApoE2 is protective. Thus it is important to understand how ApoE isoforms affect amyloid-β (Aβ) and tau toxicity, the key drivers of AD pathology. Aβ and tau accumulate to form the hallmarks of AD, plaques and neurofibrillary tangles, respectively. ApoE, primarily expressed by astrocytes, is the major lipid transporter in the brain. In this review I summarize some important historic and scientific aspects of our progress in understanding the role of the cholesterol transporter ApoE in the brain, and how the isoform ApoE4 contributes to AD pathology.
{"title":"Apolipoprotein E: Cholesterol metabolism and Alzheimer’s pathology","authors":"Theresa Pohlkamp","doi":"10.1515/nf-2019-0030","DOIUrl":"https://doi.org/10.1515/nf-2019-0030","url":null,"abstract":"Abstract Age is the greatest risk factor for Alzheimer’s disease (AD). Today, due to an increase in global life expectancy, AD-related deaths are ranked as the sixth most common cause of death. The allele isoform ɛ4 of apolipoprotein E (ApoE4) is the most important genetic risk factor for AD. Three ApoE isoforms are common in humans: ApoE2, ApoE3, and ApoE4. ApoE3 is the most frequent isoform and considered neutral with regards to AD, whereas the isoform ApoE2 is protective. Thus it is important to understand how ApoE isoforms affect amyloid-β (Aβ) and tau toxicity, the key drivers of AD pathology. Aβ and tau accumulate to form the hallmarks of AD, plaques and neurofibrillary tangles, respectively. ApoE, primarily expressed by astrocytes, is the major lipid transporter in the brain. In this review I summarize some important historic and scientific aspects of our progress in understanding the role of the cholesterol transporter ApoE in the brain, and how the isoform ApoE4 contributes to AD pathology.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"26 1","pages":"25 - 30"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/nf-2019-0030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44495820","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}
Abstract Synapses are key elements in the communication between neurons in any given network of the normal adult, developmental and pathologically altered brain. Synapses are composed of nearly the same structural subelements: a presynaptic terminal containing mitochondria with an ultrastructurally visible density at the pre- and postsynaptic apposition zone. The presynaptic density is composed of a cocktail of various synaptic proteins involved in the binding, priming and docking of synaptic vesicles inducing synaptic transmission. Individual presynaptic terminals (synaptic boutons) contain a couple of hundred up to thousands of synaptic vesicles. The pre- and postsynaptic densities are separated by a synaptic cleft. The postsynaptic density, also containing various synaptic proteins and more importantly various neurotransmitter receptors and their subunits specifically composed and arranged at individual synaptic complexes, reside at the target structures of the presynaptic boutons that could be somata, dendrites, spines or initial segments of axons. Beside the importance of the network in which synapses are integrated, their individual structural composition critically determines the dynamic properties within a given connection or the computations of the entire network, in particular, the number, size and shape of the active zone, the structural equivalent to a functional neurotransmitter release site, together with the size and organization of the three functionally defined pools of synaptic vesicles, namely the readily releasable, the recycling and the resting pool, are important structural subelements governing the ‘behavior’ of synaptic complexes within a given network such as the cortical column. In the late last century, neuroscientists started to generate quantitative 3D-models of synaptic boutons and their target structures that is one possible way to correlate structure with function, thus allowing reliable predictions about their function. The re-introduction of electron microscopy (EM) as an important tool achieved by modern high-end, high-resolution transmission-EM, focused ion beam scanning-EM, CRYO-EM and EM-tomography have enormously improved our knowledge about the synaptic organization of the brain not only in various animal species, but also allowed new insights in the ‘microcosms’ of the human brain in health and disease.
{"title":"Synapses: Multitasking Global Players in the Brain","authors":"J. Lübke, A. Rollenhagen","doi":"10.1515/nf-2019-0015","DOIUrl":"https://doi.org/10.1515/nf-2019-0015","url":null,"abstract":"Abstract Synapses are key elements in the communication between neurons in any given network of the normal adult, developmental and pathologically altered brain. Synapses are composed of nearly the same structural subelements: a presynaptic terminal containing mitochondria with an ultrastructurally visible density at the pre- and postsynaptic apposition zone. The presynaptic density is composed of a cocktail of various synaptic proteins involved in the binding, priming and docking of synaptic vesicles inducing synaptic transmission. Individual presynaptic terminals (synaptic boutons) contain a couple of hundred up to thousands of synaptic vesicles. The pre- and postsynaptic densities are separated by a synaptic cleft. The postsynaptic density, also containing various synaptic proteins and more importantly various neurotransmitter receptors and their subunits specifically composed and arranged at individual synaptic complexes, reside at the target structures of the presynaptic boutons that could be somata, dendrites, spines or initial segments of axons. Beside the importance of the network in which synapses are integrated, their individual structural composition critically determines the dynamic properties within a given connection or the computations of the entire network, in particular, the number, size and shape of the active zone, the structural equivalent to a functional neurotransmitter release site, together with the size and organization of the three functionally defined pools of synaptic vesicles, namely the readily releasable, the recycling and the resting pool, are important structural subelements governing the ‘behavior’ of synaptic complexes within a given network such as the cortical column. In the late last century, neuroscientists started to generate quantitative 3D-models of synaptic boutons and their target structures that is one possible way to correlate structure with function, thus allowing reliable predictions about their function. The re-introduction of electron microscopy (EM) as an important tool achieved by modern high-end, high-resolution transmission-EM, focused ion beam scanning-EM, CRYO-EM and EM-tomography have enormously improved our knowledge about the synaptic organization of the brain not only in various animal species, but also allowed new insights in the ‘microcosms’ of the human brain in health and disease.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"26 1","pages":"11 - 24"},"PeriodicalIF":0.0,"publicationDate":"2019-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44688972","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}
Abstract While earlier neuroscience studies on creativity have been criticized due to their heterogeneity of findings, recent studies in this field have converged to some common practices and methodological approaches, which have greatly contributed to enhance both the reliability and reproducibility of findings in this field. Relevant neuroscience findings suggest that creative cognition requires a conglomerate of neurocognitive processes involving executive functions, memory processes, internally-focused attention, or spontaneous modes of thought. Studies investigating creativity in more naturalistic, real-life settings reveal some overlap with conventional creative ideation, but also indicate that creativity and its underlying neural mechanisms are specific to the particular domain. Another trend in the neuroscience of creativity is concerned with approaches to enhance creativity, involving a broad diversity of interventions ranging from cognitively-oriented techniques to interventions using physical activity.
{"title":"The Neuroscience of Creativity","authors":"A. Fink, M. Benedek","doi":"10.1515/nf-2019-0006","DOIUrl":"https://doi.org/10.1515/nf-2019-0006","url":null,"abstract":"Abstract While earlier neuroscience studies on creativity have been criticized due to their heterogeneity of findings, recent studies in this field have converged to some common practices and methodological approaches, which have greatly contributed to enhance both the reliability and reproducibility of findings in this field. Relevant neuroscience findings suggest that creative cognition requires a conglomerate of neurocognitive processes involving executive functions, memory processes, internally-focused attention, or spontaneous modes of thought. Studies investigating creativity in more naturalistic, real-life settings reveal some overlap with conventional creative ideation, but also indicate that creativity and its underlying neural mechanisms are specific to the particular domain. Another trend in the neuroscience of creativity is concerned with approaches to enhance creativity, involving a broad diversity of interventions ranging from cognitively-oriented techniques to interventions using physical activity.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"25 1","pages":"231 - 240"},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/nf-2019-0006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45422310","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}
Abstract The analysis of large amounts of personal data with artificial neural networks for deep learning is the driving technology behind new artificial intelligence (AI) systems for all areas in science and technology. These AI methods have evolved from applications in computer vision, the automated analysis of images, and now include frameworks and methods for analyzing multimodal datasets that combine data from many different source, including biomedical devices, smartphones and common user behavior in cyberspace. For neuroscience, these widening streams of personal data and machine learning methods provide many opportunities for basic data-driven research as well as for developing new tools for diagnostic, predictive and therapeutic applications for disorders of the nervous system. The increasing automation and autonomy of AI systems, however, also creates substantial ethical challenges for basic research and medical applications. Here, scientific and medical opportunities as well ethical challenges are summarized and discussed.
{"title":"Artificial Intelligence in Basic and Clinical Neuroscience: Opportunities and Ethical Challenges","authors":"P. Kellmeyer","doi":"10.1515/nf-2019-0018","DOIUrl":"https://doi.org/10.1515/nf-2019-0018","url":null,"abstract":"Abstract The analysis of large amounts of personal data with artificial neural networks for deep learning is the driving technology behind new artificial intelligence (AI) systems for all areas in science and technology. These AI methods have evolved from applications in computer vision, the automated analysis of images, and now include frameworks and methods for analyzing multimodal datasets that combine data from many different source, including biomedical devices, smartphones and common user behavior in cyberspace. For neuroscience, these widening streams of personal data and machine learning methods provide many opportunities for basic data-driven research as well as for developing new tools for diagnostic, predictive and therapeutic applications for disorders of the nervous system. The increasing automation and autonomy of AI systems, however, also creates substantial ethical challenges for basic research and medical applications. Here, scientific and medical opportunities as well ethical challenges are summarized and discussed.","PeriodicalId":56108,"journal":{"name":"Neuroforum","volume":"25 1","pages":"241 - 250"},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/nf-2019-0018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49387877","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}
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