Yves Christen – författare

The only way we can convey our thoughts in detail to another person is through verbal language. Does this imply that our thoughts ultimately rely on words? Is there only one way in which thoughts can occur? This ambitious book takes the contrary position, arguing that many possible "languages of thought" play different roles in the life of the mind."Language" is more than communication. It is also a means of representing information in both working and long-term memory. It provides a set of rules for combining and manipulating those representations. A stellar lineup of international cognitive scientists, philosophers, and artists make the book's case that the brain is multilingual. Among topics discussed in the section on verbal languages are the learning of second languages, recovering language after brain damage, and sign language, and in the section on nonverbal languages, mental imagery, representations of motor activity, and the perception and representation of space.

Few people realize how much science can tell us about the differences between men and women. Yves Christen, provided the first comprehensive overview of research in this area when this classic book was first published in the1990s. He goes beyond simplistic "biology is destiny" arguments and constructs a convincing case for linking social and biological approaches in order to understand complex differences in behaviour.Biologists agree that the sexes differ in brain and body structure. Christen links these differences in cerebral anatomy to differences in behaviour and intellect. Taking his readers on a journey through psychology, endocrinology, demography, and many other fields, Christen shows that the biological and the social are not antagonistic. To the contrary, social factors tend to exaggerate the biological rather than neutralize it.This controversial work, Sex Differences, takes on traditional feminism for its refusal to confront the evidence on biologically determined sex differences. Christen argues for a feminism that sees traits common to women in a positive light, in the tradition of such early feminists as Clemence Royer and Margaret Sanger, as well as more contemporary feminist sociobiologists like Sarah Hardy. We deny sex differences only at the price of scientific truth and our own self-respect.

The authors address in particular the role of hormones and their links with other maternal environmental mediators in developmental programming.

Traditionally, neuroscience has considered the nervous system as an isolated entity and largely ignored influences of the social environments in which humans and many animal species live. However, there is mounting evidence that the social environment affects behavior across species, from microbes to humans.This volume brings together scholars who work with animal and human models of social behavior to discuss the challenges and opportunities in this interdisciplinary academic field.

This volume provides the reader with a pathophysiological perspective on the role of CNS in puberty and adolescence, starting from genetic/molecular aspects, going through structural/imaging changes and leading to physical/behavioral characteristics. Therefore, renowned investigators involved in both animal and human research shared recent data as well as overall appraisal of relevant questions around CNS control of puberty and adolescence. No doubt that this volume will inspire those involved in either scientific research or clinical practice or both in the fascinating field of puberty and adolescence.

Recent years have seen spectacular advances in the field of circadian biology. By integrating a circadian view within the fields of endocrinology and metabolism, researchers will be able to reveal many, yet-unsuspected aspects of how organisms cope with changes in the environment and subsequent control of homeostasis.

This book has brought together leading investigators who work in the new arena of brain connectomics. This includes ‘macro-connectome’ efforts to comprehensively chart long-distance pathways and functional networks; ‘micro-connectome’ efforts to identify every neuron, axon, dendrite, synapse, and glial process within restricted brain regions; and ‘meso-connectome’ efforts to systematically map both local and long-distance connections using anatomical tracers. This book highlights cutting-edge methods that can accelerate progress in elucidating static ‘hard-wired’ circuits of the brain as well as dynamic interactions that are vital for brain function. The power of connectomic approaches in characterizing abnormal circuits in the many brain disorders that afflict humankind is considered. Experts in computational neuroscience and network theory provide perspectives needed for synthesizing across different scales in space and time. Altogether, this book provides an integrated view of the challenges and opportunities in deciphering brain circuits in health and disease.

This book brings together leading investigators who represent various aspects of brain dynamics with the goal of presenting state-of-the-art current progress and address future developments. The individual chapters cover several fascinating facets of contemporary neuroscience from elementary computation of neurons, mesoscopic network oscillations, internally generated assembly sequences in the service of cognition, large-scale neuronal interactions within and across systems, the impact of sleep on cognition, memory, motor-sensory integration, spatial navigation, large-scale computation and consciousness. Each of these topics require appropriate levels of analyses with sufficiently high temporal and spatial resolution of neuronal activity in both local and global networks, supplemented by models and theories to explain how different levels of brain dynamics interact with each other and how the failure of such interactions results in neurologic and mental disease. While suchcomplex questions cannot be answered exhaustively by a dozen or so chapters, this volume offers a nice synthesis of current thinking and work-in-progress on micro-, meso- and macro- dynamics of the brain.

This volume provides the reader with a pathophysiological perspective on the role of CNS in puberty and adolescence, starting from genetic/molecular aspects, going through structural/imaging changes and leading to physical/behavioral characteristics.

Traditionally, neuroscience has considered the nervous system as an isolated entity and largely ignored influences of the social environments in which humans and many animal species live. However, there is mounting evidence that the social environment affects behavior across species, from microbes to humans.This volume brings together scholars who work with animal and human models of social behavior to discuss the challenges and opportunities in this interdisciplinary academic field.

This volume starts with an elementary introduction covering stem cell methodologies used to produce specific types of neurons, possibilities for their therapeutic use, and warnings of technical problems.

Recent years have seen spectacular advances in the field of circadian biology. By integrating a circadian view within the fields of endocrinology and metabolism, researchers will be able to reveal many, yet-unsuspected aspects of how organisms cope with changes in the environment and subsequent control of homeostasis.

This book brings together leading investigators who represent various aspects of brain dynamics with the goal of presenting state-of-the-art current progress and address future developments. The individual chapters cover several fascinating facets of contemporary neuroscience from elementary computation of neurons, mesoscopic network oscillations, internally generated assembly sequences in the service of cognition, large-scale neuronal interactions within and across systems, the impact of sleep on cognition, memory, motor-sensory integration, spatial navigation, large-scale computation and consciousness. Each of these topics require appropriate levels of analyses with sufficiently high temporal and spatial resolution of neuronal activity in both local and global networks, supplemented by models and theories to explain how different levels of brain dynamics interact with each other and how the failure of such interactions results in neurologic and mental disease. While suchcomplex questions cannot be answered exhaustively by a dozen or so chapters, this volume offers a nice synthesis of current thinking and work-in-progress on micro-, meso- and macro- dynamics of the brain.

This volume starts with an elementary introduction covering stem cell methodologies used to produce specific types of neurons, possibilities for their therapeutic use, and warnings of technical problems.

The advances in human genetics that have ocurred during the past 20 years have revolutionized our knowledge of the role played by inheritance in health and disase. It is clear that our DNA determines not only the emergence of catastrophic single-gene disorders, which affect millions of persons worldwide, but also interacts with environments to predispose individuals to cancer, allergy, hypertension, heart disease, diabetes, psychiatric disorders and even to some infectious diseases. Overall, the study of longevity and the demonstration of genes favouring a long lifespan suggest that such protective systems exist. In recent years, the study of genetic polymorphisms has made clear that some alleles have beneficial effects. These discoveries can substantially improve our understanding of the interactions between genetics and the environment, between pathogenetic mechanisms and new treatments.

However, cancer and neurodegeneration represent yin-yang counterpoints in the regulation of cell growth, and it is reasonable to hypothesize that key regulatory events mediated by oncogenes and tumor suppressor genes in cancer may also affect neurodegenerative processes

Fifteen of the foremost scientists in this field presented testable theoretical models of consciousness and discussed how our understanding of the role that consciousness plays in our cognitive processes is being refined with some surprising results.

Endocrine disruption is an expanding field due to the numerous chemicals involved and, as evidenced more recently, the variety of homeostatic systems that they can alter throughout life. The gathering of experts from all over the world should help to identify health disorders that are possibly or likely related to exposure to endocrine disrupters. The research needs have been discussed as well as recommendations prioritizing target groups and following the precautionary principle.

However, cancer and neurodegeneration represent yin-yang counterpoints in the regulation of cell growth, and it is reasonable to hypothesize that key regulatory events mediated by oncogenes and tumor suppressor genes in cancer may also affect neurodegenerative processes

Endocrine disruption is an expanding field due to the numerous chemicals involved and, as evidenced more recently, the variety of homeostatic systems that they can alter throughout life. The gathering of experts from all over the world should help to identify health disorders that are possibly or likely related to exposure to endocrine disrupters. The research needs have been discussed as well as recommendations prioritizing target groups and following the precautionary principle.

Neurons daily convert a variety of external stimuli into rapid or long-lasting changes in gene expression. The focus of this volume is on critical epigenetic regulation and chromatin remodeling events that occur in the nervous system and on the presumed mechanisms that operate within neurons to translate them into long-lasting neuronal responses.

The health of the proteome depends upon protein quality control to regulate the proper synthesis, folding, translocation, and clearance of proteins. The cell is challenged constantly by environmental and physiological stress, aging, and the chronic expressions of disease associated misfolded proteins. Substantial evidence supports the hypothesis that the expression of damaged proteins initiates a cascade of molecular events that leads to Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and other diseases of protein conformation.

Avoiding the hyperbole of past treatments of the subject, this book discusses maladies whose diagnoses are much different between males and females. Examples include autism, attention deficit hyperactivity disorders and congenital adrenal hyperplasia.

The misfolding and aggregation of specific proteins is an early and obligatory event in many of the age-related neurodegenerative diseases of humans. The initial cause of this pathogenic cascade and the means whereby disease spreads through the nervous system, remain uncertain. A recent surge of research, first instigated by pathologic similarities between prion disease and Alzheimer’s disease, increasingly implicates the conversion of disease-specific proteins into an aggregate-prone b-sheet-rich state as the prime mover of the neurodegenerative process. This prion-like corruptive protein templating or seeding now characterizes such clinically and etiologically diverse neurological disorders as Alzheimer´s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and frontotemporal lobar degeneration. Understanding the misfolding, aggregation, trafficking and pathogenicity of the affected proteins could therefore reveal universal pathomechanistic principles for some of the most devastating and intractable human brain disorders. It is time to accept that the prion concept is no longer confined to prionoses but is a promising concept for the understanding and treatment of a remarkable variety of diseases that afflict primarily our aging society. ​

The recent advances in Programming Somatic Cell (PSC) including induced Pluripotent Stem Cells (iPS) and Induced Neuronal phenotypes (iN), has changed our experimental landscape and opened new possibilities. The advances in PSC have provided an important tool for the study of human neuronal function as well as neurodegenerative and neurodevelopmental diseases in live human neurons in a controlled environment. For example, reprogramming cells from patients with neurological diseases allows the study of molecular pathways particular to specific subtypes of neurons such as dopaminergic neurons in Parkinson’s Disease, Motor neurons for Amyolateral Sclerosis or myelin for Multiple Sclerosis. Detecting disease-specific molecular signatures in live human brain cells, opens possibilities for early intervention therapies and new diagnostic tools. Importantly, once the neurological neural phenotype is detected in vitro, the so-called “disease-in-a-dish” approach allows for the screening of drugs that can ameliorate the disease-specific phenotype. New therapeutic drugs could either act on generalized pathways in all patients or be patient-specific and used in a personalized medicine approach. However, there are a number of pressing issues that need to be addressed and resolved before PSC technology can be extensively used for clinically relevant modeling of neurological diseases. Among these issues are the variability in PSC generation methods, variability between individuals, epigenetic/genetic instability and the ability to obtain disease-relevant subtypes of neurons . Current protocols for differentiating PSC into specific subtypes of neurons are under development, but more and better protocols are needed. Understanding the molecular pathways involved in human neural differentiation will facilitate the development of methods and tools to enrich and monitor the generation of specific subtypes of neurons that would be more relevant in modeling differentneurological diseases.

Recent years have seen spectacular advances in the filed of epigenetics. These have attracted the interest of researchers in many fields and evidence connecting epigentic regulation to brain functions has been accumulationg. Neurons daily convert a variety of external stimuli into rapid or long-lasting changes in gene expression. A variety of studies have centered on the molcular mechanisms implicated in epigentic control and how these may operte in concert. It will be critical to unravel how specifity is achieved. The focus of this volume is on critical epigenetic regulation and chromatin remodeling events that occur in the nervous system and on the presumed mechanisms that operate within neurons to translate them into long-lasting neuronal responses.

The misfolding and aggregation of specific proteins is an early and obligatory event in many of the age-related neurodegenerative diseases of humans. The initial cause of this pathogenic cascade and the means whereby disease spreads through the nervous system, remain uncertain. A recent surge of research, first instigated by pathologic similarities between prion disease and Alzheimer’s disease, increasingly implicates the conversion of disease-specific proteins into an aggregate-prone b-sheet-rich state as the prime mover of the neurodegenerative process. This prion-like corruptive protein templating or seeding now characterizes such clinically and etiologically diverse neurological disorders as Alzheimer´s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and frontotemporal lobar degeneration. Understanding the misfolding, aggregation, trafficking and pathogenicity of the affected proteins could therefore reveal universal pathomechanistic principles for some of the most devastating and intractable human brain disorders. It is time to accept that the prion concept is no longer confined to prionoses but is a promising concept for the understanding and treatment of a remarkable variety of diseases that afflict primarily our aging society. ​

The health of the proteome depends upon protein quality control to regulate the proper synthesis, folding, translocation, and clearance of proteins. The cell is challenged constantly by environmental and physiological stress, aging, and the chronic expressions of disease associated misfolded proteins. Substantial evidence supports the hypothesis that the expression of damaged proteins initiates a cascade of molecular events that leads to Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and other diseases of protein conformation.

The recent advances in Programming Somatic Cell (PSC) including induced Pluripotent Stem Cells (iPS) and Induced Neuronal phenotypes (iN), has changed our experimental landscape and opened new possibilities. The advances in PSC have provided an important tool for the study of human neuronal function as well as neurodegenerative and neurodevelopmental diseases in live human neurons in a controlled environment. For example, reprogramming cells from patients with neurological diseases allows the study of molecular pathways particular to specific subtypes of neurons such as dopaminergic neurons in Parkinson’s Disease, Motor neurons for Amyolateral Sclerosis or myelin for Multiple Sclerosis. Detecting disease-specific molecular signatures in live human brain cells, opens possibilities for early intervention therapies and new diagnostic tools. Importantly, once the neurological neural phenotype is detected in vitro, the so-called “disease-in-a-dish” approach allows for the screening of drugs that can ameliorate the disease-specific phenotype. New therapeutic drugs could either act on generalized pathways in all patients or be patient-specific and used in a personalized medicine approach. However, there are a number of pressing issues that need to be addressed and resolved before PSC technology can be extensively used for clinically relevant modeling of neurological diseases. Among these issues are the variability in PSC generation methods, variability between individuals, epigenetic/genetic instability and the ability to obtain disease-relevant subtypes of neurons . Current protocols for differentiating PSC into specific subtypes of neurons are under development, but more and better protocols are needed. Understanding the molecular pathways involved in human neural differentiation will facilitate the development of methods and tools to enrich and monitor the generation of specific subtypes of neurons that would be more relevant in modeling differentneurological diseases.