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.

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 such complex 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. In addition the authors report successes in achieving the derivation of a specific type of neuron. The dopamine neuron offers an important example and is discussed in more detail. Additional chapters cover problems obviously approachable with cells derived from stem cells, including their need in surgeries for pituitary cancers. The last chapter provides an overview of this particular field of research and presents a vision for its future directions.

Recent years have seen spectacular advances in the field of circadian biology. These have attracted the interest of researchers in many fields, including endocrinology, neurosciences, cancer, and behavior. 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 field is opening new avenues in our understanding of metabolism and endocrinology. A panel of the most distinguished investigators in the field gathered together to discuss the present state and the future of the field. The editors trust that this volume will be of use to those colleagues who will be picking up the challenge to unravel how the circadian clock can be targeted for the future development of specific pharmacological strategies toward a number of pathologies.

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 different neurological diseases.

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.

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.

In theoretical terms, sex differences in brains and behaviors of laboratory animals offer the possibility of fascinating scientific studies on a range of molecular phenomena such as genomic imprinting, DNA methylation, chromatin protein modification, non-coding DNA, potentially resulting in important neuroanatomical and neurochemical sex differences in the brain. Such sex differences could arise consequent to exposures to testosterone early in development, or to other effects deriving from the Y chromosome. However, this general subject has been treated with much hyperbole. Historically, sex differences were assumed to be present where they did not really exist, e.g. with respect to mathematics, executive leadership, etc. etc. Under what circumstances do we really care about sex differences in brain and behavior? These circumstances concern human maladies whose diagnoses are much different between boys and girls, or between women and men. Prominent examples discussed in this volume include autism, attention deficit hyperactivity disorders and congenital adrenal hyperplasia. In fact, infant boys are more susceptible than infant girls to a variety of disorders that arise early in development. This volume then ends with a consideration of effects of estrogenic hormones on the injured brain, and their roles as protective agents.

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.

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. In addition the authors report successes in achieving the derivation of a specific type of neuron. The dopamine neuron offers an important example and is discussed in more detail. Additional chapters cover problems obviously approachable with cells derived from stem cells, including their need in surgeries for pituitary cancers. The last chapter provides an overview of this particular field of research and presents a vision for its future directions.

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 such complex 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.

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 Alzheimers 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.

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 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 authors address in particular the role of hormones and their links with other maternal environmental mediators in developmental programming. The crucial nature of the placenta as an interface and target between maternal and foetal environments is addressed. Emphasis is made on the emerging science of epigenetics as a potential explanation for how environmental events that occur during brief windows of development may exert effects that impact upon somatic cells through many rounds of mitosis for much of the life span of the subsequent organism.

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. Also, this field is at the edge of several disciplines with implications of both laboratory scientists and clinicians. This symposium aims at updating mechanisms and consequences of endocrine disruption in three perspectives: neural, metabolic and reproductive. The gathering of experts from all over the world should help the participants to identify health disorders that are possibly or likely related to exposure to endocrine disrupters. The research needs will be discussed as well as recommendations prioritizing target groups and following the precautionary principle.

Homeostasis involves a delicate interplay between generative and degenerative processes to maintain a stable internal environment. In biological systems, equilibrium is established and controlled through a series of negative feedback mechanisms driven by a range of signal transduction processes. Failures in these complex communication pathways result in instability leading to disease. Cancer represents a state of imbalance caused by an excess of cell proliferation. In contrast, neurodegeneration is a consequence of excessive cell loss in the nervous system. Both of these disorders exhort profound tolls on humanity and they have been subject to a great deal of research designed to ameliorate this suffering. For the most part, the topics have been viewed as distinct and rarely do opportunities arise for transdisciplinary discussions among experts in both fields. 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

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 Alzheimers 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 two greatest medical fears of the aging population are cancer and Alzheimer's disease. Despite dramatic advances in understanding the molecular etiology of these disorders, therapeutic options for many patients with advanced disease have changed little and outcomes remain dismal. Paradoxically, recent findings suggest that some of the same molecules and biochemical processes underlying cancer may also participate in neurodegeneration. Therefore, it would be very useful to bring together experts from the fields of cancer research and neurodegeneration for discussions of the latest advances and ideas, with a particular emphasis on areas of overlap, to stimulate transdisciplinary interactions with the hope of accelerating progress. Cancer arises as a consequence of a breakdown in the genetic and epigenetic processes governing cell proliferation and cell death. Alterations in several classes of signaling molecules, both oncogenes and tumor suppressor genes, lead to uncontrolled cell growth. Over the past two decades, details of the intricate signaling pathways, from cell surface receptors through protein kinase cascades, transcription factors and modulators of chromatin, as well as the DNA damage response pathways linked to cell cycle control that guard the genome, have been uncovered. In some instances, key regulatory proteins have provided novel targets for development of small molecule inhibitors that are currently being tested in the clinic. The development of the nervous system relies on many of the signaling pathways and growth control processes that go awry in cancer. However, in mature neurons, the very same signaling proteins participate in transduction cascades linking short-term stimuli, elicited by synaptic stimulation, to long-term alterations in neuronal circuits through the regulation of gene expression and chromatin structure. These long-term adaptive modifications lead to changes in synaptic structure and function that

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.

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.