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Take a global tour of childhood that spans 50 countries and explore everyday questions such as 'Why does love matter?', 'How do children learn right from wrong'? and 'Why do adolescent relationships feel like a matter of life and death?' Combining psychology, anthropology, and evolution, you will learn about topics such as language, morality, empathy, creativity, learning and cooperation. Discover how children's skills develop, how they adapt to solve challenges, and what makes you, you. Divided into three chronological sections – early years, middle childhood, and adolescence – this book is enriched with a full set of pedagogical features, including key points to help you retain the main takeaway of each section, space for recap, a glossary of key terms, learning outcomes and chapter summaries. Embedded videos and animations throughout bring ideas to life and explain the methods researchers use to reveal the secrets of child development.
Attention is critical to our daily lives, from simple acts of reading or listening to a conversation to the more demanding situations of trying to concentrate in a noisy environment or driving on a busy roadway. This book offers a concise introduction to the science of attention, featuring real-world examples and fascinating studies of clinical disorders and brain injuries. It introduces cognitive neuroscience methods and covers the different types and core processes of attention. The links between attention, perception, and action are explained, along with exciting new insights into the brain mechanisms of attention revealed by cutting-edge research. Learning tools – including an extensive glossary, chapter reviews, and suggestions for further reading – highlight key points and provide a scaffolding for use in courses. This book is ideally suited for graduate or advanced undergraduate students as well as for anyone interested in the role attention plays in our lives.
Suicidality is a significant public health concern, with neuroimaging studies revealing abnormalities in the brains of suicidal individuals and post-mortem samples. However, the genetic architecture between suicidality and subcortical brain volumes remains poorly characterized. Using genome-wide association studies (GWAS), we investigated the genetic overlap between suicidality and subcortical brain volume. GWAS summary statistics for suicidal behaviours, including Suicide Attempts, Ever Self-Harmed, and Thoughts of Life Not Worth Living, from the UK Biobank, Suicide from the FinnGen Biobank, and data on seven subcortical brain volumes and Intracranial Volume from the ENIGMA2 study, were used to investigate the genetic correlation between phenotypes as well as potential genetic factors. A common genetic factor was identified, comprising two categories: Suicide Attempt, Ever Self-Harmed, and Thoughts of Life Not Worth Living from the UK Biobank, and Suicide from FinnGen, Intracranial Volume, and subcortical brain volumes. Cross-phenotype GWAS meta-analysis of each category at variant, gene and subnetwork levels unveils a list of significant variants (P-value <5 × 10−8), and potential hub genes (P-value <0.05) of consideration. Network, pathway, and Gene Ontology analyses of these joint categories highlighted enriched pathways and biological processes related to blood-brain barrier permeability suggesting that the presence and severity of suicidality are associated with an inflammatory signature detectable in both blood and brain tissues. This study underscores the role of brain and peripheral blood inflammation in suicide risk and holds promise for developing targeted interventions and personalized treatment strategies to reduce suicidality in at-risk populations.
This chapter comes in two related but distinct parts. The first presents general trends in the neurosciences and considers how these impact upon psychiatry as a clinical science. The second picks up a recent and important development in neuroscience which seeks to explain mental functions such as perception and has been profitably extended into explanations of psychopathology. The second part can be viewed as a working example of the first’s overarching themes.
Accounts of genetic findings involve concepts which can prove challenging. Terminology may be unfamiliar, and some words have specialised meanings and may not always be used consistently. This chapter aims to provide an overview of the key concepts. The subject matter is intrinsically dense and can be hard to take in, so the reader may wish to skim parts of this section and then refer back to it when necessary.
This chapter provides a brief review of basic neuroanatomy, followed by a more detailed description of structures and pathways important for neuropsychiatric practice. The focus will be on the limbic brain and the functional anatomy of emotion, memory, cognition and behaviour. A more comprehensive review of general neuroanatomy can be found in standard textbooks such as Johns, Clinical Neuroscience.
Information travels through the brain as electrical signals along a complex network of interconnecting nerve cells called neurons.
Neurons connect to each other at synapses, small gaps where chemicals called neurotransmitters amplify or muffle the electrical signals.
The reward pathway determines our experience of pleasure and many psychoactive drugs work by over-stimulating this pathway.
After using psychoactive drugs, the brain needs time to recover. This is often experienced as a psychological ‘crash’ or ‘come down’.
If a drug is used regularly, the desired effects become harder to achieve – a process called tolerance.
People who use drugs often increase the amount of drug they take over time in an attempt to overcome tolerance. This increases the risk of drug-related harm.
Regular psychoactive drug user ends up altering brain functioning, making it much harder to enjoy non-drug experiences. The world can become joyless.
Adolescence is the period between the onset of puberty and the point at which adult roles are assumed and involves rapid physical, psychological and social change.
In adolescence, learning takes place as the brain establishes neural networks. These networks are constantly modified by new experiences.
The adolescent brain develops in stages. One of the last areas to develop are the frontal lobes, the part of the brain responsible for decision-making and assessing risk.
Just when the adolescent brain is at this delicate developmental phase, it is also most impulsive and drug use is most likely.
Drug use in adolescence disrupts brain development, which can lead to long-term damage to brain function and increase the risk of further drug use.
Many adolescents are surprisingly poorly informed about drugs, their effects and the harms they can cause.
Adolescents tend to seek information about drugs from the internet or friends.
Accurate information is available and should be highlighted to adolescents.
The beginning of the third millennium, starting in the early noughties and increasing in strength throughout the 2010s, has seen a large shift in theoretical focus in the mind sciences. In what might be called the predictive revolution or the predictive turn, many researchers in the psychological and brain sciences have come to consider the human mind a ‘predictive engine’ or ‘prediction machine.’ Like its predecessor, the cognitive revolution, more than half a century before, the predictive revolution is grand in ambition. It tries to explain all mental processes within one common framework. In this unified theory, the functioning of the mind is no longer best explained as an information processor: Minds have become prediction systems. The predictive revolution promises to reconcile cognition and behavior as the intrinsically connected two sides of the same coin serving human interactions with the environment.
Fully updated and revised, Cognitive and Social Neuroscience of Aging, 2nd Edition provides an accessible introduction to aging and the brain. Now with full color throughout, it includes over fifty figures illustrating key research findings and anatomical diagrams. Adopting an integrative perspective across domains of psychological function, this edition features expanded coverage of multivariate methods, moral judgments, cognitive reserve, prospective memory, event boundaries, and individual differences related to aging, including sex, race, and culture. Although many declines occur with age, cognitive neuroscience research reveals plasticity and adaptation in the brain as a normal function of aging. With this perspective in mind, the book emphasizes the ways in which neuroscience methods have enriched and changed thinking about aging.
This study aimed to utilise graph theory to explore the functional brain networks in individuals with tic disorders and to investigate resting-state functional connectivity changes in critical brain regions associated with tic disorders.
Methods:
Participants comprised individuals with tic disorders and age-matched healthy controls, ranging from 6 to 18 years old, all recruited from Korea University Guro Hospital. We ensured a medication-naïve cohort by excluding participants exposed to psychotropic medications for at least three weeks prior to the study. Data included structural and resting-state functional MRI scans, analysed with the CONN-fMRI Functional Connectivity toolbox v20b. The analysis included 22 patients (18 males, 4 females) and 26 controls (14 males, 12 females).
Results:
Significantly increased global efficiency was observed in the left inferior frontal gyrus pars opercularis among tic disorder patients compared to controls. Furthermore, this region displayed enhanced resting-state functional connectivity with its right counterpart in patients versus controls.
Conclusion:
The inferior frontal gyrus pars opercularis, known for its inhibitory role, may reflect adaptive functional adjustments in response to tic symptoms. Increased hubness of the inferior frontal gyrus pars opercularis possibly represents functional adjustments in response to tic symptoms. The identified brain region with increased efficiency and connectivity presents a promising avenue for further research into tic expression and control mechanisms.
This chapter starts by summarising an experiment showing how the brain’s emotion circuitry responds to a set of words signalling threat. The main emotion activated in Brexitspeak is fear; the triggers are both linguistic and visual. They include representation of alarming scenarios, and factual misrepresentations capable of causing various negative emotions. The chapter analyses three well-known cases that illustrate such effects. The first is Vote Leave’s propaganda displayed on the side of a red bus: the slogan was an inaccurate statement that could evoke feelings of attachment, resentment and anger. This is also analysed in terms of speech acts, ambiguous and deniable assertions, and lying. The second case, the rightly controversial ‘breaking point’ poster displayed by Leave.EU had the avowed goal of emotion arousal. The visual element is analysed with reference to cognitive image schemas, and their potential for activating fear reactions. The third case, the most effective of the Vote Leave campaign, was crafted in order to prompt the fear of losing agency. This, too, likely activated the brain’s fear circuitry.
The Automatic Selective Perception (ASP) model posits that listeners make use of selective perceptual routines (SPRs) that are fast and efficient for recovering lexical meaning. These SPRs serve as filters to accentuate relevant cues and minimize irrelevant information. Years of experience with the first language (L1) lead to fairly automatic L1 SPRs; consequently, few attentional resources are needed in processing L1 speech. In contrast, L2 SPRs are less automatic. Under difficult task or stimulus conditions, listeners fall back on more automatic processes, specifically L1 SPRs. And L2 speech perception suffers where there is a mismatch between the L1 and the L2 phonetics because L1 SPRs may not extract the important cues needed for identifying L2 phonemes. This chapter will present behavioral and neurophysiology evidence that supports the ASP model, but which also indicates the need for some modification. We offer suggestions for future directions in extending this model.
Humans have the ability to recognize that when they perform actions, they produce effects in the external world. Even though humans are not the only animalsl with this mental capacity, their ability to perform actions is accompanied by a feeling of authorship, a feeling that “I” am the one who did it. This is what academics have called the sense of agency. When individuals claim reduced responsibility because they were “only obeying orders”, this defense is often viewed with skepticism, because the defendant has a clear motive of avoiding punishment. However, scientific methods can now be used to investigate the experience of receiving orders and how it influences how the brain processes information. As this chapter shows, obeying orders impacts the sense of agency and the feeling of responsibility at the brain level. Further, working and living in some highly hierarchical and sometimes coercive social structures, such as the military, can also impact the sense of agency when people make decisions. It thus appears that hierarchies provide a powerful ground to obtain a reduced feeling of responsibility and agency in individuals.
When we witness another person experiencing pain, be it emotional or physical, we have an empathic reaction. And even if we commit a harmful action against another person, we most of the time experience guilt in the aftermath, which prevents us from performing the same action in the future. Guilt and empathy are critical moral emotions that together usually prevent us from harming others. However, as this chapter shows, systematic processes of classification and dehumanization at play before a genocide can alter moral emotions towards another part of the population. Activity in empathy-related brain regions is generally reduced towards individuals that we consider as outgroup or towards dehumanized individuals. Neuroscience studies have further shown that when obeying orders to hurt another person, neural activity in empathy- and guilt-related brain regions is reduced compared to acting freely. Such results show how obeying orders diminishes our aversion to harming others.
Mitochondrial dysfunction is a common feature of brain disorders. Mitochondria play a central role in oxidative phosphorylation; thus changes in energy metabolism in the brain have been reported in conditions such as Alzheimer’s disease, Parkinson’s disease, and stroke. In addition, mitochondria regulate cellular responses associated with neuronal damage such as the production of reactive oxygen species (ROS), opening of the mitochondrial permeability transition pore (mPTP), and apoptosis. Therefore, interventions that aim to protect mitochondria may be effective against brain disorders. Fucoxanthin is a marine carotenoid that has recently gained recognition for its neuroprotective properties. However, the cellular mechanisms of fucoxanthin in brain disorders, particularly its role in mitochondrial function, have not been thoroughly discussed. This review summarises the current literature on the effects of fucoxanthin on oxidative stress, neuroinflammation, and apoptosis using in vitro and in vivo models of brain disorders. We further present the potential mechanisms by which fucoxanthin protects mitochondria, with the objective of developing dietary interventions for a spectrum of brain disorders. Although the studies reviewed are predominantly preclinical studies, they provide important insights into understanding the cellular and molecular functions of fucoxanthin in the brain. Future studies investigating the mechanisms of action and the molecular targets of fucoxanthin are warranted to develop translational approaches to brain disorders.
Epilepsy is one of the most common neurological disorders, affecting people of all ages. This chapter focusses on what has been learnt about the microRNA system in this important disease. Starting with an overview of epilepsy, it addresses what causes seizures to occur and some of the underlying mechanisms, including gene mutations and brain injuries. It explores how and which microRNAs drive complex gene changes that underpin but also oppose the enduring hyperexcitability of the epileptic brain. This includes by regulating amounts of neurotransmitter receptors, structural components of synapses, metabolic processes and inflammation. It also covers some of the earliest studies linking microRNAs to epilepsy as well as recent large-scale efforts to map every microRNA and its target in the epileptic brain. Finally, it highlights ways to model epilepsies and use of experimental tools such as antisense oligonucleotides to understand the contributions of individual microRNAs. Collectively, these studies reveal how microRNAs contribute to the molecular landscape that underlies this disease and offer the exciting possibility of targeting microRNAs to treat genetic and acquired epilepsies.
MicroRNAs were discovered during experiments designed to learn how genes coordinate animal development. This chapter begins with the early studies that taught us the importance of microRNAs for mammalian development by studying what happened when key genes were deleted in mice. It ranges from studies that knocked out genes from the entire organism towards refined approaches that removed microRNAs at defined moments from specific tissues, including the heart and the visual system. A detailed review is taken of the genes that microRNAs regulate during brain development and their contribution to the diversity of cell types. These studies reveal the essential role for the microRNA system broadly, as well as how certain developmental events are more or less tolerant of disruption to the microRNA system. This chapter also reviews which microRNAs are the first to control gene activity after fertilisation and how environmental and parental experience can change microRNA activity. The chapter also includes explanations of the scientific toolkit needed to delete or deliver biogenesis components and microRNA genes, and how microRNAs have been used as tools in stem cell research.
The genome is the totality of information that directs the making and the maintenance of you and every other living organism. Scattered among the familiar genes that code for the proteins of life are other genes. This is a book about the genes we call microRNA. It is 30 years since their discovery. They are gene regulators, every bit as vital as their more famous gene cousins. MicroRNAs fine-tune how much protein is made in our cells, each one coordinating the activity of hundreds of genes and bringing precision to the ‘noise’ of gene expression. Without them, life is virtually impossible. This introduction provides a personal account of what fascinated the author about these genes enough to make him redirect his research to microRNAs. The journey from studying pharmacology in the UK, to the USA where his interest in the brain disease epilepsy began, and later to Dublin, to work at the Royal College of Surgeons in Ireland. It lays out the contents and style of the book, which is part history of science, describing what we know and the experiments that underpin our understanding, and part memoir of the author’s own research, and the applications of microRNAs in medicine.