Progress in brain research最新文献

Understanding cognitive decline and its contributing causes, such as stress, which presents differently in different groups, is crucial given the aging population's rapid growth. This chapter looks at how stress affects older persons' cognitive decline, with a particular emphasis on the difficulties faced by medical professionals in their line of work and how to lessen the consequences. The severity and course of cognitive decline differ from person to person and are impacted by factors such as lifestyle, medical history, and stress at work. The COVID-19 pandemic has made medical practitioners' already high demands even more precarious. Stress in underprivileged areas and among veterans emphasizes the negative effects of work-related stress on mental health even more. Techniques that improve psychological well-being and lessen burnout include resilience training, digital tools, supportive leadership, and mindfulness-based stress reduction (MBSR). Enhancing work-life balance and promoting a healthier work environment can be achieved by combining these interventions with organizational changes. Aging-related cognitive impairment necessitates a multimodal strategy that includes targeted stress reduction methods and organizational adjustments. Setting mental health as a top priority in healthcare settings promotes the wellbeing of staff members, enhances patient care, and improves healthcare results.

In order to improve individual and community health outcomes, stress research is crucial for developing our understanding of human biology, psychology, and social dynamics. It also informs therapeutic practices, public health campaigns, and educational activities. The chapter explores how neurotransmitters, including glutamate, GABA, adrenaline, norepinephrine, serotonin, dopamine, and adrenaline, mediate stress responses, impact mood and behavior, and play a part in a number of stress-related disorders. The relevance of focused research and therapy approaches aimed at reestablishing equilibrium within these systems is highlighted by the fact that dysregulation of these neurotransmitters can exacerbate health problems. Additionally, it is investigated how the amygdala, hippocampus, and prefrontal cortex interact to process emotions, build resilience, and determine an individual's susceptibility to stress. These interactions are regulated by both neuroplasticity and hereditary and epigenetic factors. The chapter discusses the pharmaceutical approach to stress management, which includes a variety of drugs such as beta-blockers, anxiolytics, and antidepressants that work by targeting different neurotransmitter systems to reduce anxiety and mood disorders. Even while these therapies work, they may have negative consequences and side effects that should be carefully considered in clinical settings. The chapter promotes a comprehensive approach to stress management that combines medication, lifestyle changes, psychotherapy, and stress-reduction methods. Healthcare workers can improve patient care and ultimately the health and quality of life for people with stress-related disorders by knowing the complexity of pharmaceutical therapies and how they affect the stress response.

Cognitive performance is greatly influenced by cardiovascular health, as vascular integrity and brain perfusion are directly related to diseases including Parkinson's disease, Alzheimer's disease, and vascular dementia. Examining the intricate relationship between the heart and brain, this chapter highlights how atrial fibrillation, diabetes, hypertension, and dyslipidemia affect neurovascular coupling (NVC). Chronic inflammation, oxidative stress, and endothelial dysfunction are some of the risk factors that lead to neurodegeneration. The cerebral microvasculature is further compromised by atherosclerosis and heart failure, which exacerbates neuronal damage and increases the risk of dementia. Supported by clinical and epidemiological data, the discussion delves into the mechanisms behind vascular dementia and the vascular contributions to Alzheimer's disease. Slowing cognitive deterioration requires early intervention through lipid management, blood pressure control, and anticoagulant medication. Additionally, developments in precision medicine and neurovascular-targeted therapies present encouraging paths toward management and prevention. Through the discussion of modifiable cardiovascular risks, this chapter emphasizes how vital vascular health is to maintaining cognitive function and slowing the progression of neurodegenerative diseases.

The Merriam-Webster dictionary defines happiness as "a state of well-being and contentment". Psychologically, happiness can be defined as a state of current well-being and positivity resulting from recent stimuli, as well as long-term life satisfaction and peace of mind. This refers to two aspects of happiness discussed in psychology, first coined by Aristotle, pleasurable happiness known as "hedonia" and the long-term happiness of living a good life called "eudaimonia". These early concepts break down the vaguer and complex idea of happiness into long-term pleasure and positivity. This is where it starts to get more challenging when we try to define happiness in neurobiological terms. Many regions, pathways and circuits in the brain work in tandem to create the conscious and recognized state of happiness we cognitively perceive as humans. However, happiness is a feeling that transcends species boundaries. It is a positive state of emotions that can be expressed in different ways, including contentedness, peace, pleasure, excitement, relief, joy, and more. To do this, happiness must be broken down into constituent parts, localized to specific neuroanatomical regions, and associated with specific projects and structures to really build the anatomical architecture of happiness. Understanding how emotion is quantified and experimentally studied allows the field of neuroscience to build a comprehensive "neurobiological happiness model". Here in this chapter, we discuss historical and novel findings into this emotion; we discuss its implication as an evolutionary advantage in the adaptive response, how laughter is associated with happiness, and how a state of positive well-being plays a role in promoting positive brain health.

The blood-brain barrier (BBB) is a critical regulator of cerebral homeostasis, displaying high dynamicity of influx and efflux of substances to and from the central nervous system (CNS). In an exploration of the neurochemical pathways through which positive and negative emotions can influence the physiological characteristics of the BBB, this chapter delves into the multifaceted relationship between emotional states and BBB integrity and permeability. Negative emotions exemplified by stress, chronic anxiety, and depression have shown harmful effects on the BBB, suggesting a state of hyperpermeability that compromises the otherwise conferred protection. Few reports in literature examined the exact molecular mechanisms by which negative emotions exhibit signs of damaged and leaky BBB. Although research deciphering those mechanisms is limited, there is consensus that the disruption of tight junction (TJ) protein integrity and expression, along with neuroinflammatory processes, oxidative Stress, and excitotoxicity, plays a role in the induction of BBB damage. Conversely, positive emotions have been shown to exert protective effects, potentially reversing the increased permeability of the BBB. Compared to the research focused on the neural correlates of negative emotions, the neuroscience literature on positive emotions and well-being is still in its infancy. A deeper understanding of the mechanisms by which positive emotions modulate the BBB remains necessary. Additionally, we discuss the therapeutic implications of these findings, considering how emotional well-being can be leveraged in developing treatments for neurological disorders. By integrating neuroscience, psychology, and pharmacology insights, this chapter aims to comprehensively understand the dynamic interplay between emotions and the BBB and its potential to inform novel therapeutic strategies.

Brain cells intentionally break their DNA as a crucial step in memory formation and learning. This process allows for the expression of specific genes that are essential for these cognitive functions. While our cells are generally adept at repairing this self-inflicted DNA damage, the efficiency of this repair mechanism can decline with age or due to certain genetic factors. The deliberate DNA breakage in neurons enables the activation of rapid response genes, which in turn trigger broader transcriptional programs supporting various behaviors, including learning and memory. This process is a normal part of cellular function and gene expression. However, neurological disorders, certain syndromes, and the aging process can impair this DNA repair ability. When cells struggle to mend the intentional DNA breaks, it can lead to cellular weakening and eventual degeneration. The subsequent discussion will explore how positive and negative emotions influence the processes of brain cell regeneration and degradation.

Environmental Enrichment (EE), which provides enhanced sensory, cognitive, motor, and social stimulation, has emerged as a powerful paradigm for investigating neuroplasticity and stress resilience. This chapter explores how EE functions through hormetic mechanisms-where multiple mild stimuli trigger adaptive responses that promote beneficial outcomes. Since Hebb's pioneering work on neuronal ensembles, research has demonstrated that EE enhances neurogenesis, synaptic plasticity, and neurotrophic factor expression (BDNF and NGF) while modulating inflammatory processes, epigenetic pathways, and metabolic function. These adaptive responses operate according to biphasic dose-response patterns characteristic of hormesis, where moderate stimulation produces benefits that may diminish or become detrimental with excessive exposure. In animal models, EE has shown remarkable efficacy in mitigating cognitive decline, reducing anxiety-like behaviors, attenuating addiction vulnerability, and protecting against neurodegenerative diseases. The modulation of the hypothalamic-pituitary-adrenal (HPA) axis and the shifts in microglial phenotype observed with EE illustrate its role as a hormetic stimulus, as it can act as a mild stressor that promotes adaptive neuroplasticity, enhancing the organism's ability to cope with future stressors. In humans, analogous enrichments through physical exercise, cognitive challenges, social engagement, and music facilitate neuroplasticity, protect against cognitive decline, and promote stress resilience. The hormetic framework also explains why enrichment must be tailored to individual thresholds-excessive stimulation can overwhelm adaptive capacities, transforming beneficial eustress into harmful distress. By understanding EE as a hormetic intervention, this chapter bridges basic neuroscience with translational applications that may enhance resilience against neuropsychiatric disorders typically prevalent in aging.

Neurodegenerative disorders (NDs), such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), present increasing issues associated with the unavoidable aging of the world's population. These challenges are further highlighted by the socioeconomic consequences of these diseases. The identification and use of biomarkers for prompt diagnosis, careful observation, and efficient treatment approaches is essential to overcoming these obstacles. The primary methods for diagnosing neurodegenerative illnesses are invasive procedures like lumbar punctures to measure CSF fluid or functional brain imaging methods. Biomarkers for underlying proteinopathy in blood serum and cerebral fluid have been the focus of recent biological research, particularly in vivo. With their ability to provide novel pathways for early detection, illness progression tracking, and individualized treatment plans, biomarkers have become essential instruments in precision medicine. The classification of biomarkers including fluid, digital imaging, and molecular biomarkers is examined in this chapter, with an emphasis on their function in neurodegenerative diseases. In neurodegenerative illnesses and the aging brain, tau, amyloid-β, α-synuclein, and TDP-43 are commonly seen to be deposited together rather than separately. These may be disregarded, and it might be challenging to determine their clinicopathological significance. An overview of illness pathophysiology, diagnostic implications, and the most recent molecular and ultrastructural categories for neurodegenerative disorders are given in this chapter. Addressing these issues through interdisciplinary research and technological advancements will be crucial for the future of biomarker-driven precision medicine. This chapter provides an in-depth overview of the evolving landscape of biomarkers and their transformative impact on the early detection and personalized treatment of neurodegenerative diseases.

This chapter investigates the ways in which male and female brains are differently affected by stress during early development, which in turn affects how susceptible each group is to stress-related illnesses. When examining the structure and function of the brain, gender differences and stress must be taken into account. Male and female brain development differs in response to the prenatal testis's secretion of androgen. It appears that when it comes to responding to stress, encoding memories, feeling emotions, solving specific issues, and making decisions, men and women use distinct areas of the brain. Findings revealed that stress led to specific changes in brain structure and function, with gender-specific differences observed. The prefrontal cortex, the hippocampus, and the amygdala are among the brain regions connected to the stress response. The stress response has been linked to the presentation of numerous mental and psychosomatic conditions. The way men and women respond to stress varies on a biological and psychological level. To gain more insight into the gender differences seen throughout brain development, these disparities must also be investigated. This chapter implies that gender-specific vulnerabilities should be addressed and healthy brain development should be promoted by stress-related interventions.