Progress in brain research最新文献

This study explores the impact of positive thinking on synaptic function and connectivity. Positive thinking, characterized by optimism, constructive self-talk, and a proactive mindset, enhances resilience and supports healthy habits crucial for neuroplasticity and synaptic development. Research underscores its significant role in hormonal regulation, benefiting both physical and mental well-being. This cognitive approach amplifies positive emotions and is integral to cognitive-behavioral modification. Synaptic plasticity, essential for learning and memory, involves activity-dependent strengthening or weakening of synapses, categorized into short-term (e.g., working memory and decision-making) and long-term (e.g., learning and retention). These processes are regulated by long-term potentiation (LTP) and long-term depression (LTD), influenced by factors such as brain-derived neurotrophic factor (BDNF), astrocytes, medications, and non-invasive interventions. Positive thinking boosts serotonin production, activates dopamine neurons, and lowers cortisol levels, facilitating adaptive learning through interactions between the limbic system and prefrontal cortex. Dopamine promotes neurogenesis by maintaining neural precursor cells, while reduced cortisol levels improve hippocampal synaptic plasticity, enhancing adaptability, learning, and memory retention. Ultimately, positive thinking plays a critical role in advancing education, improving mental health treatment, and serving as the foundation for cognitive training.

Stress is an inevitable part of people's lives and is considered to have a severe impact on health, especially in the case of cardiovascular diseases and neurodegenerative diseases. This chapter aims to reveal the links between emotional stress, cardiovascular health, and neurodegenerative disease progression. Chronic stress is therefore recognized as a significant cause of cardiovascular diseases mainly because of the effects it has on the hypothalamic-pituitary-adrenal (HPA) axis and the (SNS) sympathetic which neurodegenerative nervous are diseases system such (as ALS) through inflammation of Alzheimer's mechanisms and disease, vascular such as Parkinson's functions. The mechanisms of work also establish the crosstalk between CVD and NDD, demonstrating that they share genetic, molecular, and systemic associations. It is essential to know these pathways to design interventions that will help prevent or lessen the effects of stress on health and thus enhance patient care.

Heart and brain functions are intricately connected. Previous research has explored the mechanisms behind the brain- heart axis and its clinical implications. Nonetheless, there is limited studies on the impact of heart disease on brain performance (heart-brain axis). In this context, hypoperfusion resulting from heart failure (HF) is considered a significant risk factor for cognitive impairment. Oxidative stress, immune responses, and blood perfusion contribute to cognitive dysfunction, playing a key role in this process. As such, it is important for healthcare professionals and researchers to consider the cognitive function of heart patients, particularly those having HF, to prevent the activation of this signaling pathway. Additionally, further investigation into the underlying mechanisms results in identifying new therapeutic targets for the treatment of cognitive dysfunction following heart disease. The current review aims to examine cognitive impairment in heart disease as well as its potential mechanisms, offering valuable insights for future research in related areas.

Stress, a common life experience, impacts both mental and physical health, contributing to conditions such as anxiety and cardiovascular disease. It triggers physiological and psychological responses, primarily through the Hypothalamic-Pituitary-Adrenal (HPA) and Sympathetic-Adrenal-Medullary (SAM) axes, which are coordinated by the autonomic nervous system. Dysregulation of the glucocorticoid system, mediated by mineralocorticoid and glucocorticoid receptors, plays a critical role in neurodegenerative disorders like Alzheimer's disease. Cellular pathways like PI3K/Akt, NF-κB, and AP-1 transcription factors maintain homeostasis during stress and are targets for therapeutic research. Epigenetic influences and genomic modifications highlight the long-lasting effects of stress on gene expression. Adaptive responses, such as allostasis, allow the body to maintain stability amid stress. However, excessive stress leads to allostatic load, negatively impacting the immune, endocrine, and nervous systems. Current treatments include pharmacological and lifestyle interventions, with emerging approaches such as psychobiotics and precision medicine offering future potential.

Stress is a significant determinant for a range of neurological and psychiatric illnesses, and comprehending its influence on the brain is vital for developing effective interventions. Caenorhabditis elegans (C. elegans), a tiny nematode, has become a potent model system for investigating the impact of stress on neuronal integrity, behavior, and lifespan. This chapter presents a comprehensive summary of the existing understanding of stress-induced neurodegeneration, behavioral abnormalities, and changes in lifespan in C. elegans. We explored the stress response pathways in C. elegans, specifically focusing on the heat shock response and insulin-like signaling (ILS) pathway, targeting how these pathways affect neural integrity and functions. Additionally, this chapter highlighted behavioral modifications such as changes in locomotion, feeding, pharyngeal pumping, defecation, and copulation behaviors that occur in C. elegans following exposure to stressors, and how these findings contribute to our comprehension of stress-related illnesses. Furthermore, the evolutionary preservation of stress responses in both C. elegans and humans, underscoring the significance of C. elegans studies for translational research were highlighted. In conclusion, the possible implications of C. elegans research on human well-being, with a specific emphasis on the discovery of targets for treatment and the creation of innovative approaches to address stress-related conditions are discussed in this chapter.

Dementia poses a significant challenge to global health. This chapter reviews current literature to investigate the potential protective effects of happiness and positive emotions against dementia. Studies suggest that individuals experiencing higher levels of happiness and frequent positive emotions may exhibit lower risks of developing dementia. Mechanisms proposed include the role of positive emotions in stress reduction, which could mitigate neurodegenerative processes. In addition, recent studies have begun exploring the impact of positive psychological states, such as happiness and positive emotions, on cognitive health. Furthermore, positive psychological states have been linked to healthier lifestyle choices, including physical activity and social engagement, which are known to support cognitive function. Despite promising findings, challenges remain in establishing causal relationships and elucidating specific neurobiological pathways. Future research should focus on longitudinal studies with diverse populations to clarify these relationships and inform effective interventions. Understanding how happiness and positive emotions influence dementia risk could lead to novel preventive strategies and improve quality of life for aging populations worldwide. This chapter summarizes the potential benefits of happiness and positive emotions in mitigating the risk of dementia, highlighting the need for further research to establish causal links and develop targeted interventions.

Psychedelic experiences, especially those induced by substances such as N,N-Dimethyltryptamine (DMT), are often characterized by high subjective intensity, complex visual content, and notable ineffability-that is, the difficulty of being fully expressed in words. This expressive limitation poses a significant challenge to the integration of the experience, which is essential for the therapeutic processing of these experiences. In this context, clinical studies with psychedelics are increasingly demanding innovative approaches to facilitate the assimilation of such experiences into daily life. Art, as a form of nonverbal expression, has been proposed as a promising tool in this regard. Accordingly, this article discusses the use of the mandala as a complementary expressive resource in the process of psychedelic integration, based on a Phase I clinical trial with DMT. The analysis draws on the mandalas and narratives produced by participants. The findings suggest that the creation of mandalas facilitated the symbolic expression of subjective content that was difficult to verbalize, supporting the integration process. Despite its potential, the use of expressive tools remains underexplored and unsystematized in current psychedelic clinical protocols. We concluded that the inclusion of art may represent a valuable advancement in optimizing the therapeutic benefits of psychedelics, expanding the understanding and meaning of experience.

Exercise has been central to human brain evolution. Genus Homo was a nomadic species that constantly explored novel environments, which requires the encoding of new spatial and contextual patterns and the consolidation and recall of details to localize potential food and avoid danger, functions associated with the hippocampus. Interestingly, no primates other than humans run long distances over extended periods using aerobic metabolism, a capacity described as endurance running (ER). It has been hypothesized that ER capacity may have had relevant effects on the evolution of brain structure and cognition in the genus Homo. Paradoxically, modern humans have become sedentary and no longer need to run for food or survival. The lack of exercise in the population has increased the risk of brain disorders. Studies in human and animal models show that exercise elicits functional and structural changes throughout the brain, which may serve as a mechanism to counteract the changes induced by aging and reduced physical activity. Here, we describe the cortico-hippocampal circuitry and summarize evidence from human and animal models of aging-induced and exercise-induced changes in cortical and subcortical areas that provide polymodal information and modulatory inputs to the hippocampus, respectively. We discuss how exercise-induced plasticity in the cortico-hippocampal circuit may improve brain health.

Changes in energy homeostasis in aging have significant implications for brain health. Decreased glucose utilization efficiency, mitochondrial dysfunction, loss of metabolic flexibility, and increased oxidative stress can compromise cognitive functions and increase vulnerability to neurodegenerative diseases. Understanding these changes provides valuable insights for prevention and treatment strategies, such as dietary interventions, physical exercise, and pharmacological therapies, aimed at restoring or preserving energy homeostasis in the brain and thus improving cognitive health throughout life. This chapter explores the metabolic changes in the brain associated with aging, examining the underlying biochemical and molecular mechanisms, as well as therapeutic strategies that may alleviate the detrimental effects of brain aging.