Progress in brain research最新文献

This chapter delves into the complex interplay among addiction, stress, and the reward pathways in the brain, emphasizing the ways in which various drugs affect these systems and exacerbate SUD. Drugs have physiological effects that can be both pleasurable and unpleasant. These effects change behavior through both positive and negative reinforcement. A person's genetic predisposition to addiction is mostly determined by factors such as biological sex, age of first usage, and dopamine receptor density. Drug use behaviors are also greatly influenced by environmental stressors, media exposure, and substance accessibility; nevertheless, protective variables including social support, participation in healthy activities, and preventative programs serve to reduce the dangers associated with drug use. The reinforcement of addictive behaviors is mostly dependent on the brain's reward circuits, which include the nucleus accumbens, ventral tegmental region, and prefrontal cortex, in addition to neurotransmitters such as dopamine, serotonin, and endorphins. Stress makes addiction worse by intensifying cravings and raising the possibility of relapsing. Examined are the impacts of several drug types, such as opioids, stimulants, depressants, and hallucinogens, emphasizing the long-term consequences on brain function and susceptibility to addiction. In order to create individualized interventions that target the environmental and neurological components of addiction and eventually improve treatment results, a thorough understanding of these elements is important.

The objective of this chapter is to navigate through the nexus between stress and sleep, highlighting the neurobiological systems that connect them. Starting with an overview of neuroanatomy and physiology of stress and sleep, with a further detailed breakdown of sleep stages and key neuroanatomical centers that are responsible for sleep and wakefulness. Starting with suprachiasmatic nuclei (SCN) in circadian rhythm and sleep regulation overview, with a center point on the molecular systems including the CLOCK/CRY and BMAL1/2/PER1/2 feedback loops. Following this is the neurobiological of stress, specifically the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic-adrenal (SPA) axis and influence on sleep. Vital neural circuits connecting stress and sleep are examined with the attention of the ventral tegmental area (VTA) GABA-somatostatin neurons and the locus coerules in sleep regulation in response to stress. In addition, neuroinflammation's role occurs through the cytokines IL-1β and TNF-α are investigated as a mediator of sleep disturbances caused by stress. It concludes by summarizing the implications of neuroinflammatory modulation in stress-related psychopathologies, emphasizing the opening this provides for interventions that target this inflammation helping to lighten sleep disorder.

Damage to the primary visual cortex causes homonymous visual impairments that appear to benefit from visual discrimination training. However, whether improvements persist without continued training remains to be determined and was the focus of the present study. After a baseline assessment visit, 20 participants trained twice daily in their blind-field for a minimum of six months (median=155 sessions), using a motion discrimination and integration task. At the end of training, a return study visit was used to assess recovery. Three months later, 14 of the participants returned for a third study visit to assess persistence of recovery. At each study visit, motion discrimination and integration thresholds, Humphrey visual fields, and structural MRI scans were collected. Immediately after training, all but four participants showed improvements in the trained discrimination task, and shrinkage of the perimetrically-defined visual defect. While these gains were sustained in seven out of eleven participants who improved with training, four participants lost their improvement in motion discrimination thresholds at the follow-up visit. Persistence of recovery was not related to age, time since lesion, number of training sessions performed, proportion of V1 damaged, deficit size, or optic tract degeneration measured from structural MRI scans. The present findings underscore the potential of extended visual training to induce long-term improvements in stroke-induced vision loss. However, they also highlight the need for further investigations to better understand the mechanisms driving recovery, its persistence post-training, and especially heterogeneity among participants.

Positive emotions have long been recognized for their impact on overall health, yet emerging research highlights the underlying neural mechanisms and neurotransmitter systems that mediate these effects. Several key brain regions such as the prefrontal cortex (PFC), amygdala, anterior cingulate cortex (ACC), and insula, play a role in processing positive emotions and emotional regulation. Several neurotransmitters and neuropeptides, including dopamine, serotonin, and oxytocin are involved emotional resilience and psychological health. Positive emotions can reshape neural circuits, and foster neuroplasticity and neurogenesis. Therefore, positive emotion-based interventions could play an important role in alleviating mood disorders, improve cognitive function, and enhance social and physiological health. This chapter highlights the transformative impact of integrating the science of positive emotions into therapeutic practices, showcasing their potential to improve overall well-being. It delves into the therapeutic effect of positive emotions on neural pathways and neurotransmitter systems, emphasizing their significance in fostering both mental and physical health.

The signaling pathways associated with α-Klotho, glutamate, mediators of the inflammatory response in the central nervous system (CNS) and that related to different isoforms of the Na, K-ATPase (NKA) protein as a pump and receptor for endogenous steroids (ouabain-like hormones) are associated with neuroplasticity and neuroprotection. This neuroadaptive response induced by pharmacologic (Cardiotonic Steroids, Klotho, Resveratrol, Curcumin, and other Phytochemicals), and non-pharmacologic strategies (intermittent fasting and physical exercise) involves glial and neuronal cell crosstalk through activation of different intracellular pathways involving mediators, such as glutamate, cytokines, transcription factors, and gene expression which will exert a marked influence on the adaptive processes (neuroplasticity) that prevent premature aging, in addition to playing an essential role in cognition and neurodegenerative processes. The present text addresses the effect of these agents on the Central Nervous System (CNS), exploring neuroplasticity changes associated with the neuroinflammation induced by these mediators in the presence of a modified expression or signaling of the α-Klotho and the different α-isoforms of NKA. The studies involve in vitro approaches using models of neuronal and glial cells and in vivo studies with a behavioral and biochemical approach. Studies were also done in the presence (or absence) of changes in the expression of these proteins (by using vectors, interference RNA, and transgenic animals with specific protein-modified expression, such as TNF-α and Klotho). It has been also several human studies evaluating these hermetic strategies associated with physical exercise and intermittent diet. The present chapter discusses the benefit of these strategies in the induction of neuroadaptive response.

Insomnia is characterized by difficulty initiating or maintaining sleep and affects 10-20 % of adults. Conventional pharmacotherapies for insomnia, initially comprising benzodiazepines and later the Z-drugs, often present significant adverse effects, including dependence and tolerance. Here we provide a brief review on cannabis therapy for insomnia and present a relevant case report. We first discuss the sleep stages and the main clinical aspects of insomnia. Next, we report the case of a 37 year-old patient who, after a grief situation, began to experience insomnia that was resistant to various conventional treatments, even with dosage adjustment. The insomnia diminished after replacing the conventional pharmacotherapies with full spectrum Cannabis sativa oil, rich in cannabidiol (CBD) and tetrahydrocannabinol (THC). Finally, we note that medical societies from several major countries such as England, Australia and Brazil already recommend the use of Cannabis (plants rich in THC and/or CBD) to treat insomnia. These societies base their guidelines on studies that reported a mitigation of the symptoms of insomnia with the use of cannabinoids. However, recent meta-analyses highlight the heterogeneity of the participants, interventions, and results. Further research is essential to elucidate the influence of cannabinoids on both physiological and pathological aspects of sleep.

Advances in neuroimaging are revolutionizing the landscape of precision neurology by enabling high-resolution, multimodal visualization of brain structure, function, and pathology. As traditional, symptom-based frameworks fall short in capturing the biological complexity of neurodegenerative diseases, imaging modalities such as structural MRI, diffusion tensor imaging, functional MRI, PET, and hybrid PET/MRI have emerged as essential tools for early diagnosis, patient stratification, and therapeutic monitoring. These technologies not only reveal hallmark features like hippocampal atrophy and disrupted neural networks but also uncover molecular signatures such as amyloid and tau deposition, synaptic density, and neuroinflammation. Integration with artificial intelligence (AI) and machine learning (ML) further enhances diagnostic precision by decoding subtle imaging patterns, facilitating subtype classification, and predicting disease progression. Despite transformative progress, disparities in access and implementation remain a critical challenge, particularly in low- and middle-income countries. This chapter provides a comprehensive overview of neuroimaging modalities, their diagnostic and prognostic relevance across major neurodegenerative conditions including Alzheimer's disease, Parkinson's disease, ALS, and frontotemporal dementia and the evolving role of hybrid platforms and AI integration in shaping the future of individualized neurological care.

With more cases of neuropsychiatric and chronic degenerative conditions worldwide, caregivers now play a vital role in healthcare. This chapter examines the different aspects of caregiving, including its medical, emotional and ethical sides, in cases of dementia, Parkinson's disease, stroke and spinal muscular atrophy. Emphasizing a shift from viewing caregivers as ancillary figures to recognising them as a co-therapeutic agents, highlights their impact on patient outcomes, continuity of care, and quality of life. Evidence-based interventions that use cognitive behavioural therapy, teach mindfulness and include structured routines for caregivers are assessed for how they help reduce stress on caregivers and improve the stability of those receiving care. The chapter also points out how important it is to practice culturally sensitive and ethical care in any healthcare setting, especially when resources are limited. The best practices and guidelines from the United States are reviewed to demonstrate how support for caregivers can be woven throughout the care system globally. The chapter promotes the inclusion of caregiver well-being in regular healthcare plans, making it an essential part of care rather than a secondary issue.