Progress in brain research最新文献

There is an integral relationship between stress, brain function and behavior. Over the year's extensive research has led to the development of various models to explain the intricate intersection between brain and stress. This chapter delves into some of the theoretical frameworks that explains the neurobiological and behavioral responses to stress using key models of stress such as the allostatic load model, which is the most common model that describes how chronic stress affect brain structure and function resulting in long-term changes in regions such as the hippocampus, amygdala, and prefrontal cortex which phenotypically express as cognitive impairments, emotional dysfunction seen in various forms of neurological disorder. The neuro-endocrine model, follows the glucocorticoid cascade hypothesis, that associates prolonged stress exposure to hippocampal damage and cognitive decline via alteration in the hypothalamic-pituitary-adrenal (HPA) axis and the overproduction of stress hormones like cortisol which can induce hippocampal atrophy, impair learning and memory, and promote depressive-like behaviors. The neurobiological stress model addresses the role of the hypothalamic-pituitary-adrenal (HPA) axis and stress-related neurotransmitters in shaping behavioral responses, emphasizing alterations in neuroplasticity and synaptic function. These models demonstrate how chronic stress can alter neural plasticity, neurotransmitter systems, and synaptic connectivity, affecting behavior and cognitive function. Hence by integrating molecular, neurobiological, and behavioral perspectives, these models offer a comprehensive understanding of how stress alters brain activity and behavior. The chapter further showcase how these models direct the development of medical interventions, shedding light on potential therapies that target the underlying molecular mechanisms of stress-induced brain changes.

The integrity of the visual field can be assessed using clinical techniques such as perimetry that rely on subjective report, or can be quantified objectively using functional magnetic resonance imaging (fMRI). In the case of central lesions (e.g. following strokes), fMRI visual field maps can reveal spared regions of cortex that may be missed if patient assessment relies on perimetry and anatomy of lesions alone. Even when perimetry results look stereotypical and can be categorised into hemianopia or quadrantanopia, the areas of spared cortex can be highly variable. FMRI field maps could serve as an important guide for selecting and optimising training and rehabilitation programmes for patients with damage to central visual pathway structures. Alongside a standardised battery of visual function tests, anatomical scans, and tractography data on connections between brain areas, this would provide a much richer clinical picture. Importantly, this approach may also offer useful information for a personalised approach to visual developmental disorders such as cerebral visual impairment (CVI). Here, we survey some recent results from the neuroimaging literature on measuring residual visual function, anatomy, and structural connectivity in stroke survivors, discuss recent results from rehabilitation approaches, and put forward a potential approach for characterising visual function using brain imaging in individuals with CVI.

This chapter explores sex-specific differences in brain development and hormones' critical role throughout life. Understanding these variabilities is vital for mental health, particularly concerning stress responses, aging, and the risk of neurodegenerative and cardiometabolic diseases. We examine the biological mechanisms involved, highlighting how hormones affect brain formation, neuronal plasticity, and stress responses, focusing on male and female variations. Research from animal studies and human data shows that males and females have distinct susceptibilities to diseases influenced by sex-specific hormonal effects on genes, cellular functions, and energy metabolism. Additionally, we examine the role of glucocorticoids in these diseases, considering their sex-specific effects on normal and dysfunctional physiological processes. A closer look at hormonal transition periods-such as early childhood, puberty, and menopause-emphasizes the need for sex-specific strategies in research and treatment. Overall, this chapter underscores the importance of understanding the interplay between biological sex, hormonal changes, and environmental stressors throughout life, as these factors significantly impact the onset and progression of various health conditions. Tailored approaches in health research and treatment are advocated to better address these differences.

Pharmacogenomics and CRISPR-based treatments are two areas of precision medicine that are advancing together. Pharmacogenomics involves studying how differences in someone's genes can change the effect of medications on them. Pharmacogenomics helps reduce adverse reactions to drugs and improve healing by choosing and measuring drugs according to a patient's genetic information. Additionally, CRISPR-Cas systems now serve as leading genome editing tools that allow precise alterations at given points of the genome. CRISPR technology's use in pharmacogenomics creates new opportunities for modifying gene expression, fixing harmful mutations, and creating innovative treatment approaches. A more proactive approach to illness treatment is supported by this synergy, in which genetic factors serve as both direct targets for intervention and a basis for medication selection. This chapter examines the theoretical and practical frameworks that link CRISPR-based treatments with pharmacogenomics, emphasizing recent uses in pharmacoresistance, cancer, and monogenic diseases. To guarantee safe and fair deployment, it also covers the ethical, legal, and technical issues that need to be resolved. When combined, these technologies hold the potential to revolutionize medicine by facilitating individualized and curative drugs.

Despite extensive research, Alzheimer's disease (AD) a progressive neurodegenerative disorder marked by cognitive decline, neuronal loss, and the build-up of amyloid-beta plaques and tau tangles continues to lack effective treatments. Precision medicine presents a promising shift by customizing interventions to an individual's genetic, molecular, and lifestyle profile. This chapter explores key advancements in precision therapeutics for AD, including biomarker-driven therapies, pharmacogenomics, and targeted disease-modifying agents such as monoclonal antibodies. Recent innovations, including RNA-based therapeutics, stem cell approaches, and CRISPR-mediated gene editing, are also discussed. While precision medicine holds immense promise, challenges in clinical translation, patient stratification, and regulatory pathways must be addressed. By bridging cutting-edge research with clinical applications, this chapter provides insights into the evolving landscape of individualized treatment strategies for AD.

The chapter talks about how our body and mind respond to stress and how it affects our immune system. Stress reactions, especially the fight-or-flight reaction, are helpful at first but can be harmful if they last too long. Long-term stress, caused by hormones like cortisol and adrenaline, weakens the immune system and makes people more likely to get sick. Important brain chemicals like serotonin and norepinephrine help control how our immune system works. Also, the connection between our gut and brain is an important way that mental health affects how our immune system functions. Getting older and experiencing stress early in life can affect how our immune system works. Inflammation caused by stress is connected to health issues like heart disease, depression, and autoimmune diseases. There are ways to manage stress, like being mindful and having support from friends, are important for keeping your immune system healthy and lessening harm caused by stress.

The gut microbiota-brain axis is a complex system that links the bacteria in our gut with our brain, it plays a part in what way we respond to stress. This chapter explores how stress affects the types of bacteria in the gut and shows the two-way connection between them. Stress can change the bacteria in our gut, which can cause various problems related to stress, like depression, anxiety, and irritable bowel syndrome (IBS). Figuring out how these interactions may help us develop new treatments that focus on the connection between gut bacteria and the brain. This chapter looks at how gut bacteria could help identify stress-related problems. It also discusses the difficulties and possibilities of using this research in medical practice. In the end, the chapter talks about what comes next in this quickly changing area. It highlights how important it is to include research about the gut-brain connection in overall public health plans.

Stress can have powerful and lasting effects on our bodies and behavior, partly because it changes how our genes work. These processes, such as DNA methylation, histones modifications, and non-coding RNAs, help decide when genes are active or inactive in cells experiencing stress. This can lead to lasting changes in how the cells function. It's important to understand how these changes in our genes affect our response to stress, as they can lead to problems like anxiety, depression, and heart disease. This chapter explores the link between stress and epigenetics. It talks about how our surroundings and lifestyle can impact these processes. It also shows that epigenetic treatments might help with issues created by stress. By looking at how stress affects our genes, we can discover new ways to treat stress and make medicine better for individuals, helping to lessen the bad impact of stress on our health.

The daily rise and fall in ambient temperature caused by Earth's 24-hour rotation may help regulate circadian rhythms in visually impaired individuals. In all mammals, circadian rhythms, the daily cycles of physiology and behavior, are time controlled by the suprachiasmatic nucleus (SCN), the brain's central clock. The SCN typically synchronizes circadian rhythms with the light/dark cycle through photoentrainment, a process in which specialized retinal cells capture ambient light and transmit this information to the SCN, allowing it to set its phase. Without light input, the rodent SCN's light-driven circuits can become desynchronized, potentially allowing alternative entrainment signals, such as ambient temperature, to influence central timing. Here, we consider whether a similar mechanism could benefit visually impaired humans who, due to retinal damage, have reduced or absent photic input to the central clock. Visually impaired individuals often experience circadian misalignment, whereby internal rhythms drift out of synchrony with the light-dark cycle, and we suggest that temperature information may mitigate some of this drift. Temperature entrainment could operate through heat shock pathways from the skin, via thermoregulatory brain regions with reciprocal connections to the SCN, or by shifting core body temperature through warm or cold baths, which can alter the phase of clocks in peripheral organs and potentially feedback to adjust central time. Given that temperature is a weaker cue than light, it remains unknown if, and to what extent, it may significantly impact central timing. However, if effective, temperature entrainment in the visually impaired could potentially improve circadian disorders, poor sleep, and adverse health outcomes associated with circadian dysfunction including depression, cognitive decline, and metabolic disorders, which are more prevalent in this population. Research is needed to confirm the long-term effectiveness of temperature as an entrainment cue in the visually impaired population, which may have broader implications for circadian timekeeping in mammals and the role of temperature in the absence of light.