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Based on these observations, we propose an anatomical and functional connection between the cholinergic component of the nvlDBB (Ch2) and the hippocampal CA2.The basal forebrain (BF) cholinergic system constitutes a heterogeneous cluster of large projection neurons that innervate the entire cortical mantle and amygdala. Cholinergic neuromodulation plays a critical role in regulating cognition and behavior, as well as maintenance of cellular homeostasis. Decades of postmortem histology research have demonstrated that the BF cholinergic neurons are selectively vulnerable to aging and age-related neuropathology in degenerative diseases such as Alzheimer's and Parkinson's diseases. Emerging evidence from in vivo neuroimaging research, which permits longitudinal tracking of at-risk individuals, indicates that cholinergic neurodegeneration might play an earlier and more pivotal role in these diseases than was previously appreciated. Despite these advances, our understanding of the organization and functions of the BF cholinergic system mostly derives from nonhuman animal research. In this chapter, we begin with a review of the topographical organization of the BF cholinergic system in rodent and nonhuman primate models. We then discuss basic and clinical neuroscience research in humans, which has started to translate and extend the nonhuman animal research using novel noninvasive neuroimaging techniques. We focus on converging evidence indicating that the selective vulnerability of cholinergic neurons in Alzheimer's and Parkinson's diseases is expressed along a rostral-caudal topography in the BF. We close with a discussion of why this topography of vulnerability in the BF may occur and why it is relevant to the clinician.The quality of postmortem hypothalamus research depends strongly on a thorough clinical investigation and documentation of the patient's disorder and therapies. In addition, a systematic and professional neuropathological investigation of the entire brain of both the cases and the controls is absolutely crucial. In the experience of the Netherlands Brain Bank (NBB), about 20% of the clinical neurological diagnoses, despite being made in first rate clinics, have to be revised or require extra diagnoses after a complete and thorough neuropathologic review by the NBB. The neuropathology examination may reveal for instance that the elderly "controls" already have preclinical neurodegenerative alterations. In postmortem studies, the patient and control groups must be matched for as many as possible of the known confounding factors. This is necessary to make the groups as similar as possible, except for the topic being investigated. Confounding factors are present (i) before, (ii) during, and (iii) after death. They are, respectively (i) genetic background, systemic diseases, duration and gravity of illness, medicines and addictive compounds used, age, sex, gender identity, sexual orientation, clock- and seasonal time of death, and lateralization; (ii) agonal state, stress of dying; and (iii) postmortem delay, freezing procedures, fixation, and storage time. Agonal state is generally estimated by measuring the pH of the brain. However, there are disorders in which pH is lower as a part of the disease process. Because of the large number of potentially confounding factors that differ according to, for instance, brain area and disease, a brain bank should have a large number of controls at its disposal for appropriate matching. If matching fails for some confounders, the influence of the confounders may be determined by statistical methods, such as analysis of variance or the regression models.The adult brain harbors specific niches where stem cells undergo substantial plasticity and, in some regions, generate new neurons throughout life. This phenomenon is well known in the subventricular zone of the lateral ventricles and the subgranular zone of the hippocampus and has recently also been described in the hypothalamus of several rodent and primate species. After a brief overview of preclinical studies illustrating the pathophysiologic significance of hypothalamic neurogenesis in the control of energy metabolism, reproduction, thermoregulation, sleep, and aging, we review current literature on the neurogenic niche of the human hypothalamus. A comparison of the organization of the niche between humans and rodents highlights some common features, but also substantial differences, e.g., in the distribution and extent of the hypothalamic neural stem cells. Exploring the full dynamics of hypothalamic neurogenesis in humans raises a formidable challenge however, given among others, inherent technical limitations. We close with discussing possible functional role(s) of the human hypothalamic niche, and how gaining more insights into this form of plasticity could be relevant for a better understanding of pathologies associated with disturbed hypothalamic function.Communication pathways of the hypothalamus with other brain regions and the periphery are critical to successfully control key physiological and psychological processes. With advanced functional magnetic resonance imaging (fMRI) techniques, it is possible to target hypothalamic function and infer discrete hypothalamus networks. Resting-state functional connectivity (RSFC) is a promising tool to study the functional organization of the brain and may act as a marker of individual differences and dysfunctions. Based on recent fMRI findings, the hypothalamus is mostly connected to parts of the striatum, midbrain, thalamus, insula, frontal, cingulate, and temporal cortices and the cerebellum. There is a strong interplay of the hypothalamus with these regions in response to different metabolic, hormonal, and nutritional states. In a state of hunger, hypothalamus RSFC increases with a strong shift to reward-related brain regions, especially in person with excessive weight. Nutrient signals and hormones, as insulin, act on these same connections conveying reward and internal signals to regulate homeostatic control. Moreover, dysfunctional hypothalamus communication has been documented in persons with neurological and psychiatric diseases. The results implicate that patients with depression, epilepsy, and neurodegenerative diseases show mostly a reduction in hypothalamus RSFC, whereas patients with migraine and headache display predominantly increased hypothalamus RSFC. The extent of these changes and regions affected depend on the disorder and symptom severity. Whether hypothalamus RSFC can serve as a marker for disease states or is a prodromal neurobiological feature still needs to be investigated.

The aim of the study was to evaluate the diagnostic performance of the item concerning physical activity of the Global Initiative for Asthma (GINA) asthma control questionnaire for detection of exercise-induced bronchoconstriction (EIB) in children and adolescents.

We divided participants (aged 6-18 years) with a diagnosis of asthma into two groups according to the GINA severity classification mild/moderate asthma (MMA) and severe therapy-resistant asthma (STRA). We collected anthropometric, clinical and functional data (spirometry) and performed an EIB test. We used item 4 of the GINA questionnaire regarding exercise-induced symptoms to assess the diagnostic power of this instrument.

We included 40 patients (17 with MMA and 23 with STRA) with a mean age of 11.3 years and a mean FEV

z-score of -0.33, of who 13 (32.5%) were classified as having uncontrolled asthma. Of the patients with uncontrolled asthma, 7 (53.8%) exhibited a decrease in the FEV

after the EIB test. We found a higher frequency of EIB in participants with FEV

z-score values of less than -1.0 compared to those with a z-score of -1.0 or greater (P = .05). There were no significant differences in the frequency of EIB based on disease severity and control. We also found no association of item 4 (GINA) with EIB. The area under the ROC curve demonstrated that the discriminative power of the GINA questionnaire for the detection of EIB is inadequate (P = .41), with sensitivity of 42.1% and specificity of 57.1%.

The item concerning physical activity in the GINA questionnaire has insufficient diagnostic power to detect EIB in children and adolescents with asthma.

The item concerning physical activity in the GINA questionnaire has insufficient diagnostic power to detect EIB in children and adolescents with asthma.The hypothalamic peptide oxytocin has been increasingly recognized as a hormone and neurotransmitter with important effects on energy intake, metabolism, and body weight and is under investigation as a potential novel therapeutic agent for obesity. click here The main neurons producing oxytocin and expressing the oxytocin receptor are strategically located in brain areas known to be critically involved in homeostatic energy balance as well as hedonic and motivational aspects of eating behavior. In this chapter, we will review the central and peripheral physiology of oxytocin and the interaction of oxytocin with key hormones and neural circuitries that affect food intake and metabolism. Next, we will synthesize the available data on endogenous oxytocin levels related to caloric intake, body weight, and metabolic status. We will then review the effects of exogenous oxytocin administration on eating behavior, body weight, and metabolism in humans, including in healthy individuals as well as specific populations with suspected perturbations involving oxytocin pathways. Finally, we will address the promise and fundamental challenges of translating this line of research to clinical care.Vasopressin and oxytocin are primarily synthesized in the magnocellular supraoptic and paraventricular nuclei of the hypothalamus and transported to the posterior pituitary. In the human, an extensive accessory magnocellular neuroendocrine system is present with contact to the posterior pituitary and blood vessels in the hypothalamus itself. Vasopressin and oxytocin are involved in social and behavioral functions. However, only few neocortical areas are targeted by vasopressinergic and oxytocinergic nerve fibers, which mostly project to limbic areas in the forebrain, where also their receptors are located. Vasopressinergic/oxytocinergic perikarya in the forebrain project to the brain stem and spinal cord targeting nuclei and areas involved in autonomic functions. Parvocellular neurons containing vasopressin are located in the suprachiasmatic nucleus and synchronize the activity of the pacemaker in this nucleus. From the suprachiasmatic nucleus fibers project to the parvocellular part of the paraventricular nucleus, where preautonomic neurons project to the intermediolateral nucleus in the thoracic spinal cord, from where the superior cervical ganglion is reached whose noradrenergic fibers terminate in the pineal gland to stimulate melatonin secretion at night. The pineal gland is also innervated by vasopressin- and oxytocin-containing fibers reaching the gland via the "central innervation" in the pineal stalk, which might be involve in an annual regulation of melatonin secretion.The neuropeptides oxytocin (OT) and vasopressin (VP) are known to mediate social cognition and behaviors in a sex-dependent manner. This chapter reviews the sex-dependent influence of OT and VP on social behaviors, focusing on (1) partner preference and sexual orientation, (2) memory modulation, (3) emotion regulation, and (4) trust-related behaviors. Most studies suggest that OT promotes familiar (opposite-sex) partner preference, strengthens memory, relieves anxiety, and increases trust. However, VP-regulated social cognition has been studied less than OT. VP facilitates familiar (opposite-sex) partner preference, enhances memory, induces anxiety, and influences happiness/anger perception. Detailed sex differences of these effects are reviewed. There is a male preponderance in the use of animal models and many study results are too complex to draw firm conclusions. Clarifying the complex interplay between the OT/VP system and sex hormones in the regulation of social behaviors is needed.