scholarly journals Molecular Mechanisms of Cancer-Induced Sleep Disruption

2019 ◽  
Author(s):  
William H. Walker II ◽  
Jeremy C. Borniger
Keyword(s):  
Molecular Mechanisms ◽  
Systemic Disease ◽  
Sleep Disruption ◽  
Poor Sleep ◽  
Therapeutic Approaches ◽  
Treatment Regimens ◽  
Patients With Cancer ◽  
And Behavior ◽  
The Brain

Sleep is essential for health. Indeed, poor sleep is consistently linked to the development of systemic disease, including depression, metabolic syndrome, and cognitive impairments. Further evidence has accumulated suggesting a role for sleep in cancer initiation and progression (primarily breast cancer). Indeed, patients with cancer and cancer survivors frequently experience poor sleep, manifested as insomnia, circadian misalignment, hypersomnia, somnolence syndrome, hot flushes, and nightmares. These problems are associated with a reduction in patients’ quality of life and increased mortality. Due to the heterogeneity among cancers, treatment regimens, patient populations, and lifestyle factors, the etiology of cancer-induced sleep disruption is largely unknown. Here, we discuss recent advances in understanding the pathways linking cancer and the brain and how this leads to altered sleep patterns. We describe a conceptual framework where tumors disrupt normal homeostatic processes, resulting in aberrant changes in physiology and behavior that are detrimental to health. Finally, we discuss how this knowledge can be leveraged to develop novel therapeutic approaches for cancer-associated sleep disruption, with special emphasis on host-tumor interactions.

scholarly journals Molecular Mechanisms of Cancer-Induced Sleep Disruption

2019 ◽  
Vol 20 (11) ◽  
pp. 2780 ◽  
Author(s):  
William H. Walker ◽  
Jeremy C. Borniger
Keyword(s):  
Molecular Mechanisms ◽  
Systemic Disease ◽  
Sleep Disruption ◽  
Poor Sleep ◽  
Therapeutic Approaches ◽  
Treatment Regimens ◽  
Patients With Cancer ◽  
And Behavior

Sleep is essential for health. Indeed, poor sleep is consistently linked to the development of systemic disease, including depression, metabolic syndrome, and cognitive impairments. Further evidence has accumulated suggesting the role of sleep in cancer initiation and progression (primarily breast cancer). Indeed, patients with cancer and cancer survivors frequently experience poor sleep, manifesting as insomnia, circadian misalignment, hypersomnia, somnolence syndrome, hot flushes, and nightmares. These problems are associated with a reduction in the patients’ quality of life and increased mortality. Due to the heterogeneity among cancers, treatment regimens, patient populations and lifestyle factors, the etiology of cancer-induced sleep disruption is largely unknown. Here, we discuss recent advances in understanding the pathways linking cancer and the brain and how this leads to altered sleep patterns. We describe a conceptual framework where tumors disrupt normal homeostatic processes, resulting in aberrant changes in physiology and behavior that are detrimental to health. Finally, we discuss how this knowledge can be leveraged to develop novel therapeutic approaches for cancer-associated sleep disruption, with special emphasis on host-tumor interactions.

scholarly journals Surgical management of brain metastases

2007 ◽  
Vol 22 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Moksha G. Ranasinghe ◽  
Jonas M. Sheehan
Keyword(s):  
Brain Tumors ◽  
Systemic Disease ◽  
Postoperative Management ◽  
Study Data ◽  
Preoperative Imaging ◽  
Metastatic Brain Tumors ◽  
Patients With Cancer ◽  
Proper Patient Selection ◽  
Positive Effect

✓Metastatic brain tumors continue to increase in incidence as patients with cancer live longer. The options for management continue to evolve as well, with advances in radiation-based treatment, chemotherapy, and surgery. Although metastatic brain tumors are frequently treated without surgical intervention, there continues to be a significant role for surgery in caring for patients with these lesions. Study data have proven that surgery has a positive effect on survival and quality of life in properly selected patients. Those with a suitable age, functional status, systemic disease control, and several metastases may be suitable for surgical treatment. Advances in preoperative imaging and planning as well as intraoperative surgical adjuncts have lowered the morbidity associated with resection. With proper patient selection and operative and postoperative management, resection continues to play a significant and evolving role in the care of patients with metastatic brain tumor.

scholarly journals Microbiota modulation by eating patterns and diet composition: impact on food intake

2018 ◽  
Vol 315 (6) ◽  
pp. R1254-R1260 ◽  
Author(s):  
Elizabeth Klingbeil ◽  
Claire B. de La Serre
Keyword(s):  
Diet Composition ◽  
Food Composition ◽  
Eating Patterns ◽  
Microbiota Composition ◽  
Gi Tract ◽  
Nucleus Of Solitary Tract ◽  
And Behavior ◽  
The Brain ◽  
Lps Treatment

There is accumulating evidence that the gut microbiota and its composition dynamics play a crucial role in regulating the host physiological functions and behavior. Diet composition is the primary modulator of bacterial richness and abundance in the gastrointestinal (GI) tract. Macronutrient (fat, sugar, and protein) and fiber contents are especially important in determining microbiota composition and its effect on health outcomes and behavior. In addition to food composition, time of intake and eating patterns have recently been shown to significantly affect gut bacterial makeup. Diet-driven unfavorable microbiota composition, or dysbiosis, can lead to an increased production of proinflammatory by-products such as lipopolysaccharide (LPS). Increased inflammatory potential is associated with alteration in gut permeability, resulting in elevated levels of LPS in the bloodstream, or metabolic endotoxemia. We have found that a chronic increase in circulating LPS is sufficient to induce hyperphagia in rodents. Chronic LPS treatment appears to specifically impair the gut-brain axis and vagally mediated satiety signaling. The vagus nerve relays information on the quantity and quality of nutrients in the GI tract to the nucleus of solitary tract in the brain stem. There is evidence that microbiota dysbiosis is associated with remodeling of the vagal afferent pathway and that normalizing the microbiota composition in rats fed a high-fat diet is sufficient to prevent vagal remodeling. Taken together, these data support a role for the microbiota in regulating gut-brain communication and eating behavior. Bacteria-originating inflammation may play a key role in impairment of diet-driven satiety and the development of hyperphagia.

scholarly journals Mechanismen genetischer Epilepsien

e-Neuroforum ◽  
2013 ◽  
Vol 19 (2) ◽  
Author(s):  
Ulrike Hedrich ◽  
Snezana Maljevic ◽  
Holger Lerche
Keyword(s):  
Ion Channels ◽  
Secondary Effects ◽  
Therapeutic Approaches ◽  
Neuronal Populations ◽  
The Everyday ◽  
The Common ◽  
Genetic Epilepsies ◽  
Idiopathic Epilepsies ◽  
The Brain

AbstractMechanisms of genetic epilepsies. Epilepsy is one of the most common neurological disorders. Already at the time of Hippocrates (460 - 370 BC) it was reported on as the “holy disease” (Fröscher 2004). Today it is known that an epileptic seizure is a consequence of synchronous discharges of neuronal populations in the brain, which abruptly and usually without an observ­able cause evoke involuntary behavioural dysfunction or impaired consciousness. Epilepsies can have various causes and lead to extensive implications for the everyday life of affected patients. Up to 50 % of all epilepsies are caused by genetic defects, in particular the so-called idiopathic epilepsies which occur without easily observable structural alterations of the brain. Genetically caused dysfunctions of neuronal ion channels play a central role in the formation of such epilepsies. The ion channels control the ion flux over the cell membrane of neurons and thus present the basis for the excitability of these neurons. Therefore, medications used for epilepsy treatment affect predominantly ion channels. However, the common anticonvulsants have limited success, not only because one third of epilepsy patients exhibits pharmacoresistance, but also because of the secondary effects which can dramatically affect their quality of life. Furthermore, current therapeutic approaches are mainly symptomatic and do not act on the epileptogenic mechanisms which are still largely unknown. In this review article we will highlight the current main topics of our research on genetically caused epilepsies, their pathomechanisms and therapeutic options.

scholarly journals Neurotrophins and Neurotrophic Therapy (Based on the Cerebrolysin Model) in the Treatment of Elderly Patients with Cognitive Disorders and Depression. Part 2

Psychiatry ◽  
2021 ◽  
Vol 19 (3) ◽  
pp. 80-89
Author(s):  
S. I. Gavrilova ◽  
T. P. Safarova
Keyword(s):  
Molecular Mechanisms ◽  
Common Mental Disorders ◽  
Cognitive Disorders ◽  
The Elderly ◽  
Therapeutic Approaches ◽  
Neurodegenerative Process ◽  
Target Drug ◽  
Higher Doses ◽  
The Brain ◽  
Neurotrophic Therapy

Background: сognitive impairment and late depression, along with dementia, are the most common mental disorders in elderly and senile patients. Currently, more and more attention is being paid to preventive therapeutic approaches in the treatment of these conditions and to the study of drugs with multimodal neuroprotective and neurotrophic properties that contribute to the strengthening of the so-called endogenous system of protection and recovery of the brain, which is a kind of barrier to the incipient neurodegeneration. Objective: to present a review of domestic and foreign modern studies devoted to the study of the multimodal effects of the drug cerebrolysin, which has neurotrophin-like properties, and the results of its use in the treatment of cognitive disorders that do not reach the degree of dementia, as well as late depression. Material and methods: using the keywords “late age, mild cognitive disorders, depression, MCI syndrome, therapy, cerebrolysin”, we searched for scientifi c articles in the MEDLINE and PubMed databases for the period 2000–2020. Conclusion: the data presented in the review showed that cerebrolysin, acting as a multi-target drug, affects multiple molecular mechanisms of the pathogenesis of pre-dementia cognitive disorders and late-age depression. The drug detects a neurotrophin-like effect, improves the processes of neuroplasticity and can help enhance the protection and restoration of the brain under various pathological infl uences. Neurobiological studies and the results of a pilot prospective study indicate the preventive potential of cerebrolysin in preventing the development or slowing the progression of the neurodegenerative process of Alzheimer’s type. In the studies presented in the review, the ability of cerebrolysin to increase the effectiveness of modern antidepressant therapy (with second-generation drugs) in the elderly has been shown, presumably by potentiating the therapeutic effect of antidepressants or by improving their tolerability, which makes it possible to safely use higher doses of antidepressants in the elderly and senile patients.

scholarly journals Drosophila as a Model for Microbiota Studies of Neurodegeneration

2021 ◽  
pp. 1-12
Author(s):  
Fukiko Kitani-Morii ◽  
Robert P. Friedland ◽  
Hideki Yoshida ◽  
Toshiki Mizuno
Keyword(s):  
Gut Microbiota ◽  
Molecular Mechanisms ◽  
Environmental Changes ◽  
Fruit Fly ◽  
Endocrine Regulation ◽  
Nutrient Metabolism ◽  
Host Health ◽  
And Behavior ◽  
The Brain ◽  
Lateral Sclerosis

Accumulating evidence show that the gut microbiota is deeply involved not only in host nutrient metabolism but also in immune function, endocrine regulation, and chronic disease. In neurodegenerative conditions such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis, the gut-brain axis, the bidirectional interaction between the brain and the gut, provides new route of pathological spread and potential therapeutic targets. Although studies of gut microbiota have been conducted mainly in mice, mammalian gut microbiota is highly diverse, complex, and sensitive to environmental changes. Drosophila melanogaster, a fruit fly, has many advantages as a laboratory animal: short life cycle, numerous and genetically homogenous offspring, less ethical concerns, availability of many genetic models, and low maintenance costs. Drosophila has a simpler gut microbiota than mammals and can be made to remain sterile or to have standardized gut microbiota by simple established methods. Research on the microbiota of Drosophila has revealed new molecules that regulate the brain-gut axis, and it has been shown that dysbiosis of the fly microbiota worsens lifespan, motor function, and neurodegeneration in AD and PD models. The results shown in fly studies represents a fundamental part of the immune and proteomic process involving gut-microbiota interactions that are highly conserved. Even though the fly’s gut microbiota are not simple mimics of humans, flies are a valuable system to learn the molecular mechanisms of how the gut microbiota affect host health and behavior.

scholarly journals Sleep quality with WHO Step III opioid use for cancer pain

2018 ◽  
Vol 9 (3) ◽  
pp. 307-315 ◽  
Author(s):  
Gunnhild Jakobsen ◽  
Morten Engstrøm ◽  
Peter Fayers ◽  
Marianne J Hjermstad ◽  
Stein Kaasa ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Sleep Quality ◽  
Cancer Pain ◽  
Advanced Cancer ◽  
Poor Sleep ◽  
Global Score ◽  
Patients With Cancer ◽  
Emotional Function ◽  
Financial Difficulties

ObjectiveSleep is often disturbed in patients with advanced cancer. There is limited knowledge about sleep in patients with cancer treated with strong opioids. This study examines sleep quality in patients with advanced cancer who are treated with a WHO Step III opioid for pain.MethodsAn international, multicentre, cross-sectional study with 604 adult patients with cancer pain using WHO Step III opioids. Sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI) global score (range; 0–21; score >5 indicates poor sleep). PSQI includes sleep quality, sleep latency, sleep duration, sleep efficiency, sleep disturbances, use of sleep medications and daytime dysfunction. Pain and quality of life were assessed by Brief Pain Inventory and European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire Core30.ResultsThe median age was 62 years, 42% were female, mean Karnofsky performance score (KPS) was 62.5 (±14.2) and mean oral daily morphine equivalent dose was 303 mg/24 hours (±543.8 mg). The mean PSQI global score was 8.8 (±4.2) (range 0–20). Seventy-eight per cent were poor sleepers. All PSQI components were affected, and 44% reported trouble sleeping caused by pain. In the multiple regression model, predictors of PSQI global scores were pain intensity, emotional function, constipation, financial difficulties and KPS (adjusted R2=0.21).ConclusionThe majority (78%) of these patients with cancer treated with Step III opioids experienced poor sleep quality. Pain intensity, emotional function, constipation, financial difficulties and KPS predicted poor PSQI global scores. The clinical implication is that healthcare personnel should routinely assess and treat sleep disturbance in patients with advanced cancer disease.

scholarly journals Effects of Neurological Disorders on Bone Health

2020 ◽  
Vol 11 ◽  
Author(s):  
Ryan R. Kelly ◽  
Sara J. Sidles ◽  
Amanda C. LaRue
Keyword(s):  
Bone Health ◽  
Neurological Disorders ◽  
Molecular Mechanisms ◽  
Neurological Diseases ◽  
Sensory Innervation ◽  
Current Evidence ◽  
Bone Homeostasis ◽  
Shared Risk ◽  
The Brain

Neurological diseases, particularly in the context of aging, have serious impacts on quality of life and can negatively affect bone health. The brain-bone axis is critically important for skeletal metabolism, sensory innervation, and endocrine cross-talk between these organs. This review discusses current evidence for the cellular and molecular mechanisms by which various neurological disease categories, including autoimmune, developmental, dementia-related, movement, neuromuscular, stroke, trauma, and psychological, impart changes in bone homeostasis and mass, as well as fracture risk. Likewise, how bone may affect neurological function is discussed. Gaining a better understanding of brain-bone interactions, particularly in patients with underlying neurological disorders, may lead to development of novel therapies and discovery of shared risk factors, as well as highlight the need for broad, whole-health clinical approaches toward treatment.

scholarly journals Recent Advances and Future Perspectives in the Development of Therapeutic Approaches for Neurodegenerative Diseases

2020 ◽  
Vol 10 (9) ◽  
pp. 633
Author(s):  
Melissa Bowerman
Keyword(s):  
Quality Of Life ◽  
Alzheimer’S Disease ◽  
Neurodegenerative Diseases ◽  
Huntington's Disease ◽  
Neuronal Cells ◽  
Future Perspectives ◽  
Therapeutic Approaches ◽  
Recent Advances ◽  
The Brain

Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD), severely impact the function of neuronal cells in the brain and have devastating consequences on the quality of life of patients and their families [...]

scholarly journals The Interrelation between Reactive Oxygen Species and Autophagy in Neurological Disorders

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Congcong Fang ◽  
Lijuan Gu ◽  
Daniel Smerin ◽  
Shanping Mao ◽  
Xiaoxing Xiong
Keyword(s):  
Cerebral Ischemia ◽  
Neurological Disorders ◽  
Molecular Mechanisms ◽  
Cell Damage ◽  
Cellular Defense ◽  
Neuronal Homeostasis ◽  
Pathogenic Factors ◽  
The Brain ◽  
Cytotoxic Substance

Neurological function deficits due to cerebral ischemia or neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) have long been considered a thorny issue in clinical treatment. Recovery after neurologic impairment is fairly limited, which poses a major threat to health and quality of life. Accumulating evidences support that ROS and autophagy are both implicated in the onset and development of neurological disorders. Notably, oxidative stress triggered by excess of ROS not only puts the brain in a vulnerable state but also enhances the virulence of other pathogenic factors, just like mitochondrial dysfunction, which is described as the culprit of nerve cell damage. Nevertheless, autophagy is proposed as a subtle cellular defense mode against destructive stimulus by timely removal of damaged and cytotoxic substance. Emerging evidence suggests that the interplay of ROS and autophagy may establish a determinant role in the modulation of neuronal homeostasis. However, the underlying regulatory mechanisms are still largely unexplored. This review sets out to afford an overview of the crosstalk between ROS and autophagy and discusses relevant molecular mechanisms in cerebral ischemia, AD, and PD, so as to provide new insights into promising therapeutic targets for the abovementioned neurological conditions.

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