scholarly journals The hypothalamus for whole-body physiology: from metabolism to aging

2021 ◽  
Author(s):  
Tiemin Liu ◽  
Yong Xu ◽  
Chun-Xia Yi ◽  
Qingchun Tong ◽  
Dongsheng Cai
Keyword(s):  
Treatment Strategies ◽  
Brain Dysfunction ◽  
Brain Inflammation ◽  
Whole Body ◽  
Health Issues ◽  
Root Cause ◽  
Metabolic Physiology ◽  
Key Issues ◽  
New Treatment ◽  
The Brain

AbstractObesity and aging are two important epidemic factors for metabolic syndrome and many other health issues, which contribute to devastating diseases such as cardiovascular diseases, stroke and cancers. The brain plays a central role in controlling metabolic physiology in that it integrates information from other metabolic organs, sends regulatory projections and orchestrates the whole-body function. Emerging studies suggest that brain dysfunction in sensing various internal cues or processing external cues may have profound effects on metabolic and other physiological functions. This review highlights brain dysfunction linked to genetic mutations, sex, brain inflammation, microbiota, stress as causes for whole-body pathophysiology, arguing brain dysfunction as a root cause for the epidemic of aging and obesity-related disorders. We also speculate key issues that need to be addressed on how to reveal relevant brain dysfunction that underlines the development of these disorders and diseases in order to develop new treatment strategies against these health problems.

Endometrial Cancer State of the Science Meeting

2009 ◽  
Vol 19 (1) ◽  
pp. 134-140 ◽  
Author(s):  
Henry C. Kitchener ◽  
Edward L. Trimble
Keyword(s):  
Endometrial Cancer ◽  
Current Knowledge ◽  
Gynecological Cancer ◽  
Treatment Strategies ◽  
List Type ◽  
Uterine Carcinosarcoma ◽  
National Cancer Research Institute ◽  
Key Issues ◽  
New Treatment ◽  
State Of The Science

There is a pressing need to improve our understanding of endometrial cancer (EC) and uterine carcinosarcoma and to develop new treatment strategies to improve outcomes. In recognition of this, a State of the Science meeting on EC was held last November 28 and 29, 2006, in Manchester, United Kingdom. The meeting was cosponsored by the National Cancer Research Institute (UK), the National Cancer Institute (US), and the Gynecological Cancer Intergroup.The objectives of the meeting were as follows: To review current knowledge and understanding of EC and its treatments.To identify key issues for translational research and clinical trials.To identify the most important trials for women with endometrial carcinoma and uterine carcinosarcoma, both those already underway or to be done, for which the Gynecological Cancer Intergroup might facilitate international cooperation.

scholarly journals The Role of 2-Oxoglutarate Dependent Dioxygenases in Gliomas and Glioblastomas: A Review of Epigenetic Reprogramming and Hypoxic Response

2021 ◽  
Vol 11 ◽  
Author(s):  
Rebekah L. I. Crake ◽  
Eleanor R. Burgess ◽  
Janice A. Royds ◽  
Elisabeth Phillips ◽  
Margreet C. M. Vissers ◽  
...  
Keyword(s):  
Patient Survival ◽  
Hypoxia Inducible Factor ◽  
Treatment Strategies ◽  
Low Grade ◽  
Histone Demethylases ◽  
Dioxygenase Enzymes ◽  
New Treatment ◽  
New Treatments ◽  
The Brain

Gliomas are a heterogeneous group of cancers that predominantly arise from glial cells in the brain, but may also arise from neural stem cells, encompassing low-grade glioma and high-grade glioblastoma. Whereas better diagnosis and new treatments have improved patient survival for many cancers, glioblastomas remain challenging with a highly unfavorable prognosis. This review discusses a super-family of enzymes, the 2-oxoglutarate dependent dioxygenase enzymes (2-OGDD) that control numerous processes including epigenetic modifications and oxygen sensing, and considers their many roles in the pathology of gliomas. We specifically describe in more detail the DNA and histone demethylases, and the hypoxia-inducible factor hydroxylases in the context of glioma, and discuss the substrate and cofactor requirements of the 2-OGDD enzymes. Better understanding of how these enzymes contribute to gliomas could lead to the development of new treatment strategies.

Epidemiologia zaburzeń neuropoznawczych u pacjentów w wieku podeszłym

2018 ◽  
Vol 21 (3) ◽  
Author(s):  
Wioletta Mędrzycka-Dąbrowska ◽  
Katarzyna Kwiecień-Jaguś ◽  
Renata Piotrkowska ◽  
Piotr Jarzynkowski
Keyword(s):  
The Elderly ◽  
Brain Dysfunction ◽  
Aging Brain ◽  
Psychomotor Slowing ◽  
Functional Changes ◽  
Slowing Down ◽  
Memory Functioning ◽  
Compensation Mechanisms ◽  
Key Issues ◽  
The Brain

The phenomenon of progressive impairment of cognitive functions is characteristic for the aging process. More than half of people over 50 complain about weakening of their previous intellectual performance, reduced mood, impaired memory, psychomotor slowing down, decreased ability to concentrate and divide attention, extend reaction time and reduce motor performance. The basis of mental changes in the elderly are changes in the brain. The changes arising in the aging brain are the result of pathological processes: metabolic and altered cerebral circulation. These changes, and mainly their extent, consequently cause brain dysfunction and are manifested mainly in the deterioration of mental functions. The brain is first and foremost the material basis of a mental life. With age, slow, cumulative and irreversible morphological and functional changes occur in the human brain. This process is slow, which is why it is accompanied by a number of compensation mechanisms. This phenomenon occurs regardless of gender. The aim of this article is to present the key issues related to memory functioning in the elderly, with particular emphasis on neurocognitive impairment after surgery.

Endophenotypes

2020 ◽  
pp. 184-192
Author(s):  
David Braff
Keyword(s):  
De Novo ◽  
Statistical Significance ◽  
Treatment Strategies ◽  
De Novo Mutations ◽  
Treatment Development ◽  
Cognitive Domains ◽  
Gene Transcripts ◽  
Key Issues ◽  
New Treatment ◽  
Control Designs

Since Gottesman introduced the concept of endophenotypes in schizophrenia research, the endophenotype strategy for understanding the genetics of schizophrenia has been used widely. Endophenotypes are wide-ranging laboratory-based quantitative measures from gene transcripts to neurocognition that show deficits in schizophrenia patients and their first-degree relatives. In addition, these deficits are primarily state related and cosegregate with the disorder. Quantitative endophenotypes, such as working memory, share many genes with schizophrenia itself but have 100 times the efficiency and require about 10 times fewer subjects than case-control designs to reach statistical significance for gene finding. Endophenotypes are also platforms for collaborations with scientists studying key issues including de novo mutations and methylation events in psychosis. In addition, the endophenotypes most commonly used in psychosis research are neurocognitive and tap into cognitive domains that have been identified by the FDA and MATRICS project as targets for new treatment development. Thus, the endophenotype strategy is an exciting and dynamic path for gene discovery and personalized treatment strategies in the future.

Toward Precision Medicine in Brain Metastases

2018 ◽  
Vol 38 (01) ◽  
pp. 095-103 ◽  
Author(s):  
Anna Berghoff ◽  
Priscilla Brastianos
Keyword(s):  
Brain Metastases ◽  
Genetic Divergence ◽  
Metastatic Cancer ◽  
Treatment Strategies ◽  
Whole Brain Radiotherapy ◽  
Genetic Alterations ◽  
Brain Radiotherapy ◽  
Genomic Technologies ◽  
New Treatment ◽  
The Brain

AbstractBrain metastases (BMs) reflect an area of high clinical need, as up to 40% of patients with metastatic cancer will develop this morbid and highly fatal complication. Historically, treatment strategies have relied on local approaches including radiosurgery, whole-brain radiotherapy, and neurosurgical resection. Recently, targeted and immune-modulating therapies have shown promising responses and have been introduced in the clinical management of patients with BMs. Recent improvements in genomic technologies have enriched our understanding of BMs and have demonstrated that BMs present with significant genetic divergence from the originating primary tumor, such that potentially targetable genetic alterations are detected only in the BMs. However, this genetic divergence also results in genetic alterations associated with resistance to targeted therapies. A deeper insight on the genetic alterations of BMs and the interaction with the brain microenvironment will likely reveal new treatment targets, moving toward more precision therapies for patients with BMs.

Neurotrophic factors and the pathophysiology of schizophrenic psychoses

2004 ◽  
Vol 19 (6) ◽  
pp. 326-337 ◽  
Author(s):  
Nuria Durany ◽  
Johannes Thome
Keyword(s):  
Neurotrophic Factors ◽  
Neurotrophic Factor ◽  
Treatment Strategies ◽  
Extensive Literature ◽  
National Library ◽  
Gene Level ◽  
Schizophrenic Patients ◽  
Conceptual Paper ◽  
New Treatment ◽  
The Brain

AbstractThe aim of this review is to summarize the present state of findings on altered neurotrophic factor levels in schizophrenic psychoses, on variations in genes coding for neurotrophic factors, and on the effect of antipsychotic drugs on the expression level of neurotrophic factors. This is a conceptual paper that aims to establish the link between the neuromaldevelopment theory of schizophrenia and neurotrophic factors. An extensive literature review has been done using the Pub Med database, a service of the National Library of Medicine, which includes over 14 million citations for biomedical articles back to the 1950s. The majority of studies discussed in this review support the notion of alterations of neurotrophic factors at the protein and gene level, respectively, and support the hypothesis that these alterations could, at least partially, explain some of the morphological, cytoarchitectural and neurobiochemical abnormalities found in the brain of schizophrenic patients. However, the results are not always conclusive and the clinical significance of these alterations is not fully understood. It is, thus, important to further neurotrophic factor research in order to better understand the etiopathogenesis of schizophrenic psychoses and, thus, potentially develop new treatment strategies urgently needed for patients suffering from these devastating disorders.

scholarly journals New Treatment Strategies of Depression: Based on Mechanisms Related to Neuroplasticity

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Yu-Jhen Huang ◽  
Hsien-Yuan Lane ◽  
Chieh-Hsin Lin
Keyword(s):  
Nmda Receptor ◽  
Brain Stimulation ◽  
Depressive Disorders ◽  
Treatment Strategies ◽  
Nmda Receptor Antagonist ◽  
Brain Dysfunction ◽  
Antidepressant Effect ◽  
Noninvasive Brain Stimulation ◽  
Magnetic Seizure Therapy ◽  
New Treatment

Major depressive disorder is a severe and complex mental disorder. Impaired neurotransmission and disrupted signalling pathways may influence neuroplasticity, which is involved in the brain dysfunction in depression. Traditional neurobiological theories of depression, such as monoamine hypothesis, cannot fully explain the whole picture of depressive disorders. In this review, we discussed new treatment directions of depression, including modulation of glutamatergic system and noninvasive brain stimulation. Dysfunction of glutamatergic neurotransmission plays an important role in the pathophysiology of depression. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has rapid and lasting antidepressive effects in previous studies. In addition to ketamine, other glutamatergic modulators, such as sarcosine, also show potential antidepressant effect in animal models or clinical trials. Noninvasive brain stimulation is another new treatment strategy beyond pharmacotherapy. Growing evidence has demonstrated that superficial brain stimulations, such as transcranial magnetic stimulation, transcranial direct current stimulation, cranial electrotherapy stimulation, and magnetic seizure therapy, can improve depressive symptoms. The antidepressive effect of these brain stimulations may be through modulating neuroplasticity. In conclusion, drugs that modulate neurotransmission via NMDA receptor and noninvasive brain stimulation may provide new directions of treatment for depression. Furthermore, exploring the underlying mechanisms will help in developing novel therapies for depression in the future.

scholarly journals Hypoxia Augments Cerebral Inflammation in a Dextran Sulfate Sodium-Induced Colitis Mouse Model

2020 ◽  
Vol 14 ◽  
Author(s):  
Ying Han ◽  
Liping Ding ◽  
Xiang Cheng ◽  
Ming Zhao ◽  
Tong Zhao ◽  
...  
Keyword(s):  
Mouse Model ◽  
Inflammatory Responses ◽  
Brain Dysfunction ◽  
Brain Inflammation ◽  
Control Group ◽  
Hypoxia Exposure ◽  
Hypoxic Conditions ◽  
Hypoxia Group ◽  
Cerebral Inflammation ◽  
The Brain

The importance of hypoxia in the pathophysiology of inflammatory bowel disease (IBD) is increasingly being realized; also, hypoxia seems to be an important accelerator of brain inflammation, as has been reported by our group and others. IBD is a chronic intestinal disorder that leads to the development of inflammation, which is related to brain dysfunction. However, no studies have reported whether hypoxia is associated with IBD-induced neuroinflammation. Therefore, the objective of the present study was to determine whether hypoxia augments cerebral inflammation in a DSS-induced colitis mouse model. The mouse model was developed using 3% DSS for five days combined with exposure to hypoxic conditions (6,000 m) for two days. Mice were randomly divided into four groups: control group, DSS group, hypoxia group, and DSS plus hypoxia group. The results demonstrated that DSS combined with hypoxia resulted in up-regulation of colonic and plasmatic proinflammatory cytokines. Meanwhile, DSS plus hypoxia increased expression of Iba1, which is a marker of activated microglia, accompanied by increased expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the brain. Moreover, the expression of tight junction proteins, such as zonula occludens-1 (ZO-1), occludin, and claudin-5, was markedly downregulated. The current study provides new insight into how hypoxia exposure induces excessive inflammatory responses andpathophysiological consequences in the brain in a DSS-induced colitis model.

Brain–body communication in stroke

Neuroforum ◽  
2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Katarzyna Winek ◽  
Daniel Cuervo Zanatta ◽  
Marietta Zille
Keyword(s):  
Risk Factors ◽  
Atrial Fibrillation ◽  
Stroke Risk ◽  
Treatment Strategies ◽  
The Body ◽  
Cns Injury ◽  
Stroke Risk Factors ◽  
The Central Nervous System ◽  
New Treatment ◽  
The Brain

Abstract Stroke is a leading cause of death and disability worldwide with limited therapeutic options available for selected groups of patients. The susceptibility to stroke depends also on systemic parameters, and some stroke risk factors are modifiable, such as atrial fibrillation (AF) or hypertension. When considering new treatment strategies, it is important to remember that the consequences of stroke are not limited to the central nervous system (CNS) injury, but reach beyond the boundaries of the brain. We provide here a brief overview of the mechanisms of how the brain communicates with the body, focusing on the heart, immune system, and gut microbiota (GM).

scholarly journals Monitoring in vivo neural activity to understand gut-brain signaling

Endocrinology ◽  
2021 ◽  
Author(s):  
Amber L Alhadeff
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Neural Activity ◽  
Weight Control ◽  
Treatment Strategies ◽  
New Treatment ◽  
Body Weight Control ◽  
The Brain ◽  
Intake Control

Abstract Appropriate food intake requires exquisite coordination between the gut and the brain. Indeed, it has long been known that gastrointestinal signals communicate with the brain to promote or inhibit feeding behavior. Recent advances in the ability to monitor and manipulate neural activity in awake, behaving rodents has facilitated important discoveries about how gut signaling influences neural activity and feeding behavior. This review emphasizes recent studies that have advanced our knowledge of gut-brain signaling and food intake control, with a focus on how gut signaling influences in vivo neural activity in animal models. Moving forward, dissecting the complex pathways and circuits that transmit nutritive signals from the gut to the brain will reveal fundamental principles of energy balance, ultimately enabling new treatment strategies for diseases rooted in body weight control.

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