scholarly journals Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms

2021 ◽  
Vol 22 (14) ◽  
pp. 7272
Author(s):  
Omar Hahad ◽  
Andreas Daiber ◽  
Matthias Michal ◽  
Marin Kuntic ◽  
Klaus Lieb ◽  
...  
Keyword(s):  
Risk Factor ◽  
Experimental Studies ◽  
Public Health Perspective ◽  
Neuropsychiatric Disease ◽  
Global Epidemic ◽  
Neuropsychiatric Diseases ◽  
Disease Associations ◽  
The Central Nervous System ◽  
Underlying Mechanisms ◽  
And Oxidative Stress

Despite extensive efforts to combat cigarette smoking/tobacco use, it still remains a leading cause of global morbidity and mortality, killing more than eight million people each year. While tobacco smoking is a major risk factor for non-communicable diseases related to the four main groups—cardiovascular disease, cancer, chronic lung disease, and diabetes—its impact on neuropsychiatric risk is rather elusive. The aim of this review article is to emphasize the importance of smoking as a potential risk factor for neuropsychiatric disease and to identify central pathophysiological mechanisms that may contribute to this relationship. There is strong evidence from epidemiological and experimental studies indicating that smoking may increase the risk of various neuropsychiatric diseases, such as dementia/cognitive decline, schizophrenia/psychosis, depression, anxiety disorder, and suicidal behavior induced by structural and functional alterations of the central nervous system, mainly centered on inflammatory and oxidative stress pathways. From a public health perspective, preventive measures and policies designed to counteract the global epidemic of smoking should necessarily include warnings and actions that address the risk of neuropsychiatric disease.

scholarly journals The Synergistic Effects of APOE Genotype and Obesity on Alzheimer’s Disease Risk

2018 ◽  
Vol 20 (1) ◽  
pp. 63 ◽  
Author(s):  
Nahdia Jones ◽  
G. Rebeck
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Cognitive Deficits ◽  
Disease Risk ◽  
Synergistic Effects ◽  
Apoe Genotype ◽  
Global Epidemic ◽  
Underlying Mechanisms ◽  
Apoe Genotypes

The APOE gene has three common alleles—E2, E3, and E4, with APOE4 being the strongest genetic risk factor for developing Alzheimer’s Disease (AD). Obesity is a global epidemic and contributes to multiple metabolic problems. Obesity is also a risk factor for cognitive decline. Here, we review the effects of APOE4 and obesity on cognition and AD development, independently and together. We describe studies that have associated APOE4 with cognitive deficits and AD, as well as studies that have associated obesity to cognitive deficits and AD. We then describe studies that have examined the effects of obesity and APOE genotypes together, with a focus on APOE4 and high fat diets. Both human studies and rodent models have contributed to understanding the effects of obesity on the different APOE genotypes, and we outline possible underlying mechanisms associated with these effects. Data across approaches support a model in which APOE4 and obesity combine for greater detrimental effects on metabolism and cognition, in ways that are influenced by both age and sex.

Dispositional negativity, cognition, and anxiety disorders: An integrative translational neuroscience framework

2019 ◽  
Author(s):  
Juyoen Hur ◽  
Melissa D. Stockbridge ◽  
Andrew S. Fox ◽  
Alexander J. Shackman
Keyword(s):  
Risk Factor ◽  
Anxiety Disorders ◽  
Executive Control ◽  
Intervention Strategies ◽  
Attentional Biases ◽  
Translational Neuroscience ◽  
Adult Personality ◽  
Fundamental Dimension ◽  
To Come ◽  
Underlying Mechanisms

When extreme, anxiety can become debilitating. Anxiety disorders, which often first emerge early in development, are common and challenging to treat, yet the underlying mechanisms have only recently begun to come into focus. Here, we review new insights into the nature and biological bases of dispositional negativity, a fundamental dimension of childhood temperament and adult personality and a prominent risk factor for the development of pediatric and adult anxiety disorders. Converging lines of epidemiological, neurobiological, and mechanistic evidence suggest that dispositional negativity increases the likelihood of psychopathology via specific neurocognitive mechanisms, including attentional biases to threat and deficits in executive control. Collectively, these observations provide an integrative translational framework for understanding the development and maintenance of anxiety disorders in adults and youth and set the stage for developing improved intervention strategies.

Mechanisms underlying heart failure in type 2 diabetes mellitus

2019 ◽  
pp. 37-39
Keyword(s):  
Diabetes Mellitus ◽  
Heart Failure ◽  
Experimental Studies ◽  
Vascular Complications ◽  
Molecular Alterations ◽  
Increased Risk ◽  
Cardioprotective Effects ◽  
Underlying Mechanisms ◽  
Cardio Vascular

The prevalence of heart failure is markedly increased in individuals with diabetes mellitus. Numerous observational studies suggest that this increased risk for heart failure can be attributed to exacerbated vascular complications and the presence of increased risk factors in diabetic subjects. In addition, experimental studies revealed the presence of a number of distinct molecular alterations in the myocardium that occur independently of vascular disease and hypertension. Many of these molecular alterations are similarly observed in failing hearts of nondiabetic patients and have thus been proposed to contribute to the increased risk for heart failure in diabetes. The interest in understanding the underlying mechanisms of impaired cardio- vascular outcomes in diabetic individuals has much increased since the demonstration of cardioprotective effects of SGLT-2 inhibitors and GLP-1 receptor agonists in recent clinical trials. The current review therefore summarizes the distinct mechanisms that have been proposed to increase the risk for heart failure in diabetes mellitus.

Prediction of Disease Comorbidity Using HeteSim Scores based on Multiple Heterogeneous Networks

2019 ◽  
Vol 19 (4) ◽  
pp. 232-241 ◽  
Author(s):  
Xuegong Chen ◽  
Wanwan Shi ◽  
Lei Deng
Keyword(s):  
Protein Interactions ◽  
Experimental Studies ◽  
Treatment Strategies ◽  
Computational Method ◽  
Biological Information ◽  
Support Vector ◽  
Protein Protein Interactions ◽  
Efficient Treatment ◽  
Disease Associations ◽  
Previous State

Background: Accumulating experimental studies have indicated that disease comorbidity causes additional pain to patients and leads to the failure of standard treatments compared to patients who have a single disease. Therefore, accurate prediction of potential comorbidity is essential to design more efficient treatment strategies. However, only a few disease comorbidities have been discovered in the clinic. Objective: In this work, we propose PCHS, an effective computational method for predicting disease comorbidity. Materials and Methods: We utilized the HeteSim measure to calculate the relatedness score for different disease pairs in the global heterogeneous network, which integrates six networks based on biological information, including disease-disease associations, drug-drug interactions, protein-protein interactions and associations among them. We built the prediction model using the Support Vector Machine (SVM) based on the HeteSim scores. Results and Conclusion: The results showed that PCHS performed significantly better than previous state-of-the-art approaches and achieved an AUC score of 0.90 in 10-fold cross-validation. Furthermore, some of our predictions have been verified in literatures, indicating the effectiveness of our method.

scholarly journals The neuropathological impact of COVID-19: a review

2021 ◽  
Vol 45 (1) ◽  
Author(s):  
Ghadha Ibrahim Fouad
Keyword(s):  
Main Body ◽  
Respiratory Dysfunction ◽  
Behavior Understanding ◽  
Vital Functions ◽  
Global Issue ◽  
The Central Nervous System ◽  
Underlying Mechanisms ◽  
Neural Disorders ◽  
High Adaptation ◽  
Viral Outbreak

Abstract Background The Coronavirus disease 2019 (COVID-19) outbreak has become a challenging global issue after its emergence in December 2019. Due to the high adaptation of the virus, COVID-19 demonstrated a high transmission and infectivity potentials. Several studies demonstrated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induce deleterious neurological manifestations through interacting with the central nervous system (CNS). Main body The neuroinvasive potential of SARS-CoV-2 might contribute to its fatal behavior. Understanding the underlying mechanisms of this novel neuropathogen might contribute to the development of effective therapeutic strategies. The manifestations of neural damage in COVID-19 patients ranged from headache to severe encephalopathy and progression of preexisting neural disorders, it is speculated that neuroinvasion is strongly linked to the fatal respiratory dysfunction. The underlying neuropathological impact of emerging pneumonia (COVID-19) is still unclear. Conclusion This review demonstrated the urgent need to understand the neuropathology of COVID-19, to manage the current borderless viral outbreak of SARS-CoV-2 and its comorbidities. Moreover, SARS-CoV-2 could be regarded as an opportunistic neuropathogen that affects several vital functions in the human body.

scholarly journals Overexpression of neuregulin 1 in GABAergic interneurons results in reversible cortical disinhibition

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yao-Yi Wang ◽  
Bing Zhao ◽  
Meng-Meng Wu ◽  
Xiao-Li Zheng ◽  
Longnian Lin ◽  
...  
Keyword(s):  
Neural Network ◽  
Intellectual Disabilities ◽  
Sodium Channel ◽  
Susceptibility Gene ◽  
Gabaergic Interneurons ◽  
Neuregulin 1 ◽  
Neuropsychiatric Diseases ◽  
Underlying Mechanisms ◽  
Gabaergic Function ◽  
Schizophrenia Susceptibility

AbstractCortical disinhibition is a common feature of several neuropsychiatric diseases such as schizophrenia, autism and intellectual disabilities. However, the underlying mechanisms are not fully understood. To mimic increased expression of Nrg1, a schizophrenia susceptibility gene in GABAergic interneurons from patients with schizophrenia, we generated gtoNrg1 mice with overexpression of Nrg1 in GABAergic interneurons. gtoNrg1 mice showed cortical disinhibition at the cellular, synaptic, neural network and behavioral levels. We revealed that the intracellular domain of NRG1 interacts with the cytoplasmic loop 1 of Nav1.1, a sodium channel critical for the excitability of GABAergic interneurons, and inhibits Nav currents. Intriguingly, activation of GABAergic interneurons or restoring NRG1 expression in adulthood could rescue the hyperactivity and impaired social novelty in gtoNrg1 mice. These results identify mechanisms underlying cortical disinhibition related to schizophrenia and raise the possibility that restoration of NRG1 signaling and GABAergic function is beneficial in certain neuropsychiatric disorders.

scholarly journals Current Evidence on the Role of the Gut Microbiome in ADHD Pathophysiology and Therapeutic Implications

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 249
Author(s):  
Ana Checa-Ros ◽  
Antonio Jeréz-Calero ◽  
Antonio Molina-Carballo ◽  
Cristina Campoy ◽  
Antonio Muñoz-Hoyos
Keyword(s):  
Gut Microbiome ◽  
Pediatric Patients ◽  
Neurodevelopmental Disorder ◽  
Current Evidence ◽  
Omega 3 ◽  
Therapeutic Implications ◽  
Neuropsychiatric Diseases ◽  
Bidirectional Relationship ◽  
The Central Nervous System

Studies suggest that the bidirectional relationship existent between the gut microbiome (GM) and the central nervous system (CNS), or so-called the microbiome–gut–brain axis (MGBA), is involved in diverse neuropsychiatric diseases in children and adults. In pediatric age, most studies have focused on patients with autism. However, evidence of the role played by the MGBA in attention deficit/hyperactivity disorder (ADHD), the most common neurodevelopmental disorder in childhood, is still scanty and heterogeneous. This review aims to provide the current evidence on the functioning of the MGBA in pediatric patients with ADHD and the specific role of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) in this interaction, as well as the potential of the GM as a therapeutic target for ADHD. We will explore: (1) the diverse communication pathways between the GM and the CNS; (2) changes in the GM composition in children and adolescents with ADHD and association with ADHD pathophysiology; (3) influence of the GM on the ω-3 PUFA imbalance characteristically found in ADHD; (4) interaction between the GM and circadian rhythm regulation, as sleep disorders are frequently comorbid with ADHD; (5) finally, we will evaluate the most recent studies on the use of probiotics in pediatric patients with ADHD.

scholarly journals Infectious disease-associated encephalopathies

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Maria C. Barbosa-Silva ◽  
Maiara N. Lima ◽  
Denise Battaglini ◽  
Chiara Robba ◽  
Paolo Pelosi ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Cognitive Deficits ◽  
Brain Function ◽  
Cell Activation ◽  
Therapeutic Strategies ◽  
Barrier Dysfunction ◽  
Glial Cell Activation ◽  
The Central Nervous System ◽  
Underlying Mechanisms

AbstractInfectious diseases may affect brain function and cause encephalopathy even when the pathogen does not directly infect the central nervous system, known as infectious disease-associated encephalopathy. The systemic inflammatory process may result in neuroinflammation, with glial cell activation and increased levels of cytokines, reduced neurotrophic factors, blood–brain barrier dysfunction, neurotransmitter metabolism imbalances, and neurotoxicity, and behavioral and cognitive impairments often occur in the late course. Even though infectious disease-associated encephalopathies may cause devastating neurologic and cognitive deficits, the concept of infectious disease-associated encephalopathies is still under-investigated; knowledge of the underlying mechanisms, which may be distinct from those of encephalopathies of non-infectious cause, is still limited. In this review, we focus on the pathophysiology of encephalopathies associated with peripheral (sepsis, malaria, influenza, and COVID-19), emerging therapeutic strategies, and the role of neuroinflammation. Graphic abstract

scholarly journals Does Social Exclusion Alter Sensory and Pain Thresholds in Children and Adolescents with Functional Abdominal Pain? – Results from a Preliminary Study

Pain Medicine ◽  
2018 ◽  
Vol 20 (8) ◽  
pp. 1472-1478
Author(s):  
Marco Daniel Gulewitsch ◽  
Aiste Jusyte ◽  
Katja Weimer ◽  
Michael Schönenberg
Keyword(s):  
Abdominal Pain ◽  
Social Exclusion ◽  
Experimental Studies ◽  
Control Group ◽  
Childhood And Adolescence ◽  
Sensory Threshold ◽  
Functional Abdominal Pain ◽  
Pain Thresholds ◽  
Before And After ◽  
Underlying Mechanisms

Abstract Objective Functional abdominal pain (AP) is a prevalent issue in childhood and adolescence. The contribution of psychosocial factors in the development and maintenance of this health problem is rather unclear, and experimental studies about underlying mechanisms are lacking. This study investigates whether experimentally induced social exclusion decreases sensory and pain thresholds in children suffering from AP. Subjects Twenty children/adolescents with AP and 22 healthy controls. Methods Children/adolescents participated in the Cyberball paradigm, which affects an experience of social exclusion. Thermal sensory and pain thresholds were measured before and after Cyberball. Results Children/adolescents with AP showed a divergent reaction regarding their sensory threshold after social exclusion: The control group exhibited a tendency toward a decreased sensory threshold whereas the AP group remained stable. Concerning the pain threshold, no effect of social exclusion could be identified. The increase of both thresholds (“numbing”) after Cyberball was positively correlated with symptoms of mental health issues. Conclusions This is the first study to investigate changes in sensory and pain thresholds following painful social interactions in a sample of children/adolescents with a chronic pain condition. Results suggest that AP and control children differ in their reaction of sensory thresholds, which might indicate an altered processing of social exclusion. Replication and further methodological improvements are needed.

scholarly journals The Molecular Biology of Brain Metastasis

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Gazanfar Rahmathulla ◽  
Steven A. Toms ◽  
Robert J. Weil
Keyword(s):  
Molecular Biology ◽  
Brain Metastasis ◽  
Targeted Drug Delivery ◽  
Rapid Expansion ◽  
Genetic Mechanisms ◽  
The Central Nervous System ◽  
Targeted Drug ◽  
Underlying Mechanisms ◽  
The Brain ◽  
New Location

Metastasis to the central nervous system (CNS) remains a major cause of morbidity and mortality in patients with systemic cancers. Various crucial interactions between the brain environment and tumor cells take place during the development of the cancer at its new location. The rapid expansion in molecular biology and genetics has advanced our knowledge of the underlying mechanisms involved, from invasion to final colonization of new organ tissues. Understanding the various events occurring at each stage should enable targeted drug delivery and individualized treatments for patients, with better outcomes and fewer side effects. This paper summarizes the principal molecular and genetic mechanisms that underlie the development of brain metastasis (BrM).

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