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Developmental Neuroscience 2022Therapeutic hypothermia (TH) is now a standard treatment for infants with moderate-to-severe neonatal encephalopathy (NE), and improves brain damage on neuroimaging and... (Review)
Review
Therapeutic hypothermia (TH) is now a standard treatment for infants with moderate-to-severe neonatal encephalopathy (NE), and improves brain damage on neuroimaging and neurodevelopmental outcomes. Critically, for effective neuroprotection, hypothermia should be started within 6 h from birth. There is compelling evidence to suggest that a proportion of infants with mild NE have material risk of developing brain damage and poor outcomes. This cohort is increasingly being offered TH, despite lack of trial evidence for its benefit. In current practice, infants need to be diagnosed within 6 h of birth for therapeutic treatment, compared to retrospective NE grading in the pre-hypothermia era. This presents challenges as NE is a dynamic brain disorder that can worsen or resolve over time. Neurological symptoms of NE can be difficult to discern in the first few hours after birth, and confounded by analgesics and anesthetic treatment. Using current enrolment criteria, a significant number of infants with NE that would benefit from hypothermia are not treated, and vice versa, some infants receive hypothermia when its benefit will be limited. Better biomarkers are needed to further improve management and treatment of these neonates. In the present review, we examine the latest research, and highlight a central limitation of most current biomarkers: that their predictive value is consistently greatest after most neuroprotective therapies are no longer effective.
Topics: Biomarkers; Brain Injuries; Humans; Hypothermia; Hypothermia, Induced; Hypoxia-Ischemia, Brain; Infant; Infant, Newborn; Infant, Newborn, Diseases; Prognosis; Retrospective Studies
PubMed: 35168240
DOI: 10.1159/000522617 -
Epilepsy & Behavior : E&B Aug 2021Epilepsy is a brain disorder that leads to seizures and neurobiological, cognitive, psychological, and social consequences. Physical inactivity can contribute to worse... (Review)
Review
OBJECTIVE
Epilepsy is a brain disorder that leads to seizures and neurobiological, cognitive, psychological, and social consequences. Physical inactivity can contribute to worse epilepsy pathophysiology. Here, we review how physical exercise affects epilepsy physiopathology.
METHODS
An extensive literature search was performed and the mechanisms of physical exercise on epilepsy were discussed. The search was conducted in Scopus and PubMed. Articles with relevant information were included. Only studies written in English were considered.
RESULTS
The regular practice of physical exercise can be beneficial for individuals with neurodegenerative diseases, such as epilepsy by decreasing the production of pro-inflammatory and stress biomarkers, increasing socialization, and reducing the incidence of epileptic seizures. Physical exercise is also capable of reducing the symptoms of depression and anxiety in epilepsy. Physical exercise can also improve cognitive function in epilepsy. The regular practice of physical exercise enhances the levels of brain-derived neuro factor (BDNF) in the hippocampi, induces neurogenesis, inhibits oxidative stress and reactive gliosis, avoids cognitive impairment, and stimulates the production of dopamine in the epileptic brain.
CONCLUSION
Physical exercise is an excellent non-pharmacological tool that can be used in the treatment of epilepsy.
Topics: Cognitive Dysfunction; Epilepsy; Exercise; Exercise Therapy; Humans; Seizures
PubMed: 34058490
DOI: 10.1016/j.yebeh.2021.108079 -
Alcohol Research & Health : the Journal... 2003Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and... (Review)
Review
Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver before toxins are removed. As a result, toxins such as ammonia and manganese can accumulate in the blood and enter the brain, where they can damage nerve cells and supporting cells called astrocytes. Positron emission tomography analyses have determined that ammonia levels are elevated in the brains of HE patients; ammonia accumulation can alter the expression of various important brain genes. Magnetic resonance images show that manganese is deposited in a brain area called the globus pallidus; manganese deposits may be responsible for structural changes in the astrocytes that are characteristic of HE. Treatment of patients with HE involves measures to lower ammonia levels in the blood, medications to counteract ammonia's effects on brain cell function, devices to compensate for liver dysfunction, and liver transplantation.
Topics: Brain; Hepatic Encephalopathy; Humans; Liver Diseases, Alcoholic
PubMed: 15535452
DOI: No ID Found -
International Journal of Molecular... Feb 2019Brain histamine is a neurotransmitter and regulates diverse physiological functions. Previous studies have shown the involvement of histamine depletion in several... (Review)
Review
Brain histamine is a neurotransmitter and regulates diverse physiological functions. Previous studies have shown the involvement of histamine depletion in several neurological disorders, indicating the importance of drug development targeting the brain histamine system. Histamine -methyltransferase (HNMT) is a histamine-metabolising enzyme expressed in the brain. Although pharmacological studies using HNMT inhibitors have been conducted to reveal the direct involvement of HNMT in brain functions, HNMT inhibitors with high specificity and sufficient blood⁻brain barrier permeability have not been available until now. Recently, we have phenotyped -deficient mice to elucidate the importance of HNMT in the central nervous system. disruption resulted in a robust increase in brain histamine concentration, demonstrating the essential role of HNMT in the brain histamine system. Clinical studies have suggested that single nucleotide polymorphisms of the human gene are associated with several brain disorders such as Parkinson's disease and attention deficit hyperactivity disorder. Postmortem studies also have indicated that HNMT expression is altered in human brain diseases. These findings emphasise that an increase in brain histamine levels by novel HNMT inhibitors could contribute to the improvement of brain disorders.
Topics: Amine Oxidase (Copper-Containing); Animals; Brain; Brain Diseases; Disease Models, Animal; Disease Susceptibility; Enzyme Activation; Enzyme Inhibitors; Gene Expression Regulation, Enzymologic; Histamine; Histamine N-Methyltransferase; Humans; Metabolic Networks and Pathways; Mice; Mice, Knockout; Phenotype; Receptors, Histamine
PubMed: 30744146
DOI: 10.3390/ijms20030737 -
Hellenic Journal of Nuclear Medicine 2017In the past two decades much has been published on whiplash injury, yet both the confusion regarding the condition, and the medicolegal discussion about it have...
In the past two decades much has been published on whiplash injury, yet both the confusion regarding the condition, and the medicolegal discussion about it have increased. In this paper, functional imaging research results are summarized using MRIcroGL 3D visualization software and assembled in an image comprising regions of cerebral activation and deactivation.
Topics: Brain; Brain Diseases; Brain Injuries; Brain Mapping; Evidence-Based Medicine; Humans; Whiplash Injuries
PubMed: 28697186
DOI: 10.1967/s002449910550 -
Tidsskrift For Den Norske Laegeforening... Oct 2022
Topics: Alcohol Amnestic Disorder; Brain Diseases; Humans
PubMed: 36226426
DOI: 10.4045/tidsskr.22.0136 -
Brain Pathology (Zurich, Switzerland) Mar 2023The blood-brain barrier (BBB) is a physiological barrier maintaining a specialized brain micromilieu that is necessary for proper neuronal function. Endothelial tight... (Review)
Review
The blood-brain barrier (BBB) is a physiological barrier maintaining a specialized brain micromilieu that is necessary for proper neuronal function. Endothelial tight junctions and specific transcellular/efflux transport systems provide a protective barrier against toxins, pathogens, and immune cells. The barrier function is critically supported by other cell types of the neurovascular unit, including pericytes, astrocytes, microglia, and interneurons. The dysfunctionality of the BBB is a hallmark of neurological diseases, such as ischemia, brain tumors, neurodegenerative diseases, infections, and autoimmune neuroinflammatory disorders. Moreover, BBB dysfunction is critically involved in epilepsy, a brain disorder characterized by spontaneously occurring seizures because of abnormally synchronized neuronal activity. While resistance to antiseizure drugs that aim to reduce neuronal hyperexcitability remains a clinical challenge, drugs targeting the neurovasculature in epilepsy patients have not been explored. The use of novel imaging techniques permits early detection of BBB leakage in epilepsy; however, the detailed mechanistic understanding of causes and consequences of BBB compromise remains unknown. Here, we discuss the current knowledge of BBB involvement in temporal lobe epilepsy with the emphasis on the neurovasculature as a therapeutic target.
Topics: Humans; Epilepsy, Temporal Lobe; Blood-Brain Barrier; Brain; Astrocytes; Epilepsy
PubMed: 36599709
DOI: 10.1111/bpa.13147 -
Brain Research Bulletin Jan 2018Astrocytes are key active elements of the brain that contribute to information processing. They not only provide neurons with metabolic and structural support, but also... (Review)
Review
Astrocytes are key active elements of the brain that contribute to information processing. They not only provide neurons with metabolic and structural support, but also regulate neurogenesis and brain wiring. Furthermore, astrocytes modulate synaptic activity and plasticity in part by controlling the extracellular space volume, as well as ion and neurotransmitter homeostasis. These findings, together with the discovery that human astrocytes display contrasting characteristics with their rodent counterparts, point to a role for astrocytes in higher cognitive functions. Dysfunction of astrocytes can thereby induce major alterations in neuronal functions, contributing to the pathogenesis of several brain disorders. In this review we summarize the current knowledge on the structural and functional alterations occurring in astrocytes from the human brain in pathological conditions such as epilepsy, primary tumours, Alzheimer's disease, major depressive disorder and Down syndrome. Compelling evidence thus shows that dysregulations of astrocyte functions and interplay with neurons contribute to the development and progression of various neurological diseases. Targeting astrocytes is thus a promising alternative approach that could contribute to the development of novel and effective therapies to treat brain disorders.
Topics: Astrocytes; Brain; Brain Diseases; Gliosis; Humans
PubMed: 28212850
DOI: 10.1016/j.brainresbull.2017.02.001 -
Nature Reviews. Neuroscience Jul 2019Many human brain disorders are associated with characteristic alterations in the structural and functional connectivity of the brain. In this article, we explore how... (Review)
Review
Many human brain disorders are associated with characteristic alterations in the structural and functional connectivity of the brain. In this article, we explore how commonalities and differences in connectome alterations can reveal relationships across disorders. We survey recent literature on connectivity changes in neurological and psychiatric disorders in the context of key organizational principles of the human connectome and observe that several disturbances to network properties of the human brain have a common role in a wide range of brain disorders and point towards potentially shared network mechanisms underpinning disorders. We hypothesize that the distinct dimensions along which connectome networks are organized (for example, 'modularity' and 'integration') provide a general coordinate system that allows description and categorization of relationships between seemingly disparate disorders. We outline a cross-disorder 'connectome landscape of dysconnectivity' along these principal dimensions of network organization that may place shared connectome alterations between brain disorders in a common framework.
Topics: Animals; Brain; Brain Diseases; Connectome; Humans; Nerve Net
PubMed: 31127193
DOI: 10.1038/s41583-019-0177-6 -
Biomolecules Dec 2020The incidence of brain pathologies has increased during last decades. Better diagnosis (autism spectrum disorders) and longer life expectancy (Parkinson's disease,... (Review)
Review
The incidence of brain pathologies has increased during last decades. Better diagnosis (autism spectrum disorders) and longer life expectancy (Parkinson's disease, Alzheimer's disease) partly explain this increase, while emerging data suggest pollutant exposures as a possible but still underestimated cause of major brain disorders. Taking into account that the brain parenchyma is rich in gap junctions and that most pollutants inhibit their function; brain disorders might be the consequence of gap-junctional alterations due to long-term exposures to pollutants. In this article, this hypothesis is addressed through three complementary aspects: (1) the gap-junctional organization and connexin expression in brain parenchyma and their function; (2) the effect of major pollutants (pesticides, bisphenol A, phthalates, heavy metals, airborne particles, etc.) on gap-junctional and connexin functions; (3) a description of the major brain disorders categorized as neurodevelopmental (autism spectrum disorders, attention deficit hyperactivity disorders, epilepsy), neurobehavioral (migraines, major depressive disorders), neurodegenerative (Parkinson's and Alzheimer's diseases) and cancers (glioma), in which both connexin dysfunction and pollutant involvement have been described. Based on these different aspects, the possible involvement of pollutant-inhibited gap junctions in brain disorders is discussed for prenatal and postnatal exposures.
Topics: Air Pollutants; Alzheimer Disease; Brain; Brain Diseases; Cell Communication; Connexin 43; Depressive Disorder, Major; Female; Gap Junctions; Humans; Pregnancy
PubMed: 33396565
DOI: 10.3390/biom11010051