28,353 results match your criteria Lead Encephalopathy


Acute encephalitis in immunocompetent adults.

Lancet 2019 Feb 14;393(10172):702-716. Epub 2019 Feb 14.

National Institute for Health Research Health Protection Research Unit in Emerging and Zoonotic Infections, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK; Department of Neurology, the Walton Center NHS Foundation Trust, Liverpool, UK.

Encephalitis is a condition of inflammation of the brain parenchyma, occurs as a result of infectious or autoimmune causes, and can lead to encephalopathy, seizures, focal neurological deficits, neurological disability, and death. Viral causes account for the largest proportion, but in the last decade there has been growing recognition of anti-neuronal antibody syndromes. This Seminar focuses on the diagnosis and management of acute encephalitis in adults. Read More

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http://dx.doi.org/10.1016/S0140-6736(18)32526-1DOI Listing
February 2019

The mouse as a model of fundamental concepts related to Turner syndrome.

Authors:
Arthur P Arnold

Am J Med Genet C Semin Med Genet 2019 Feb 19. Epub 2019 Feb 19.

Department of Integrative Biology and Physiology, Laboratory of Neuroendocrinology of the Brain Research Institute, University of California, Los Angeles, California.

Although XO mice do not show many of the overt phenotypic features of Turner syndrome (TS; 45,X or XO), mice and humans share different classes of genes on the X chromosome that are more or less likely to cause TS phenotypes. Based on the evolutionary history of the sex chromosomes, and the pattern of dosage balancing among sex chromosomal and autosomal genes in functional gene networks, it is possible to prioritize types of X genes for study as potential causes of features of TS. For example, X-Y gene pairs are among the most interesting because of the convergent effects of X and Y genes that both are likely to prevent the effects of TS in XX and XY individuals. Read More

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http://dx.doi.org/10.1002/ajmg.c.31681DOI Listing
February 2019

Role of Methylprednisolone in the Management of Hemodynamically Unstable Brain-Dead Cases.

Exp Clin Transplant 2019 Jan;17(Suppl 1):257-259

From the Organ Procurement Unit (OPU), Lung Transplantation Research Center (LTRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.

Objectives: Optimal care of potential donors can lead to successful transplantation. Hemodynamic instability is a common complication in deceased potential donors. The most common underlying causes are hormonal and electrolyte disturbances as well as a hyperinflammatory state, which is rooted in activation of the cytokine cascade. Read More

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http://dx.doi.org/10.6002/ect.MESOT2018.P113DOI Listing
January 2019

Clinical heterogeneity of frontotemporal dementia and Parkinsonism linked to chromosome 17 caused by MAPT N279K mutation in relation to tau positron emission tomography features.

Mov Disord 2019 Feb 17. Epub 2019 Feb 17.

Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.

Background: While mechanistic links between tau abnormalities and neurodegeneration have been proven in frontotemporal dementia and parkinsonism linked to chromosome 17 caused by MAPT mutations, variability of the tau pathogenesis and its relation to clinical progressions in the same MAPT mutation carriers are yet to be clarified.

Objectives: The present study aimed to analyze clinical profiles, tau accumulations, and their correlations in 3 kindreds with frontotemporal dementia and parkinsonism linked to chromosome 17 attributed to the MAPT N279K mutation.

Methods: Four patients with N279K mutant frontotemporal dementia and parkinsonism linked to chromosome 17/MAPT underwent [ C]PBB3-PET to estimate regional tau loads. Read More

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http://dx.doi.org/10.1002/mds.27623DOI Listing
February 2019

SHARQnet - Sophisticated harmonic artifact reduction in quantitative susceptibility mapping using a deep convolutional neural network.

Z Med Phys 2019 Feb 14. Epub 2019 Feb 14.

Centre for Advanced Imaging, The University of Queensland, Building 57 of University Dr, St Lucia, QLD 4072, Brisbane, Australia.

Quantitative susceptibility mapping (QSM) reveals pathological changes in widespread diseases such as Parkinson's disease, Multiple Sclerosis, or hepatic iron overload. QSM requires multiple processing steps after the acquisition of magnetic resonance imaging (MRI) phase measurements such as unwrapping, background field removal and the solution of an ill-posed field-to-source-inversion. Current techniques utilize iterative optimization procedures to solve the inversion and background field correction, which are computationally expensive and lead to suboptimal or over-regularized solutions requiring a careful choice of parameters that make a clinical application of QSM challenging. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09393889183016
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http://dx.doi.org/10.1016/j.zemedi.2019.01.001DOI Listing
February 2019
1 Read

Antiepileptic therapy approaches in KCNQ2 related epilepsy: A systematic review.

Eur J Med Genet 2019 Feb 13. Epub 2019 Feb 13.

Division of Pediatric Neurology, Developmental Medicine and Social Pediatrics, Dr. von Haunersches Children's Hospital, LMU Munich, Lindwurmstraße4, 80337, Munich, Germany; Comprehensive Epilepsy Center for Children, Adolescents and Adults, LMU Munich, Lindwurmstraße 4, 80337, Munich, Germany. Electronic address:

Background: KCNQ2 related disorders comprise both benign seizure disorders and early onset epileptic encephalopathies. Especially within the latter group, patients suffer from refractory seizures to standard antiepileptic drugs and developmental delay. Besides the hope of personalized medical approaches to treat the recently unraveled large amount of genetic channelopathies, there are sparse systematic data on treatment responses in KCNQ2 related epilepsy in larger cohorts. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S17697212183066
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http://dx.doi.org/10.1016/j.ejmg.2019.02.001DOI Listing
February 2019
3 Reads

The Contribution of Pluripotent Stem Cell (PSC)-Based Models to the Study of Fragile X Syndrome (FXS).

Brain Sci 2019 Feb 15;9(2). Epub 2019 Feb 15.

Stem Cell Research Laboratory, Medical Genetics Institute, Shaare Zedek Medical Center, Jerusalem 91031, Israel.

Fragile X syndrome (FXS) is the most common heritable form of cognitive impairment. It results from a deficiency in the fragile X mental retardation protein (FMRP) due to a CGG repeat expansion in the 5'-UTR of the X-linked gene. When CGGs expand beyond 200 copies, they lead to epigenetic gene silencing of the gene. Read More

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http://dx.doi.org/10.3390/brainsci9020042DOI Listing
February 2019

Evaluation of brain volume alterations in HCV-infected patients after interferon-free therapy: A pilot study.

J Neurol Sci 2019 Feb 7;399:36-43. Epub 2019 Feb 7.

Department of General Radiology, Interventional Radiology and Neuroradiology, Radiology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland.

The study was performed to evaluate cerebral volume changes in HCV-infected subjects before and after interferon-free therapy with direct-acting antiviral agents (DAA). We aimed also to estimate the impact of successful DAA therapy on the neuropsychological state of patients. Eleven HCV genotype 1 (GT1) patients treated with ombitasvir/paritaprevir (boosted with ritonavir) and dasabuvir, with or without ribavirin underwent brain magnetic resonance (MR) before and 24 weeks after completion of therapy. Read More

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http://dx.doi.org/10.1016/j.jns.2019.02.002DOI Listing
February 2019
1 Read

Berardinelli-Seip syndrome and progressive myoclonus epilepsy.

Epileptic Disord 2019 Feb 15. Epub 2019 Feb 15.

Child Neurology and Psychiatry Unit, "Regina Montis Regalis" Hospital, Mondovì.

Berardinelli-Seip syndrome, or congenital generalized lipodystrophy type 2 (CGL2), is characterized by a lack of subcutaneous adipose tissue and precocious metabolic syndrome with insulin resistance, resulting in diabetes, dyslipidaemia, hepatic steatosis, cardiomyopathy, and acanthosis nigricans. Most reported mutations are associated with mild, non-progressive neurological impairment. We describe the clinical and EEG data of a patient with progressive myoclonus epilepsy (PME), CGL2, and progressive neurological impairment, carrying a homozygous BSCL2 nonsense mutation. Read More

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http://dx.doi.org/10.1684/epd.2019.1038DOI Listing
February 2019
1 Read

Differential Response Following Infection of Mouse CNS with Virulent and Attenuated Vaccinia Virus Strains.

Vaccines (Basel) 2019 Feb 12;7(1). Epub 2019 Feb 12.

Department of Infectious Diseases, Israel Institute of Biological Research (IIBR), Ness-Ziona, Israel.

Viral infections of the central nervous system (CNS) lead to a broad range of pathologies. CNS infections with Orthopox viruses have been mainly documented as an adverse reaction to smallpox vaccination with vaccinia virus. To date, there is insufficient data regarding the mechanisms underlying pathological viral replication or viral clearance. Read More

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http://www.mdpi.com/2076-393X/7/1/19
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http://dx.doi.org/10.3390/vaccines7010019DOI Listing
February 2019
3 Reads

The Astrocytic cAMP Pathway in Health and Disease.

Int J Mol Sci 2019 Feb 12;20(3). Epub 2019 Feb 12.

Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-0033, Japan.

Astrocytes are major glial cells that play critical roles in brain homeostasis. Abnormalities in astrocytic functions can lead to brain disorders. Astrocytes also respond to injury and disease through gliosis and immune activation, which can be both protective and detrimental. Read More

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http://dx.doi.org/10.3390/ijms20030779DOI Listing
February 2019

[The unusual couple: a clinical case of coexistence between aHUS and Fabry's disease].

G Ital Nefrol 2019 Feb;36(1)

Professore Ordinario di Nefrologia, Università degli Studi della Campania, Luigi Vanvitelli.

Atypical hemolytic-uremic syndrome (aHUS) is a rare, potentially lethal (1-4) systemic disorder, capable of affecting both adults and children, causing thrombotic microangiopathy (TMA) (5) that leads to the formation of thrombus within small blood vessels with multiple organ failure. The pathogenesis of the aHUS is part of a sort of chronic and uncontrolled activation of the complement system by genetic mutation of some proteins usually responsible for its self-regulation (6,7). Today, the rapid diagnosis of the disease and the timely start of treatment with eculizumab, improve outcomes of renal failure, stroke and heart attack (8-10). Read More

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February 2019
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Clinical, neuroradiological, and biochemical features of SLC35A2-CDG patients.

J Inherit Metab Dis 2019 Jan 12. Epub 2019 Jan 12.

Department of Clinical Genetics, United Laboratories, Tartu University Hospital, Tartu, Estonia.

SLC35A2-CDG is caused by mutations in the X-linked SLC35A2 gene encoding the UDP-galactose transporter. SLC35A2 mutations lead to hypogalactosylation of N-glycans. SLC35A2-CDG is characterized by severe neurological symptoms and, in many patients, early-onset epileptic encephalopathy. Read More

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http://dx.doi.org/10.1002/jimd.12055DOI Listing
January 2019
1 Read

Novel Homozygous Mutation in the WWOX Gene Causes Seizures and Global Developmental Delay: Report and Review.

Transl Neurosci 2018 31;9:203-208. Epub 2018 Dec 31.

King Abdullah International Medical Research Centre (KAIMRC), King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs (MNGHA), Riyadh, Saudi Arabia.

The gene has a WW domain containing oxidoreductase, which is located at the common fragile site FRA16D at chromosome 16q23. is a tumor suppressor gene that has been associated with several types of cancer such as hepatic, breast, lung, prostate, gastric, and ovarian. Recently WWOX has been implicated in epilepsy, where studies show homozygous loss-of-function mutation lead to early-infantile epileptic encephalopathy, spinocerebellar ataxia, intractable seizures and developmental delay, and early lethal microcephaly syndrome with epilepsy. Read More

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http://dx.doi.org/10.1515/tnsci-2018-0029DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368664PMC
December 2018
2 Reads

Risk and Protective Environmental Factors Associated with Autism Spectrum Disorder: Evidence-Based Principles and Recommendations.

J Clin Med 2019 Feb 8;8(2). Epub 2019 Feb 8.

Child Neurology and Psychiatry Unit, Systems Medicine Department, Tor Vergata University of Rome, 00133 Rome, Italy.

Autism Spectrum Disorder (ASD) is a complex condition with early childhood onset, characterized by a set of common behavioral features. The etiology of ASD is not yet fully understood; however, it reflects the interaction between genetics and environment. While genetics is now a well-established risk factor, several data support a contribution of the environment as well. Read More

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http://dx.doi.org/10.3390/jcm8020217DOI Listing
February 2019
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Protein misfolding and aggregation in neurodegenerative diseases: a review of pathogeneses, novel detection strategies, and potential therapeutics.

Rev Neurosci 2019 Feb 12. Epub 2019 Feb 12.

Department of Physiology and Biophysics, Stony Brook University School of Medicine, 101 Nicolls Road, Health Sciences Center, Stony Brook, NY 11794-8434, USA.

Protein folding is a complex, multisystem process characterized by heavy molecular and cellular footprints. Chaperone machinery enables proper protein folding and stable conformation. Other pathways concomitant with the protein folding process include transcription, translation, post-translational modifications, degradation through the ubiquitin-proteasome system, and autophagy. Read More

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http://dx.doi.org/10.1515/revneuro-2016-0035DOI Listing
February 2019
2 Reads

Inborn errors of coenzyme A metabolism and neurodegeneration.

J Inherit Metab Dis 2019 Jan;42(1):49-56

Unit of Molecular Neurogenetics - Pierfranco and Luisa Mariani Centre for the Study of Mitochondrial Disorders in Children, Foundation IRCCS Neurological Institute C. Besta, Via Temolo 4, Milan 20126, Italy.

Two inborn errors of coenzyme A (CoA) metabolism are responsible for distinct forms of neurodegeneration with brain iron accumulation (NBIA), a heterogeneous group of neurodegenerative diseases having as a common denominator iron accumulation mainly in the inner portion of globus pallidus. Pantothenate kinase-associated neurodegeneration (PKAN), an autosomal recessive disorder with progressive impairment of movement, vision and cognition, is the most common form of NBIA and is caused by mutations in the pantothenate kinase 2 gene (PANK2), coding for a mitochondrial enzyme, which phosphorylates vitamin B5 in the first reaction of the CoA biosynthetic pathway. Another very rare but similar disorder, denominated CoPAN, is caused by mutations in coenzyme A synthase gene (COASY) coding for a bi-functional mitochondrial enzyme, which catalyzes the final steps of CoA biosynthesis. Read More

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http://dx.doi.org/10.1002/jimd.12026DOI Listing
January 2019

Impact of epilepsy duration, seizure control and EEG abnormalities on cognitive impairment in drug-resistant epilepsy patients.

Acta Neurol Belg 2019 Feb 8. Epub 2019 Feb 8.

Faculty of Medical Sciences, Department of Infectious Diseases, University of Kragujevac, Serbia, 69 Svetozara Markovica St., 34000, Kragujevac, Serbia.

Cognitive impairment frequently occurs in epilepsy patients. Patients with drug-resistant epilepsy (DRE) have poor drug responsivity and higher seizure frequency which consequently lead to brain damage and may have implications on cognitive status. In the present study, we assessed a frequency and degree of cognitive impairment in 52 patients with drug-sensitive epilepsy (DSE) and 103 DRE patients at three time points (baseline, after 12 and 18 months). Read More

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http://dx.doi.org/10.1007/s13760-019-01090-xDOI Listing
February 2019

Complete recovery in Wernicke's encephalopathy complicating hyperemesis gravidarum.

BMJ Case Rep 2019 Feb 7;12(2). Epub 2019 Feb 7.

Department of Obstetrics and Gynecology, Jawaharlal Institute of Post-graduate Medical Education and Research, Pondicherry, India.

Wernicke's encephalopathy (WE) is an uncommon neurological complication in pregnancies complicated with hyperemesis due to thiamine deficiency. In women with hyperemesis, inadvertent glucose administration prior to thiamine supplementation triggers the development of neurological manifestations. Delay in the diagnosis can lead to maternal morbidity, and in one-third of cases may lead to persistence of some neurological deficit. Read More

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http://dx.doi.org/10.1136/bcr-2018-227530DOI Listing
February 2019
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[Retinovascular Findings in Susac's Syndrome].

Laryngorhinootologie 2019 Feb 8;98(2):108-113. Epub 2019 Feb 8.

Background: Susac syndrome is a vasculopathy affecting the central nervous system, retina and cochlea leading to the triad encephalopathy, branch retinal artery occlusions and hearing loss. To date, about 300 cases have been described in the literature.

Patients/methods: Three patients with confirmed Susac syndrome were evaluated for disease-specific retinal pathologies. Read More

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http://dx.doi.org/10.1055/a-0747-6968DOI Listing
February 2019

[Psychosocial Care For Patients With Amyotrophic Lateral Sclerosis: A Narrative Review].

Psychother Psychosom Med Psychol 2019 Feb 7. Epub 2019 Feb 7.

Abteilung für Medizinische Psychologie und Medizinische Soziologie, Universitätsklinikum Leipzig.

This narrative review gives a broad summary of the psychosocial strain in patients with amyotrophic lateral sclerosis (ALS) and psychotherapeutic interventions addressing these issues. ALS is a fatal, rapidly progressing neurodegenerative disease, which leads to weakness and atrophy in almost all muscles of the body, resulting in impairment and finally inability in all domains of daily life including mobility, food intake, respiration or communication. In addition to these mainly motor impairments, most patients are also affected by severe cognitive-emotional and behavioral alterations and deficits which may lead to additional distress. Read More

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http://dx.doi.org/10.1055/a-0806-7862DOI Listing
February 2019
1 Read

Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis.

JCI Insight 2019 Feb 7;4(3). Epub 2019 Feb 7.

Departments of Biomedical Sciences and Pediatrics, Divisions of Infectious Diseases and Immunology.

Kawasaki disease (KD), the leading cause of acquired cardiac disease among children, is often associated with myocarditis that may lead to long-term myocardial dysfunction and fibrosis. Although those myocardial changes develop during the acute phase, they may persist for decades and closely correlate with long-term myocardial sequelae. Using the Lactobacillus casei cell wall extract-induced (LCWE-induced) KD vasculitis murine model, we investigated long-term cardiovascular sequelae, such as myocardial dysfunction, fibrosis, and coronary microvascular lesions following adrenergic stimuli after established KD vasculitis. Read More

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https://insight.jci.org/articles/view/126279
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http://dx.doi.org/10.1172/jci.insight.126279DOI Listing
February 2019
2 Reads

Less Is More - Estimation of the Number of Strides Required to Assess Gait Variability in Spatially Confined Settings.

Front Aging Neurosci 2018 21;10:435. Epub 2019 Jan 21.

Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Neurocure Cluster of Excellence, Berlin, Germany.

Gait variability is an established marker of gait function that can be assessed using sensor-based approaches. In clinical settings, spatial constraints and patient condition impede the execution of longer distance walks for the recording of gait parameters. Turning paradigms are often used to overcome these constraints and commercial gait analysis systems algorithmically exclude turns for gait parameters calculations. Read More

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http://dx.doi.org/10.3389/fnagi.2018.00435DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348278PMC
January 2019
1 Read

Investigation of occupational exposure to lead and its relation with blood lead levels in electrical solderers.

Environ Monit Assess 2019 Feb 4;191(3):126. Epub 2019 Feb 4.

Health Sciences Research Center, Addiction Institute, Mazandaran University of Medical Sciences, Sari, Mazandaran, Iran.

Occupational exposure to lead compounds can cause headache, nausea, encephalopathy, anemia, chronic muscle pain, and saturnism. Exposure to lead in women can affect fertility, and cause abortion or low IQ in the offspring. The aim of this study was to investigate occupational exposure to lead and its relation with blood lead levels in female electrical parts solderers. Read More

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http://link.springer.com/10.1007/s10661-019-7258-x
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http://dx.doi.org/10.1007/s10661-019-7258-xDOI Listing
February 2019
2 Reads

Levofloxacin-associated Encephalopathy with Severe Hyperventilation.

Intern Med 2019 Feb 1. Epub 2019 Feb 1.

Department of Internal Medicine, Tokyo Women's Medical University Medical Center East, Japan.

A 64-year-old woman with no previous mental illness took a single 500 mg tablet of levofloxacin for cystitis. Two hours later, she developed psychosis with involuntary movement and severe hyperventilation with respiratory alkalosis. Cranial magnetic resonance imaging findings were unremarkable, and an electroencephalogram revealed no epileptiform discharge. Read More

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http://dx.doi.org/10.2169/internalmedicine.1619-18DOI Listing
February 2019
1 Read

The Ca-Binding S100B Protein: An Important Diagnostic and Prognostic Neurobiomarker in Pediatric Laboratory Medicine.

Methods Mol Biol 2019 ;1929:701-728

Neonatal Intensive Care Unit, Department of Pediatrics, University of Chieti, Chieti, Italy.

In recent decades a significant scientific effort has focused on projects regarding the use of neurobiomarkers in perinatal medicine with a view to understanding the mechanisms that interfere with physiological patterns of brain development and lead to ominous effects in several human diseases. Numerous potential neurobiomarkers have been proposed for use in monitoring high-risk fetuses and newborns, including markers of oxidative stress, neuroproteins, and vasoactive agents. Nonetheless, the use of these markers in clinical practice remains a matter of debate. Read More

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http://dx.doi.org/10.1007/978-1-4939-9030-6_44DOI Listing
January 2019

Mutations in and in a patient with early-onset epileptic encephalopathy and respiratory depression.

Cold Spring Harb Mol Case Stud 2019 Feb 1;5(1). Epub 2019 Feb 1.

Epilepsy Genetics Program, Department of Neurology, Boston Children's Hospital, Boston, Massachusetts 02115, USA.

Early infantile epileptic encephalopathy (EIEE) is a severe disorder associated with epilepsy, developmental delay and intellectual disability, and in some cases premature mortality. We report the case of a female infant with EIEE and strikingly suppressed respiratory dysfunction that led to death. Postmortem research evaluation revealed hypoplasia of the arcuate nucleus of the medulla, a candidate region for respiratory regulation. Read More

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http://dx.doi.org/10.1101/mcs.a003442DOI Listing
February 2019
2 Reads

Hepatic Encephalopathy in Cirrhosis: Pathology and Pathophysiology.

Drugs 2019 Jan 31. Epub 2019 Jan 31.

Department of Medicine, University of Montreal, 45143 Cabot Trail, Englishtown, NS, B0C 1H0, Canada.

Neuropathology of hepatic encephalopathy (HE) in cirrhosis is primarily astroglial in nature characterized by Alzheimer type 2 astrocytosis together with activation of microglia indicative of neuroinflammation. Focal loss of neurons may also occur in the basal ganglia, thalamus and cerebellum. Pathophysiology of HE in cirrhosis is multifactorial, involving brain accumulation of ammonia and manganese, systemic and central inflammation, nutritional/metabolic factors and activation of the GABAergic neurotransmitter system. Read More

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http://dx.doi.org/10.1007/s40265-018-1017-0DOI Listing
January 2019
1 Read

Concussion Evaluation and Management.

Med Clin North Am 2019 Mar 3;103(2):251-261. Epub 2018 Dec 3.

Department of Neurology, Mayo Clinic College of Medicine, 13400 East Shea Boulevard, Scottsdale, AZ 85259, USA. Electronic address:

Concussion is a public health crisis affecting vulnerable populations including youth athletes. As awareness increases, more patients with acute concussion are seeking medical evaluations. Internists are frontline medical providers and thus should be able to identify, diagnose, manage, and know when to refer patients with concussion. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00257125183012
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http://dx.doi.org/10.1016/j.mcna.2018.10.005DOI Listing
March 2019
3 Reads

Methamphetamine and its immune-modulating effects.

Maturitas 2019 Mar 5;121:13-21. Epub 2018 Dec 5.

Institute for Health and Sport, Victoria University, Melbourne, VIC, Australia. Electronic address:

The recreational use of methamphetamine (METH, or ice) is a global burden. It pervades and plagues contemporary society; it has been estimated that there are up to 35 million users worldwide. METH is a highly addictive psychotropic compound which acts on the central nervous system, and chronic use can induce psychotic behavior. Read More

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http://dx.doi.org/10.1016/j.maturitas.2018.12.003DOI Listing
March 2019
2 Reads
2.942 Impact Factor

Inflammatory Mechanisms in Neurodegeneration.

J Neurochem 2019 Jan 31. Epub 2019 Jan 31.

Department of Biomedical Sciences, University of North, Dakota School of Medicine and Health Sciences, Grand Forks, ND, USA.

This review discusses the profound connection between microglia, neuroinflammation, and Alzheimer's disease (AD) . Theories have been postulated, tested, and modified over several decades. The findings have further bolstered the belief that microglia-mediated inflammation is both a product and contributor to AD pathology and progression. Read More

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http://dx.doi.org/10.1111/jnc.14674DOI Listing
January 2019

Minimal hepatic encephalopathy: current clinical and pathogenetic aspects.

Authors:
I V Damulin

Ter Arkh 2018 Feb;90(2):89-93

I.M. First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.

The review considers modern ideas about the clinic and pathogenesis of minimal hepatic encephalopathy (MHE). It is discussed the present of cognitive impairment in this category of patients. The data of functional MRI are analyzed, and these results allow taking a fresh look at the origin of clinical disorders in this condition. Read More

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http://dx.doi.org/10.26442/terarkh201890289-93DOI Listing
February 2018
1 Read

National Trends in Hospitalizations for Stroke Associated With Infective Endocarditis and Opioid Use Between 1993 and 2015.

Stroke 2019 Jan 30:STROKEAHA118024436. Epub 2019 Jan 30.

From the Clinical and Translational Neuroscience Unit, Department of Neurology, Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY (S.S.O., A.C., M.L.C., M.P.L., A.E.M., H.K.).

Background and Purpose- There has been a recent sharp rise in opioid-related deaths in the United States. Intravenous opioid use can lead to infective endocarditis (IE) which can result in stroke. There are scant data on recent trends in this neurological complication of opioid abuse. Read More

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http://dx.doi.org/10.1161/STROKEAHA.118.024436DOI Listing
January 2019
1 Read

Profiling of Argonaute-2-loaded microRNAs in a mouse model of frontotemporal dementia with parkinsonism-17.

Int J Physiol Pathophysiol Pharmacol 2018 25;10(6):172-183. Epub 2018 Dec 25.

Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland Dublin 2, Ireland.

Tauopathies are a group of neurodegenerative diseases characterized by the pathological aggregation of the microtubule-associated protein tau. These include more than 20 diseases, with Alzheimer's disease being the most frequent. While pathological and neurotoxic effects of tau are well documented, the mechanisms by which tau can promote neurodegeneration are less clear. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334219PMC
December 2018
1 Read

Clinical and EEG Characteristics of Ifosfamide-Related Encephalopathy.

J Clin Neurophysiol 2019 Jan 30. Epub 2019 Jan 30.

Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, New York, U.S.A.

Purpose: Ifosfamide can lead to a syndrome of central nervous system toxicity. Here, we investigate the clinical and EEG characteristics of patients with ifosfamide-related encephalopathy.

Methods: Retrospective data were collected on patients from Memorial Sloan Kettering Cancer Center, who developed encephalopathy associated with ifosfamide between 2007 and 2017. Read More

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http://Insights.ovid.com/crossref?an=00004691-900000000-9948
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http://dx.doi.org/10.1097/WNP.0000000000000539DOI Listing
January 2019
1 Read

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer's Disease.

Front Neurosci 2018 14;12:1027. Epub 2019 Jan 14.

Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Cross-talk between adipose tissue and central nervous system (CNS) underlies the increased risk of obese people to develop brain diseases such as cognitive and mood disorders. Detailed mechanisms for how peripheral changes caused by adipose tissue accumulation in obesity impact the CNS to cause brain dysfunction are poorly understood. Adipokines are a large group of substances secreted by the white adipose tissue to regulate a wide range of homeostatic processes including, but not limited to, energy metabolism and immunity. Read More

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http://dx.doi.org/10.3389/fnins.2018.01027DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6340072PMC
January 2019
1 Read

PD-1/PD-L1 checkpoint blockade harnesses monocyte-derived macrophages to combat cognitive impairment in a tauopathy mouse model.

Nat Commun 2019 01 28;10(1):465. Epub 2019 Jan 28.

Department of Neurobiology, Weizmann Institute of Science, Rehovot, 7610001, Israel.

Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies. Harnessing the immune system by blocking the programmed cell death receptor (PD)-1 pathway in an amyloid beta mouse model was shown to evoke a sequence of immune responses that lead to disease modification. Here, blocking PD-L1, a PD-1 ligand, was found to have similar efficacy to that of PD-1 blocking in disease modification, in both animal models of AD and of tauopathy. Read More

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http://www.nature.com/articles/s41467-019-08352-5
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http://dx.doi.org/10.1038/s41467-019-08352-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349941PMC
January 2019
4 Reads

Dyschromatosis symmetrica hereditaria and reticulate acropigmentation of Kitamura: An update.

J Dermatol Sci 2019 Jan 15. Epub 2019 Jan 15.

Department of Dermatology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.

Dyschromatosis symmetrica hereditaria (DSH) and reticulate acropigmentation of Kitamura (RAK) are rare, inherited pigmentary diseases. DSH shows a mixture of pigmented and depigmented macules on the extremities. RAK shows reticulated, slightly depressed pigmented macules on the extremities. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09231811193000
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http://dx.doi.org/10.1016/j.jdermsci.2019.01.004DOI Listing
January 2019
7 Reads

Novel Approach for the Search for Chemical Scaffolds with Dual Activity with Acetylcholinesterase and the α7 Nicotinic Acetylcholine Receptor-A Perspective for the Treatment of Neurodegenerative Disorders.

Molecules 2019 Jan 27;24(3). Epub 2019 Jan 27.

Sydney School of Pharmacy, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia.

Neurodegenerative disorders, including Alzheimer's disease, belong to the group of the most difficult and challenging conditions with very limited treatment options. Attempts to find new drugs in most cases fail at the clinical stage. New tactics to develop better drug candidates to manage these diseases are urgently needed. Read More

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http://dx.doi.org/10.3390/molecules24030446DOI Listing
January 2019
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Activin Receptor-Like Kinase 1 Combined With VEGF-A Affects Migration and Proliferation of Endothelial Cells From Sporadic Human Cerebral AVMs.

Front Cell Neurosci 2018 9;12:525. Epub 2019 Jan 9.

Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Heterozygous loss of activin receptor-like kinase 1 (Alk1) can lead to hereditary hemorrhagic telangiectasia (HHT), which is a kind of vascular disease characterized by direct connections between arteries and veins with the lacking of capillaries, and develops into arteriovenous malformations (AVMs) in later stage. However, the changes of Alk1 in human sporadic cerebral AVMs (cAVMs) remain unknown. In the present study, we used endothelial cells (ECs) derived from human cAVMs (cAVM-ECs) specimens, to explore the characteristics of cAVM-ECs and the relationship between Alk1 and human sporadic cAVMs. Read More

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http://dx.doi.org/10.3389/fncel.2018.00525DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333867PMC
January 2019
2 Reads

[Significance of kallikrein-kinin system in central nervous system diseases].

Wiad Lek 2018 ;71(8):1615-1620

Katedra Podstawowych Nauk Biomedycznych, Wydział Farmaceutyczny z Oddziałem Medycyny Laboratoryjnej w Sosnowcu, Śląski Uniwersytet Medyczny w Katowicach., Sosnowiec, Polska, Szpital Wielospecjalistyczny w Jaworznie, Jaworzno, Polska.

Kallikreins cleave kininogens to release kinins. Kinins exert their biological effect by activating constitutive bradykinin receptor-2 (BR2) and inducible by inflammatory cytokines bradykinin receptor-1 (BR1). Studies in animal models and some clinical observations indicate tat the activation of kallikrein - kinin system may have relevance to central nervous system (CNS) diseases, including multiple sclerosis, Alzheimer's disease, epilepsy as well as cerebral ischemia and neoplasmatic tumors. Read More

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January 2018
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Pathogenic variants in USP7 cause a neurodevelopmental disorder with speech delays, altered behavior, and neurologic anomalies.

Genet Med 2019 Jan 25. Epub 2019 Jan 25.

Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA.

Purpose: Haploinsufficiency of USP7, located at chromosome 16p13.2, has recently been reported in seven individuals with neurodevelopmental phenotypes, including developmental delay/intellectual disability (DD/ID), autism spectrum disorder (ASD), seizures, and hypogonadism. Further, USP7 was identified to critically incorporate into the MAGEL2-USP7-TRIM27 (MUST), such that pathogenic variants in USP7 lead to altered endosomal F-actin polymerization and dysregulated protein recycling. Read More

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http://www.nature.com/articles/s41436-019-0433-1
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http://dx.doi.org/10.1038/s41436-019-0433-1DOI Listing
January 2019
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The adjuvant effect of C(OH) nanoparticles promoting both humoral and cellular immune responses to HCV recombinant proteins.

Mater Sci Eng C Mater Biol Appl 2019 Apr 27;97:753-759. Epub 2018 Dec 27.

CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety and CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing 100190, China. Electronic address:

Hepatitis c virus (HCV) infection is one of major causes for chronic liver diseases worldwide and could lead to death. Development of effective HCV vaccines is a powerful auxiliary method of existing treatments. Adjuvants are necessary for modern vaccines to promote immune responses. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09284931183171
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http://dx.doi.org/10.1016/j.msec.2018.12.088DOI Listing
April 2019
4 Reads

L-Ferritin: One Gene, Five Diseases; from Hereditary Hyperferritinemia to Hypoferritinemia-Report of New Cases.

Pharmaceuticals (Basel) 2019 Jan 23;12(1). Epub 2019 Jan 23.

BloodGenetics SL, Esplugues de Llobregat, 08950 Barcelona, Spain.

Ferritin is a multimeric protein composed of light (L-ferritin) and heavy (H-ferritin) subunits that binds and stores iron inside the cell. A variety of mutations have been reported in the L-ferritin subunit gene ( gene) that cause the following five diseases: (1) hereditary hyperferritinemia with cataract syndrome (HHCS), (2) neuroferritinopathy, a subtype of neurodegeneration with brain iron accumulation (NBIA), (3) benign hyperferritinemia, (4) L-ferritin deficiency with autosomal dominant inheritance, and (5) L-ferritin deficiency with autosomal recessive inheritance. Defects in the gene lead to abnormally high levels of serum ferritin (hyperferritinemia) in HHCS and benign hyperferritinemia, while low levels (hypoferritinemia) are present in neuroferritinopathy and in autosomal dominant and recessive L-ferritin deficiency. Read More

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http://www.mdpi.com/1424-8247/12/1/17
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http://dx.doi.org/10.3390/ph12010017DOI Listing
January 2019
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Astrocyte activation and altered metabolism in normal aging, age-related CNS diseases, and HAND.

J Neurovirol 2019 Jan 22. Epub 2019 Jan 22.

Department of Neuroscience and Center for Neurovirology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.

Astrocytes regulate local cerebral blood flow, maintain ion and neurotransmitter homeostasis, provide metabolic support, regulate synaptic activity, and respond to brain injury, insults, and infection. Because of their abundance, extensive connectivity, and multiple roles in the brain, astrocytes are intimately involved in normal functioning of the CNS and their dysregulation can lead to neuronal dysfunction. In normal aging, decreased biological functioning and reduced cognitive abilities are commonly experienced in individuals free of overt neurological disease. Read More

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http://dx.doi.org/10.1007/s13365-019-00721-6DOI Listing
January 2019

Hyperglycemia aggravates decrease in alpha-synuclein expression in a middle cerebral artery occlusion model.

Lab Anim Res 2018 Dec 31;34(4):195-202. Epub 2018 Dec 31.

Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, Jinju, Korea.

Hyperglycemia is one of the major risk factors for stroke. Hyperglycemia can lead to a more extensive infarct volume, aggravate neuronal damage after cerebral ischemia. α-Synuclein is especially abundant in neuronal tissue, where it underlies the etiopathology of several neurodegenerative diseases. Read More

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http://dx.doi.org/10.5625/lar.2018.34.4.195DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333603PMC
December 2018

The Neonatal Acute Bilirubin Encephalopathy Registry (NABER): Background, Aims, and Protocol.

Neonatology 2019 Jan 22;115(3):242-246. Epub 2019 Jan 22.

Division of Neonatal and Developmental Medicine, Department of Pediatrics, Stanford University School of Medicine and the Lucile Salter Packard Children's Hospital, Stanford, California, USA.

Background: Acute bilirubin encephalopathy (ABE) is a potentially devastating condition that can lead to death or life-long neurodevelopmental handicaps. ABE is particularly tragic because it is, in theory, completely preventable. Progress toward its prevention has been hampered by the perception that the extreme hyperbilirubinemia giving rise to ABE typically has no clear causation, with the majority of previous cases being labeled as "idiopathic" neonatal jaundice. Read More

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http://dx.doi.org/10.1159/000495518DOI Listing
January 2019
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Transient Cognitive Impairment in Epilepsy.

Front Mol Neurosci 2018 7;11:458. Epub 2019 Jan 7.

NEST, Istituto Nanoscienze-CNR and Scuola Normale Superiore, Pisa, Italy.

Impairments of the dialog between excitation and inhibition (E/I) is commonly associated to neuropsychiatric disorders like autism, bipolar disorders and epilepsy. Moderate levels of hyperexcitability can lead to mild alterations of the EEG and are often associated with cognitive deficits even in the absence of overt seizures. Indeed, various testing paradigms have shown degraded performances in presence of acute or chronic non-ictal epileptiform activity. Read More

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http://dx.doi.org/10.3389/fnmol.2018.00458DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330286PMC
January 2019
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Studies towards the development of a PET radiotracer for imaging of the P2Y receptors in the brain: synthesis, F-labeling and preliminary biological evaluation.

Eur J Med Chem 2019 Mar 7;165:142-159. Epub 2019 Jan 7.

Helmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Permoserstraße 15, 04318, Leipzig, Germany.

Purine nucleotides such as ATP and ADP are important extracellular signaling molecules in almost all tissues activating various subtypes of purinoreceptors. In the brain, the P2Y receptor (P2YR) subtype mediates trophic functions like differentiation and proliferation, and modulates fast synaptic transmission, both suggested to be affected in diseases of the central nervous system. Research on P2YR is limited because suitable brain-penetrating P2YR-selective tracers are not yet available. Read More

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http://dx.doi.org/10.1016/j.ejmech.2019.01.006DOI Listing
March 2019
8 Reads