neurolizer

I like to think that both MIB and SHIELD are real, and any time something happens in NY (or London, or wherever else) all of the civilians are neurolized after the event and again after reconstruction (if necessary, depending on damage).

Late-onset spinal form xanthomatosis without brain lesion: a case report.

PubMed: Late-onset spinal form xanthomatosis without brain lesion: a case report.

BMC Neurol. 2016;16(1):21

Authors: Yanagihashi M, Kano O, Terashima T, Kawase Y, Hanashiro S, Sawada M, Ishikawa Y, Shiraga N, Ikeda K, Iwasaki Y

Abstract
BACKGROUND: Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive sterol storage disease caused by a mutated sterol 27-hydroxylase (CYP27A1) gene. Patients with typical CTX show neurological dysfunction including bilateral cataracts, paresis, cerebral ataxia, dementia, and psychiatric disorders, and magnetic resonance imaging (MRI) has revealed symmetrical lesions in the cerebellar white matter.
CASE PRESENTATION: We report the case of a patient with late-onset spinal form CTX without brain lesion. He showed pyramidal tract signs, and impaired joint position and vibration sensation in the lower limbs. Cervical sagittal MRI demonstrated a longitudinally extensive white matter abnormality in the dorsal column of the C2-C7 spinal cord; however, a brain MRI revealed an absence of lesions, including in the cerebellar white matter. Genetic analysis of CYP27A1 revealed that the patient was compound heterozygous for p.Gln85Arg in exon 1, a novel mutation, and p.Arg405Gln in exon 7, a previously reported mutation.
CONCLUSION: This is the first report of late-onset spinal form CTX without typical neurological symptoms, and the first report of p.Gln85Arg in CYP27A1. We speculate that spinal form CTX without brain lesion is a clinically and radiologically rare variation of CTX. Therefore, spinal xanthomatosis should be included in the differential diagnosis of chronic myelopathy even with late-onset and/or no other typical neurological findings.

PMID: 26861945 [PubMed - in process] http://dlvr.it/KTWnTN

This reviews the evidence, efficacy and effectiveness of THC-CBD oromucosal spray in symptom management for patients with spasticity due to MS.

PMID:  Ther Adv Neurol Disord. 2016 Jan ;9(1):9-30. PMID: 26788128 Abstract Title:  Evidence for the efficacy and effectiveness of THC-CBD oromucosal spray in symptom management of patients with spasticity due to multiple sclerosis. Abstract:  Spasticity, one of the main symptoms of multiple sclerosis (MS), can affect more than 80% of MS patients during the course of their disease and is often not treated adequately.δ-9-Tetrahydrocannabinol-cannabidiol (THC-CBD) oromucosal spray is a plant-derived, standardized cannabinoid-based oromucosal spray medicine for add-on treatment of moderate to severe, resistant multiple sclerosis-induced spasticity. This article reviews the current evidence for the efficacy and safety, with dizziness and fatigue as the most common treatment-related adverse events, being mostly mild to moderate in severity. Results from both randomized controlled phase III studies involving about,1600 MS patients or 1500 patient-years and recently published studies on everyday clinical practice involving more than 1000 patients or more than,1000 patient-years are presented.

from Rimedi Sources http://ift.tt/1nT3Kny

This reviews the evidence, efficacy and effectiveness of THC-CBD oromucosal spray in symptom management for patients with spasticity due to MS.

PMID:  Ther Adv Neurol Disord. 2016 Jan ;9(1):9-30. PMID: 26788128 Abstract Title:  Evidence for the efficacy and effectiveness of THC-CBD oromucosal spray in symptom management of patients with spasticity due to multiple sclerosis. Abstract:  Spasticity, one of the main symptoms of multiple sclerosis (MS), can affect more than 80% of MS patients during the course of their disease and is often not treated adequately.δ-9-Tetrahydrocannabinol-cannabidiol (THC-CBD) oromucosal spray is a plant-derived, standardized cannabinoid-based oromucosal spray medicine for add-on treatment of moderate to severe, resistant multiple sclerosis-induced spasticity. This article reviews the current evidence for the efficacy and safety, with dizziness and fatigue as the most common treatment-related adverse events, being mostly mild to moderate in severity. Results from both randomized controlled phase III studies involving about,1600 MS patients or 1500 patient-years and recently published studies on everyday clinical practice involving more than 1000 patients or more than,1000 patient-years are presented.

from Health News Spirulina http://www.greenmedinfo.com/article/reviews-evidence-efficacy-and-effectiveness-thc-cbd-oromucosal-spray-symptom
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Alteration of phospholipids in the blood of patients with Duchenne muscular dystrophy (DMD): in vitro, high resolution (31)P NMR-based study.

Alteration of phospholipids in the blood of patients with Duchenne muscular dystrophy (DMD): in vitro, high resolution (31)P NMR-based study.

Acta Neurol Belg. 2016 Feb 9;

Authors: Srivastava NK, Mukherjee S, Sinha N

Abstract
In vitro, high-resolution (31)P NMR (Nuclear Magnetic Resonance) spectroscopy-based analysis of phospholipids in serum is well recognized in leukemia, lymphoma, non-hematological cancers and renal cell carcinoma. In context of these studies, phospholipids were analyzed in blood of thirty-two (n = 32) patients with Duchenne muscular dystrophy (DMD) (Age, Mean ± SD; 8.0 ± 1.6 years) and sixteen (n = 16) healthy subjects (Age, Mean ± SD; 8.6 ± 2.3 years). Quantity of phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI), phosphatidylserine (PS) and lyso-phosphatidylcholine (Lys-PC) was significantly higher (p < 0.05) in DMD patients as compared to healthy subjects. There were no significant differences (p > 0.05) observed for the quantity of phospholipids in blood of gene deletion positive cases of DMD as compared to negative gene deletion cases of DMD. Quantity of phospholipids in negative gene deletion cases of DMD patients as well as DMD cases with positive gene deletion was significantly higher (p < 0.05) as compared to normal individuals. The present study distinguishes the patients with DMD from the healthy subjects on the basis of the quantity of phospholipids in blood. These observations may be useful in future for the development of new diagnostic method of DMD.

PMID: 26861054 [PubMed - as supplied by publisher]



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Intranasal delivery of hypoxia-preconditioned bone marrow-derived mesenchymal stem cells enhanced regenerative effects after intracerebral hemorrhagic stroke in mice.

PubMed: Related Articles

Intranasal delivery of hypoxia-preconditioned bone marrow-derived mesenchymal stem cells enhanced regenerative effects after intracerebral hemorrhagic stroke in mice.

Exp Neurol. 2015 Oct;272:78-87

Authors: Sun J, Wei ZZ, Gu X, Zhang JY, Zhang Y, Li J, Wei L

Abstract
Intracerebral hemorrhagic stroke (ICH) causes high mortality and morbidity with very limited treatment options. Cell-based therapy has emerged as a novel approach to replace damaged brain tissues and promote regenerative processes. In this study we tested the hypothesis that intranasally delivered hypoxia-preconditioned BMSCs could reach the brain, promote tissue repair and improve functional recovery after ICH. Hemorrhagic stroke was induced in adult C57/B6 mice by injection of collagenase IV into the striatum. Animals were randomly divided into three groups: sham group, intranasal BMSC treatment group, and vehicle treatment group. BMSCs were pre-treated with hypoxic preconditioning (HP) and pre-labeled with Hoechst before transplantation. Behavior tests, including the mNSS score, rotarod test, adhesive removal test, and locomotor function evaluation were performed at varying days, up to 21days, after ICH to evaluate the therapeutic effects of BMSC transplantation. Western blots and immunohistochemistry were performed to analyze the neurotrophic effects. Intranasally delivered HP-BMSCs were identified in peri-injury regions. NeuN+/BrdU+ co-labeled cells were markedly increased around the hematoma region, and growth factors, including BDNF, GDNF, and VEGF were significantly upregulated in the ICH brain after BMSC treatment. The BMSC treatment group showed significant improvement in behavioral performance compared with the vehicle group. Our data also showed that intranasally delivered HP-BMSCs migrated to peri-injury regions and provided growth factors to increase neurogenesis after ICH. We conclude that intranasal administration of BMSC is an effective treatment for ICH, and that it enhanced neuroregenerative effects and promoted neurological functional recovery after ICH. Overall, the investigation supports the potential therapeutic strategy for BMSC transplantation therapy against hemorrhagic stroke.

PMID: 25797577 [PubMed - indexed for MEDLINE] http://dlvr.it/KQxG2Q

A case report of a healthy 10-year-old boy with acute disseminated encephalomyelitis associated with acute acquired Toxoplasma gondii infection.

PMID:  Pediatr Neurol. 2013 Mar ;48(3):236-9. PMID: 23419476 Abstract Title:  Acute disseminated encephalomyelitis associated with acute Toxoplasma gondii Infection. Abstract:  Acute disseminated encephalomyelitis is an acute demyelinating disorder of the central nervous system, which principally affects the brain and spinal cord. It usually follows a benign infection or vaccination in children. Although a number of infectious agents have been implicated in acute disseminated encephalomyelitis, Toxoplasma gondii infection has not been described previously in children. Acquired T. gondii infection presents with lymphadenopathy and fever and usually spontaneously resolves in immunocompetent patients. We describe a previously healthy 10-year-old boy with acute disseminated encephalomyelitis associated with acute acquired Toxoplasma gondii infection, the symptoms of which initially began with nuchal stiffness, difficulty in walking, and urinary and stool incontinence; he later had development of motor and sensory impairment in both lower extremities and classical magnetic resonance imaging lesions suggestive of the disease. The patient recovered completely after the specific therapy for acquired T. gondii infection and pulse prednisolone. Although acute acquired Toxoplasma gondii infection has not been reported previously in association with acute disseminated encephalomyelitis, clinicians should keep in mind this uncommon cause of a common disease when evaluatinga patient with acute disseminated encephalomyelitis.

from Rimedi Sources http://ift.tt/20qpKCb

A case report of a healthy 10-year-old boy with acute disseminated encephalomyelitis associated with acute acquired Toxoplasma gondii infection.

PMID:  Pediatr Neurol. 2013 Mar ;48(3):236-9. PMID: 23419476 Abstract Title:  Acute disseminated encephalomyelitis associated with acute Toxoplasma gondii Infection. Abstract:  Acute disseminated encephalomyelitis is an acute demyelinating disorder of the central nervous system, which principally affects the brain and spinal cord. It usually follows a benign infection or vaccination in children. Although a number of infectious agents have been implicated in acute disseminated encephalomyelitis, Toxoplasma gondii infection has not been described previously in children. Acquired T. gondii infection presents with lymphadenopathy and fever and usually spontaneously resolves in immunocompetent patients. We describe a previously healthy 10-year-old boy with acute disseminated encephalomyelitis associated with acute acquired Toxoplasma gondii infection, the symptoms of which initially began with nuchal stiffness, difficulty in walking, and urinary and stool incontinence; he later had development of motor and sensory impairment in both lower extremities and classical magnetic resonance imaging lesions suggestive of the disease. The patient recovered completely after the specific therapy for acquired T. gondii infection and pulse prednisolone. Although acute acquired Toxoplasma gondii infection has not been reported previously in association with acute disseminated encephalomyelitis, clinicians should keep in mind this uncommon cause of a common disease when evaluatinga patient with acute disseminated encephalomyelitis.

from Health News Spirulina http://www.greenmedinfo.com/article/case-report-healthy-10-year-old-boy-acute-disseminated-encephalomyelitis
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PubMed: Paranoid delusion as lead symptom in two siblings with late-onset Tay-Sachs disease and a novel mutation in the HEXA gene.: Related Articles

Paranoid delusion as lead symptom in two siblings with late-onset Tay-Sachs disease and a novel mutation in the HEXA gene.

J Neurol. 2015;262(4):1072-3

Authors: Stendel C, Gallenmüller C, Peters K, Bürger F, Gramer G, Biskup S, Klopstock T

PMID: 25860343 [PubMed - indexed for MEDLINE] http://dlvr.it/KMVfW9

Neurological presentations of intravascular lymphoma (IVL): meta-analysis of 654 patients.

Neurological presentations of intravascular lymphoma (IVL): meta-analysis of 654 patients.

BMC Neurol. 2016;16(1):9

Authors: Fonkem E, Dayawansa S, Stroberg E, Lok E, Bricker PC, Kirmani B, Wong ET, Huang JH

Abstract
BACKGROUND: Patients with intravascular lymphoma (IVL) frequently have neurological signs and symptoms. Prompt diagnosis and treatment is therefore crucial for their survival. However, the spectrum of neurological presentations and their respective frequencies have not been adequately characterized. Our aim is to document the spectrum of clinical symptoms and their respective frequencies and to create a clinical framework for the prompt diagnosis of IVL.
METHODS: A comprehensive meta-analysis of 654 cases of IVL published between 1957 and 2012 was performed to provide better insight into the neurological presentations of this disease. Neurologic complications were mainly divided into central nervous system (CNS) and peripheral nervous system (PNS) presentations.
RESULTS: There were no differences in occurrences of CNS IVL based on gender or geographic locations (Asian Vs non-Asian). However, most patients with CNS IVL were younger than 70 years of age (p < 0.05). Our limited data do not support the treatment efficacy of methotrexate. CNS symptoms were seen in 42 % of all cases. The most common CNS complications identified were cognitive impairment/dementia (60.9 %), paralysis (22.2 %), and seizures (13.4 %). PNS complications were seen in 9.5 % of cases. Out of these, muscle weakness (59.7 %), neurogenic bladder (37.1 %), and paresthesia (16.1 %) were the most common presentations.
CONCLUSIONS: CNS complications are more common among IVL patients. Out of these, dementia and seizures outnumber stroke-like presentations.

PMID: 26849888 [PubMed - as supplied by publisher]



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Alzheimer plaques in brain injury

Alzheimer plaques in brain injury

Alzheimer plaques in brain injury

Larry H. Bernstein, MD, FCAP, Curator

LPBI

Alzheimer’s Plaques Linked to Brain Injury in Middle-Aged People

Bevin Fletcher, Associate Editor   http://www.biosciencetechnology.com/news/2016/02/alzheimers-plaques-linked-brain-injury-middle-aged-people

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A new Neurol…

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Apoptotic neurons induce proliferative responses of progenitor cells in the postnatal neocortex
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Journal Reference

Exp Neurol. 2015 Nov;273:126-37.

Petrenko V1, Mihhailova J1, Salmon P1, Kiss JZ2.

Show Affiliations
  1. Department of Neurosciences, University of Geneva Medical School, CH-1211 Geneva 4, Switzerland.
  2. Department of Neurosciences, University of Geneva Medical School, CH-1211 Geneva 4, Switzerland. Electronic address: Jozsef.Kiss@unige.ch.

Abstract

Apoptotic cell death is the leading cause of neuronal loss after neonatal brain injury. Little is known about the intrinsic capacity of the immature cerebral cortex for replacing dead cells. Here we test the hypothesis that neuronal apoptosis is able to trigger compensatory proliferation in surrounding cells. In order to establish a “pure” apoptotic cell death model and to avoid the confounding effects of broken blood-brain barrier and inflammatory reactions, we used a diphtheria toxin (DT) and diphtheria toxin receptor (DTR) system to induce ablation of layer IV neurons in the rodent somatosensory cortex during the early postnatal period. We found that DT-triggered apoptosis is a slowly progressing event lasting about for 7days. While dying cells expressed the morphological features of apoptosis, we could not detect immunoreactivity for activated caspase-3 in these cells. Microglia activation and proliferation represented the earliest cellular responses to apoptotic cell death. In addition, we found that induced apoptosis triggered a massive proliferation of undifferentiated progenitor cell pool including Sox2 as well as NG2 cells. The default differentiation pattern of proliferating progenitors appears to be the glial phenotype; we could not find evidence for newly generated neurons in response to apoptotic neuronal death. These results suggest that mitotically active progenitor populations are intrinsically capable to contribute to the repair process of injured cortical tissue and may represent a potential target for neuronal replacement strategies.

Copyright © 2015. Published by Elsevier Inc.

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PubMed: Emerging microtubule targets in glioma therapy.: Related Articles

Emerging microtubule targets in glioma therapy.

Semin Pediatr Neurol. 2015 Mar;22(1):49-72

Authors: Katsetos CD, Reginato MJ, Baas PW, D'Agostino L, Legido A, Tuszyn Ski JA, Dráberová E, Dráber P

Abstract
Major advances in the genomics and epigenomics of diffuse gliomas and glioblastoma to date have not been translated into effective therapy, necessitating pursuit of alternative treatment approaches for these therapeutically challenging tumors. Current knowledge of microtubules in cancer and the development of new microtubule-based treatment strategies for high-grade gliomas are the topic in this review article. Discussed are cellular, molecular, and pharmacologic aspects of the microtubule cytoskeleton underlying mitosis and interactions with other cellular partners involved in cell cycle progression, directional cell migration, and tumor invasion. Special focus is placed on (1) the aberrant overexpression of βIII-tubulin, a survival factor associated with hypoxic tumor microenvironment and dynamic instability of microtubules; (2) the ectopic overexpression of γ-tubulin, which in addition to its conventional role as a microtubule-nucleating protein has recently emerged as a transcription factor interacting with oncogenes and kinases; (3) the microtubule-severing ATPase spastin and its emerging role in cell motility of glioblastoma cells; and (4) the modulating role of posttranslational modifications of tubulin in the context of interaction of microtubules with motor proteins. Specific antineoplastic strategies discussed include downregulation of targeted molecules aimed at achieving a sensitization effect on currently used mainstay therapies. The potential role of new classes of tubulin-binding agents and ATPase inhibitors is also examined. Understanding the cellular and molecular mechanisms underpinning the distinct behaviors of microtubules in glioma tumorigenesis and drug resistance is key to the discovery of novel molecular targets that will fundamentally change the prognostic outlook of patients with diffuse high-grade gliomas.

PMID: 25976261 [PubMed - indexed for MEDLINE] http://dlvr.it/KMRx61

Vitamin C mitigated ethanol-induced oxidative stress, neuroinflammation and apoptotic neuronal loss.

PMID:  CNS Neurol Disord Drug Targets. 2015 Nov 10. Epub 2015 Nov 10. PMID: 26831257 Abstract Title:  Neuroprotection by vitamin C against ethanol -induced neuroinflammation associated neurodegeneration in developing rat brain. Abstract:  Ethanol induces oxidative stress and its exposure during early developmental age causes neuronal cell death which leads to several neurological disorders. We previously reported that vitamin C can protect against ethanol-induced apoptotic cell death in developing rat brain. Here, we extended our study to know the therapeutic efficacy of vitamin C against ethanol-induced oxidative stress, neuroinflammation mediated neurodegeneration in postnatal day 7 (PND7) rats. A single episode of ethanol (5g/kg) subcutaneous administration to PND7 rats significantly induced the production of reactive oxygen species (ROS), activation of both microglia and astrocytes followed by the induction of different apoptotic markers. On the other hand due to its free radical scavenging properties vitamin C treatment significantly reduced ROS production, suppressed both activated microglia and astrocytes and reversed other changes including elevated level of Bax/Bcl-2 ratio, cytochrome c and different caspases such as caspase-9 and caspase-3 induced by ethanol in developing rat brain. Moreover, vitamin C treatment also reduced ethanol-induced activation of PARP-1 and neurodegeneration as evident from Flouro-Jade-B and Nissl stainined neuronal cell death in PND7 rat brain. These findings suggest that vitamin C mitigated ethanol-induced oxidative stress, neuroinflammation and apoptotic neuronal loss and may be beneficial against ethanol abusing in brain development.

from Health News Spirulina http://www.greenmedinfo.com/article/vitamin-c-mitigated-ethanol-induced-oxidative-stress-neuroinflammation-and
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