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https://www.readbyqxmd.com/read/28542502/in-vivo-transduction-of-neurons-with-tat-uch-l1-protects-brain-against-controlled-cortical-impact-injury
#1
Hao Liu, Marie E Rose, Xiecheng Ma, Sherman Culver, C Edward Dixon, Steven H Graham
Many mechanisms or pathways are involved in secondary post-traumatic brain injury, such as the ubiquitin-proteasome pathway (UPP), axonal degeneration and neuronal cell apoptosis. UCH-L1 is a protein that is expressed in high levels in neurons and may have important roles in the UPP, autophagy and axonal integrity. The current study aims to evaluate the role of UCH-L1 in post-traumatic brain injury (TBI) and its potential therapeutic effects. A novel protein was constructed that fused the protein transduction domain (PTD) of trans-activating transduction (TAT) protein with UCH-L1 (TAT-UCH-L1) in order to promote neuronal transduction...
2017: PloS One
https://www.readbyqxmd.com/read/28539419/microglia-are-irrelevant-for-neuronal-degeneration-and-axon-regeneration-after-acute-injury
#2
Alexander M Hilla, Heike Diekmann, Dietmar Fischer
The role of microglia in de- and regenerative processes after damage of the nervous system still remains ambiguous, partially due to the paucity of appropriate investigative methods. Here, we show that treatment with the pharmacological colony stimulating factor 1 receptor inhibitor PLX5622 specifically eliminated microglia in murine retinae and optic nerves. Interestingly, time course and extent of retinal ganglion cell (RGC) degeneration after optic nerve crush remained unaffected upon microglia depletion, although remnants of pre-labeled apoptotic RGCs were not cleared from the retina in these animals...
May 24, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28536832/proteomic-profiling-reveals-crucial-retinal-protein-alterations-in-the-early-phase-of-an-experimental-glaucoma-model
#3
Fabian Anders, Julia Teister, Sebstian Funke, Norbert Pfeiffer, Franz Grus, Thanos Solon, Verena Prokosch
PURPOSE: Clinical glaucoma is difficult to assess in terms of molecular pathophysiology, prompting studies in experimental models of glaucoma. The purpose of this study was to investigate quantitative changes in retinal protein expression at the onset of experimental glaucoma in rats. Analyzing the proteome provides a suitable tool to decipher the pathophysiological processes in glaucomatous degeneration. METHODS: Thermic cauterization of episcleral veins was utilized to elevate the intraocular pressure in Sprague Dawley rats...
May 24, 2017: Graefe's Archive for Clinical and Experimental Ophthalmology
https://www.readbyqxmd.com/read/28535586/an-experimental-infarct-targeting-the-internal-capsule-histopathological-and-ultrastructural-changes
#4
Chang-Woo Han, Kyung-Hwa Lee, Myung Giun Noh, Jin-Myung Kim, Hyung-Seok Kim, Hyung-Sun Kim, Ra Gyung Kim, Jongwook Cho, Hyoung-Ihl Kim, Min-Cheol Lee
BACKGROUND: Stroke involving the cerebral white matter (WM) has increased in prevalence, but most experimental studies have focused on ischemic injury of the gray matter. This study was performed to investigate the WM in a unique rat model of photothrombotic infarct targeting the posterior limb of internal capsule (PLIC), focusing on the identification of the most vulnerable structure in WM by ischemic injury, subsequent glial reaction to the injury, and the fundamental histopathologic feature causing different neurologic outcomes...
May 2017: Journal of Pathology and Translational Medicine
https://www.readbyqxmd.com/read/28534083/synthetic-alpha-synuclein-fibrils-cause-mitochondrial-impairment-and-selective-dopamine-neurodegeneration-in-part-via-inos-mediated-nitric-oxide-production
#5
Victor Tapias, Xiaoping Hu, Kelvin C Luk, Laurie H Sanders, Virginia M Lee, J Timothy Greenamyre
Intracellular accumulation of α-synuclein (α-syn) are hallmarks of synucleinopathies, including Parkinson's disease (PD). Exogenous addition of preformed α-syn fibrils (PFFs) into primary hippocampal neurons induced α-syn aggregation and accumulation. Likewise, intrastriatal inoculation of PFFs into mice and non-human primates generates Lewy bodies and Lewy neurites associated with PD-like neurodegeneration. Herein, we investigate the putative effects of synthetic human PFFs on cultured rat ventral midbrain dopamine (DA) neurons...
May 22, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28534077/white-matter-injury-in-the-preterm-infant-pathology-and-mechanisms
#6
REVIEW
Stephen A Back
The human preterm brain is particularly susceptible to cerebral white matter injury (WMI) that disrupts the normal progression of developmental myelination. Advances in the care of preterm infants have resulted in a sustained reduction in the severity of WMI that has shifted from more severe focal necrotic lesions to milder diffuse WMI. Nevertheless, WMI remains a global health problem and the most common cause of chronic neurological morbidity from cerebral palsy and diverse neurobehavioral disabilities. Diffuse WMI involves maturation-dependent vulnerability of the oligodendrocyte (OL) lineage with selective degeneration of late oligodendrocyte progenitors (preOLs) triggered by oxidative stress and other insults...
May 22, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28528135/presymptomatically-applied-ampa-receptor-antagonist-prevents-calcium-increase-in-vulnerable-type-of-motor-axon-terminals-of-mice-modeling-amyotrophic-lateral-sclerosis
#7
Roland Patai, Melinda Paizs, Massimo Tortarolo, Caterina Bendotti, Izabella Obál, József I Engelhardt, László Siklós
Increased intracellular calcium (Ca), which might be the consequence of an excess influx through Ca-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, plays a crucial role in degeneration of motor neurons. Previously we demonstrated that the presymptomatic application of AMPA receptor antagonist, talampanel, could reduce Ca elevation in spinal motor neurons of mice carrying the G93A mutation of superoxide dismutase 1 (SOD1), modeling amyotrophic lateral sclerosis (ALS). It remained to be examined whether the remote, functionally semi-autonomous motor axon terminals could be rescued from the Ca overload, or if the terminals, where the degeneration possibly starts, already experience intractable changes at early time points...
May 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28526658/nonclinical-pharmacology-and-toxicology-of-the-first-biosimilar-insulin-glargine-drug-product-basaglar-%C3%A2-abasaglar-%C3%A2-approved-in-the-european-union
#8
Richard A Byrd, Rebecca A Owens, Jamie L Blackbourne, David E Coutant, Mark W Farmen, M Dodson Michael, Julie S Moyers, A Eric Schultze, Michael K Sievert, Niraj K Tripathi, John L Vahle
Basaglar(®)/Abasaglar(®) (Lilly insulin glargine [LY IGlar]) is a long-acting human insulin analogue drug product granted marketing authorisation as a biosimilar to Lantus(®) (Sanofi insulin glargine [SA IGlar]) by the European Medicines Agency. We assessed the similarity of LY IGlar to the reference drug product, European Union-sourced SA IGlar (EU-SA IGlar), using nonclinical in vitro and in vivo studies. No biologically relevant differences were observed for receptor binding affinity at either the insulin or insulin-like growth factor-1 (IGF-1) receptors, or in assays of functional or de novo lipogenic activity...
May 16, 2017: Regulatory Toxicology and Pharmacology: RTP
https://www.readbyqxmd.com/read/28519902/reduced-gliotransmitter-release-from-astrocytes-mediates-tau-induced-synaptic-dysfunction-in-cultured-hippocampal-neurons
#9
Roberto Piacentini, Domenica Donatella Li Puma, Marco Mainardi, Giacomo Lazzarino, Barbara Tavazzi, Ottavio Arancio, Claudio Grassi
Tau is a microtubule-associated protein exerting several physiological functions in neurons. In Alzheimer's disease (AD) misfolded tau accumulates intraneuronally and leads to axonal degeneration. However, tau has also been found in the extracellular medium. Recent studies indicated that extracellular tau uploaded from neurons causes synaptic dysfunction and contributes to tau pathology propagation. Here we report novel evidence that extracellular tau oligomers are abundantly and rapidly accumulated in astrocytes where they disrupt intracellular Ca(2+) signaling and Ca(2+) -dependent release of gliotransmitters, especially ATP...
May 18, 2017: Glia
https://www.readbyqxmd.com/read/28513333/atg9a-deficiency-causes-axon-specific-lesions-including-neuronal-circuit-dysgenesis
#10
Junji Yamaguchi, Chigure Suzuki, Tomohisa Nanao, Soichirou Kakuta, Kentarou Ozawa, Isei Tanida, Tatsuya Saitoh, Takehiko Sunabori, Masaaki Komatsu, Keiji Tanaka, Shigeki Aoki, Kenji Sakimura, Yasuo Uchiyama
Conditional knockout mice for Atg9a, specifically in brain tissue, were generated to understand the roles of ATG9A in the neural tissue cells. The mice were born normally, but half of them died within one week, and none lived beyond 4 weeks of age. SQSTM1/p62 and NBR1, receptor proteins for selective autophagy, together with ubiquitin, accumulated in Atg9a-deficient neurosoma at postnatal day 15 (P15), indicating an inhibition of autophagy, whereas these proteins were significantly decreased at P28, as evidenced by immunohistochemistry, electron microscopy and western blot...
May 17, 2017: Autophagy
https://www.readbyqxmd.com/read/28507529/parkinson-disease-an-evolutionary-perspective
#11
Pedro J Garcia-Ruiz, Alberto J Espay
There are two central premises to this evolutionary view of Parkinson disease (PD). First, PD is a specific human disease. Second, the prevalence of PD has increased over the course of human history. Several lines of evidence may explain why PD appears to be restricted to the human species. The major manifestations of PD are the consequence of degeneration in the dopamine-synthesizing neurons of the mesostriatal neuronal pathway. It is of note the enormous expansion of the human dopamine mesencephalic neurons onto the striatum compared with other mammals...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28506594/fingolimod-and-teriflunomide-attenuate-neurodegeneration-in-mouse-models-of-neuronal-ceroid-lipofuscinosis
#12
Janos Groh, Kristina Berve, Rudolf Martini
CLN diseases are rare lysosomal storage diseases characterized by progressive axonal degeneration and neuron loss in the CNS, manifesting in disability, blindness, and premature death. We have previously demonstrated that, in animal models of infantile and juvenile forms of CLN disease (CLN1 and CLN3, respectively), secondary neuroinflammation in the CNS substantially amplifies neural damage, opening the possibility that immunomodulatory treatment might improve disease outcome. First, we recapitulated the inflammatory phenotype, originally seen in mice in autopsies of CLN patients...
May 13, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28506346/-role-of-short-latency-somatosensory-evoked-potential-in-the-diagnosis-of-chronic-inflammatory-demyelinating-polyneuropathy
#13
Rui-Di Sun, Bing Fu, Jun Jiang
OBJECTIVE: To investigate the role of short-latency somatosensory evoked potential (SSEP) in the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). METHODS: A total of 48 children with a confirmed or suspected CIDP and 40 healthy children were enrolled. Nerve electrophysiological examination and/or SSEP examination was performed (the children in the healthy control group only underwent SSEP examination). Four-lead electromyography was used for nerve electrophysiological examination, including at least 4 motor nerves and 2 sensory nerves...
May 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28503425/neuroprotective-effects-of-gypenosides-in-experimental-autoimmune-optic-neuritis
#14
Hong-Kan Zhang, Yuan Ye, Zhen-Ni Zhao, Kai-Jun Li, Yi Du, Qiu-Ming Hu, Jian-Feng He
AIM: To determine whether gypenosides have protective effects in experimental autoimmune optic neuritis (EAON). METHODS: Mice were randomly divided into seven groups: control group, model group, three different density gypenosides monotherapy, methylprednisolone monotherapy, combination of gypenosides and methylprednisolone group. The control group was subcutaneously injected with oil emulsion adjuvant and all other groups were subcutaneously immunized with an emulsified mixture of myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide to induce EAON...
2017: International Journal of Ophthalmology
https://www.readbyqxmd.com/read/28502476/purkinje-cells-are-more-vulnerable-to-the-specific-depletion-of-cathepsin-d-than-to-that-of-atg7
#15
Masato Koike, Masahiro Shibata, Takehiko Sunabori, Junji Yamaguchi, Kenji Sakimura, Masaaki Komatsu, Keiji Tanaka, Yasuo Uchiyama
Neurologic phenotypes of cathepsin D (CTSD)-deficient mice, a murine model of neuronal ceroid lipofuscinoses, indicate the importance of CTSD for the maintenance of metabolism in central nervous system neurons. To further understand the role of CTSD in central nervous system neurons, we generated mice with a CTSD deficiency specifically in the Purkinje cells (PCs) (CTSD(Flox/Flox);GRID2-Cre) and compared their phenotypes with those of PC-selective Atg7-deficient (Atg7(Flox/Flox);GRID2-Cre) mice. In both strains of mice, PCs underwent degeneration, but the CTSD-deficient PCs disappeared more rapidly than their Atg7-deficient counterparts...
May 11, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28495474/late-effect-of-developmental-exposure-to-glycidol-on-hippocampal-neurogenesis-in-mice-loss-of-parvalbumin-expressing-interneurons
#16
Masashi Kawashima, Yousuke Watanabe, Kota Nakajima, Hirotada Murayama, Rei Nagahara, Meilan Jin, Toshinori Yoshida, Makoto Shibutani
Developmental exposure to glycidol of rats causes axonal injury targeting axon terminals in dams and transient disruption of late-stage differentiation of hippocampal neurogenesis, accompanying sustained increase in the number of reelin-producing or calretinin-expressing interneurons in offspring. The molecular mechanism of disruptive neurogenesis probably targets the newly generating nerve terminals. We previously found differences between mice and rats in the effects on hippocampal neurogenesis after developmental exposure to the same neurotoxic substances...
May 8, 2017: Experimental and Toxicologic Pathology: Official Journal of the Gesellschaft Für Toxikologische Pathologie
https://www.readbyqxmd.com/read/28487632/nicotinamide-and-wld-s-act-together-to-prevent-neurodegeneration-in-glaucoma
#17
Pete A Williams, Jeffrey M Harder, Nicole E Foxworth, Brynn H Cardozo, Kelly E Cochran, Simon W M John
Glaucoma is a complex neurodegenerative disease characterized by progressive visual dysfunction leading to vision loss. Retinal ganglion cells are the primary affected neuronal population, with a critical insult damaging their axons in the optic nerve head. This insult is typically secondary to harmfully high levels of intraocular pressure (IOP). We have previously determined that early mitochondrial abnormalities within retinal ganglion cells lead to neuronal dysfunction, with age-related declines in NAD (NAD(+) and NADH) rendering retinal ganglion cell mitochondria vulnerable to IOP-dependent stresses...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28485482/deletion-of-sarm1-gene-is-neuroprotective-in-two-models-of-peripheral-neuropathy
#18
Elliot Turkiew, Debbie Falconer, Nicole Reed, Ahmet Höke
Distal axon degeneration seen in many peripheral neuropathies is likely to share common molecular mechanisms with Wallerian degeneration. Although several studies in mouse models of peripheral neuropathy showed prevention of axon degeneration in the slow Wallerian degeneration (Wlds) mouse, the role of a recently identified player in Wallerian degeneration, Sarm1, has not been explored extensively. In this study we show that mice lacking the Sarm1 gene are resistant to distal axonal degeneration in a model of chemotherapy induced peripheral neuropathy caused by paclitaxel and a model of high fat diet induced putative metabolic neuropathy...
May 9, 2017: Journal of the Peripheral Nervous System: JPNS
https://www.readbyqxmd.com/read/28483540/peripheral-nervous-system-involvement-in-systemic-lupus-erythematosus-prevalence-clinical-and-immunological-characteristics-treatment-and-outcome-of-a-large-cohort-from-a-single-centre
#19
REVIEW
Pilar Toledano, Ramón Orueta, Ignasi Rodríguez-Pintó, Josep Valls-Solé, Ricard Cervera, Gerard Espinosa
Disorders of peripheral nervous system in patients with systemic lupus erythematosus (PNS-SLE) are a major cause of morbidity. The aims of the present study were to determine the prevalence of PNS-SLE involvement in a large cohort of SLE patients from a single centre, to characterize such involvement, treatment modalities and outcome, and to identify the possible variables that may be associated with its presence. We performed an observational cross-sectional study that included all SLE patients being followed in our department between March and December 2015 who met at least one of the PNS-SLE case definitions proposed in 1999 by the American College of Rheumatology...
May 5, 2017: Autoimmunity Reviews
https://www.readbyqxmd.com/read/28482594/a-bridging-sf-alg-composite-scaffold-loaded-ngf-for-spinal-cord-injury-repair
#20
Genlong Jiao, Yongqin Pan, Cunchuang Wang, ZhaoXia Li, Zhizhong Li, Rui Guo
Neurons loss and axons degeneration after spinal cord injury (SCI) gradually give rise to result in functional motor and sensory impairment. A bridging biomaterial scaffold that allows the axons to grow through has been investigated for the repair of injured spinal cord. In this study, we introduced a silk fibroin (SF)-based neurobridge as scaffold enriched with/without nerve growth factor (NGF) that can be utilized as a therapeutic approach for spinal cord repair. NGF released from alginate (Alg) microspheres on SF scaffold (SF/Alg composites scaffolds) to the central lesion site of SCI significantly enhanced the sparing of spinal cord tissue and increased the number of surviving neurons...
July 1, 2017: Materials Science & Engineering. C, Materials for Biological Applications
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