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axon degenerate

Işık Odaman Al, Başak Koç, Cengiz Bayram, Ezgi Uysalol Paslı, Edibe Pembegül Yıldız, Ali Ayçiçek, Mine Çalışkan, Gül Nihal Özdemir
Lymphomas are solid tumors characterized by the malignant proliferation of lymphoid cells. Neurologic signs encountered in patients with Hodgkin's lymphoma can be due to the direct spread of tumor to the nervous system, secondary to chemotherapy or radiation, secondary to tumor mass compression, infectious causes and paraneoplastic syndromes. Paraneoplastic neurologic syndromes are rarely encountered in patients with Hodgkin's lymphoma and non-Hodgkin's lymphoma. Except for paraneoplastic cerebellar degeneration in Hodgkin's lymphoma and dermato/polymyositis in both Hodgkin's lymphoma and non-Hodgkin's lymphoma, other paraneoplastic syndromes are uncommon and have only been reported as isolated case reports or short series...
December 2018: Türk Pediatri Arşivi
Eva Leitzen, Barbara B Raddatz, Wen Jin, Sandra Goebbels, Klaus-Armin Nave, Wolfgang Baumgärtner, Florian Hansmann
Theiler's murine encephalomyelitis virus (TMEV)-induces a demyelinating disease in the spinal cord (SC) of susceptible but not in resistant (B6) mouse strains. The aim of the present study was to induce SC demyelination and a peripheral neuropathy in resistant mice by switching the infection site from cerebrum to SC. B6 mice were intraspinally inoculated with TMEV. Infected mice showed clinical signs starting at 7 days post infection (dpi). Histopathology revealed a mononuclear myelitis, centred on the injection site at 3 dpi with subsequent antero- and retrograde spread, accompanied by demyelination and axonal damage within the SC...
March 14, 2019: Scientific Reports
Stéphanie Hostenbach, Ayla Pauwels, Veronique Michiels, Hubert Raeymaekers, Anne-Marie Van Binst, Annick Van Merhaeghen-Wieleman, Peter Van Schuerbeek, Jacques De Keyser, Miguel D'Haeseleer
BACKGROUND: Axonal degeneration is related to long-term disability in patients with multiple sclerosis (MS). The underlying mechanism remains ill understood but appears to involve axonal energetic dysfunction. A globally impaired cerebral blood flow (CBF) has been observed in the normal-appearing white matter (NAWM) of patients with MS, which is probably related to astrocytic overexpression of endothelin-1 (ET-1). Cerebral hypoperfusion has been associated with reduced mitochondrial activity and disabling symptoms (e...
March 14, 2019: Trials
Uta Chrzanowski, Sudip Bhattarai, Miriam Scheld, Tim Clarner, Petra Fallier-Becker, Cordian Beyer, Sven Olaf Rohr, Christoph Schmitz, Tanja Hochstrasser, Felix Schweiger, Sandra Amor, Anja Horn-Bochtler, Bernd Denecke, Stella Nyamoya, Markus Kipp
Brain-intrinsic degenerative cascades are a proposed factor driving inflammatory lesion formation in multiple sclerosis (MS) patients. We recently showed that encephalitogenic lymphocytes are recruited to the sites of active demyelination induced by cuprizone. Here, we investigated whether cuprizone-induced oligodendrocyte and myelin pathology is sufficient to trigger peripheral immune cell recruitment into the forebrain. We show that early cuprizone-induced white matter lesions display a striking similarity to early MS lesions, i...
March 10, 2019: Neurochemistry International
J D Triplett, G A Nicholson, C M Sue, T Hornemann, C Yiannikas
Hereditary sensory and autonomic neuropathy type I (HSAN-1) is an autosomal dominant sensory neuropathy occurring secondary to mutations in the SPTLC1 and SPTLC2 genes. We present two generations of a single family with Ser384Phe mutation in the SPTLC2 gene located on chromosome 14q24 characterized by a typical HSAN-1c presentation, with additional findings upper motor neuron signs, early demyelinating features on nerve conduction studies and type II juxtafoveal retinal telangiectasias also known as macular telangiectasias (MacTel II)...
March 13, 2019: Journal of the Peripheral Nervous System: JPNS
Chongyang Chen, Xin Jiang, Yingchao Li, Haitao Yu, Shupeng Li, Zaijun Zhang, Hua Xu, Ying Yang, Gongping Liu, Feiqi Zhu, Xiaohu Ren, Liangyu Zou, Benhong Xu, Jianjun Liu, Peter S Spencer, Xifei Yang
Excessive copper can cause neurotoxicity and contribute to the development of some neurological diseases; however, copper neurotoxicity and the potential mechanisms remain poorly understood. We used proteomics and phosphoproteomics to quantify protein changes in the hippocampus of wild-type and 3xTg-AD mice, both of which were treated at 6 months of age with 2 months of drinking water with or without added copper chloride (0.13 ppm concentration). A total of 3960 unique phosphopeptides (5290 phosphorylation sites) from 1406 phosphoproteins was identified...
March 9, 2019: Free Radical Biology & Medicine
Isabelle Bos, Stephanie Vos, Frans Verhey, Philip Scheltens, Charlotte Teunissen, Sebastiaan Engelborghs, Kristel Sleegers, Giovanni Frisoni, Olivier Blin, Jill C Richardson, Régis Bordet, Magda Tsolaki, Julius Popp, Gwendoline Peyratout, Pablo Martinez-Lage, Mikel Tainta, Alberto Lleó, Peter Johannsen, Yvonne Freund-Levi, Lutz Frölich, Rik Vandenberghe, Sarah Westwood, Valerija Dobricic, Frederik Barkhof, Cristina Legido-Quigley, Lars Bertram, Simon Lovestone, Johannes Streffer, Ulf Andreasson, Kaj Blennow, Henrik Zetterberg, Pieter Jelle Visser
INTRODUCTION: We investigated relations between amyloid-β (Aβ) status, apolipoprotein E (APOE) ε4, and cognition, with cerebrospinal fluid markers of neurogranin (Ng), neurofilament light (NFL), YKL-40, and total tau (T-tau). METHODS: We included 770 individuals with normal cognition, mild cognitive impairment, and Alzheimer's disease (AD)-type dementia from the EMIF-AD Multimodal Biomarker Discovery study. We tested the association of Ng, NFL, YKL-40, and T-tau with Aβ status (Aβ- vs...
March 7, 2019: Alzheimer's & Dementia: the Journal of the Alzheimer's Association
Vahideh Oveissi, Mahboobe Ram, Roodabeh Bahramsoltani, Farnaz Ebrahimi, Roja Rahimi, Rozita Naseri, Tarun Belwal, Hari Prasad Devkota, Zahra Abbasabadi, Mohammad Hosein Farzaei
BACKGROUND: Chemotherapy, as one of the main approaches of cancer treatment, is accompanied with several adverse effects, including chemotherapy-induced peripheral neuropathy (CIPN). Since current methods to control the condition are not completely effective, new treatment options should be introduced. Medicinal plants can be suitable candidates to be assessed regarding their effects in CIPN. Current paper reviews the available preclinical and clinical studies on the efficacy of herbal medicines in CIPN...
March 9, 2019: Daru: Journal of Faculty of Pharmacy, Tehran University of Medical Sciences
Macarena S Arrázola, Cristian Saquel, Romina J Catalán, Sebastián A Barrientos, Diego E Hernandez, Alejandra Catenaccio, Felipe A Court
Axonal degeneration contributes to functional impairment in several disorders of the nervous system, constituting an important target for neuroprotection. Several individual factors and subcellular events have been implicated in axonal degeneration, but the identification of an integrative signaling pathway activating this self-destructive process has remained elusive. Through pharmacological and genetic approaches, we tested whether necroptosis, a regulated cell death mechanism, implicated in the pathogenesis of several neurodegenerative diseases, is involved in axonal degeneration...
March 8, 2019: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Xiaoping Wang, Xiaojia Li, Wu Jingfen, Deng Fei, Peng Mei
Cerebral ischemia reperfusion (I/R) injury is associated with a high incidence of neurological morbidity and mortality worldwide. Higenamine has anti-inflammatory, anti-oxidative and anti-apoptotic capacities and has been successfully used in myocardial and intestinal ischemia reperfusion. We hypothesized that higenamine might serve the same effects in cerebral I/R. In a rat model of cerebral I/R, higenamine improved functional state of nerves, significantly inhibited the I/R-induced increase in the serum level of tumor necrosis factor α (TNF-alpha) and interleukins (ILs) such as IL-1, IL-6 and IL-18, and CD14+ cells, while decreasing the axonal nerve degeneration...
March 1, 2019: Frontiers in Bioscience (Landmark Edition)
S Tozza, S Magri, E M Pennisi, E Schirinzi, C Pisciotta, F Balistreri, D Severi, G Ricci, G Siciliano, F Taroni, L Santoro, F Manganelli
EGR2 (Early Growth Response 2) is one of the most important transcription factors involved in myelination in the peripheral nervous system. EGR2 mutations typically cause different forms of demyelinating neuropathy, i.e. Charcot-Marie-Tooth type 1D (CMT1D), Dejerine-Sottas Syndrome (DSS) and Congenital Hypomyelinating Neuropathy (CHN). However, the EGR2 gene has been recently associated with an axonal phenotype (CMT2) in a large CMT family. Here, we report another CMT family exhibiting an axonal phenotype associated with a missense change (c...
March 6, 2019: Journal of the Peripheral Nervous System: JPNS
Yo Shinoda, Shunsuke Ehara, Satoshi Tatsumi, Eiko Yoshida, Tsutomu Takahashi, Komyo Eto, Toshiyuki Kaji, Yasuyuki Fujiwara
Exposure to organic mercury, especially methylmercury (MeHg), causes Minamata disease, a severe chronic neurological disorder. Minamata disease predominantly affects the central nervous system, and therefore, studies on the mechanisms of MeHg neurotoxicity have focused primarily on the brain. Although the peripheral nervous system is also affected by the organometallic compound and shows signs of neural degeneration, the mechanisms of peripheral MeHg neurotoxicity remain unclear. In the present study, we performed quantitative immunohistochemical analyses of the dorsal root ganglion (DRG) and associated sensory and motor fibers to clarify the mechanisms of MeHg-induced peripheral neurotoxicity in Wistar rats...
2019: Journal of Toxicological Sciences
M-Marsel Mesulam, Nava Lalehzari, Farzan Rahmani, Daniel Ohm, Ryan Shahidehpour, Garam Kim, Tamar Gefen, Sandra Weintraub, Eileen Bigio, Changiz Geula
OBJECTIVE: To investigate the status of the basal forebrain cholinergic system in primary progressive aphasia (PPA) as justification for cholinergic therapy. METHODS: A cohort of 36 brains from PPA participants with the neuropathology of Alzheimer disease (PPA-AD, n = 14) or frontotemporal lobar degeneration (PPA-tau, n = 12; PPA-TDP, n = 10) were used for semiquantitative rating of degeneration and gliosis of basal forebrain cholinergic neurons (BFCN). A subpopulation of 5 PPA-AD and 7 control brains underwent detailed analysis of BFCN pathology and cortical cholinergic axonal loss employing immunohistochemical and histochemical methods and stereologic analysis...
March 6, 2019: Neurology
Xi Chen, Jennifer K Kordich, Erin T Williams, Nathan Levine, Allyson Cole-Strauss, Lee Marshall, Viviane Labrie, Jiyan Ma, Jack W Lipton, Darren J Moore
Mutations in the vacuolar protein sorting 35 ortholog ( VPS35 ) gene represent a cause of late-onset, autosomal dominant familial Parkinson's disease (PD). A single missense mutation, D620N, is considered pathogenic based upon its segregation with disease in multiple families with PD. At present, the mechanism(s) by which familial VPS35 mutations precipitate neurodegeneration in PD are poorly understood. Here, we employ a germline D620N VPS35 knockin (KI) mouse model of PD to formally establish the age-related pathogenic effects of the D620N mutation at physiological expression levels...
March 6, 2019: Proceedings of the National Academy of Sciences of the United States of America
Caihong Zhu, Bei Li, Karl Frontzek, Yingjun Liu, Adriano Aguzzi
SARM1 (sterile α and HEAT/armadillo motif-containing protein) is a member of the MyD88 (myeloid differentiation primary response gene 88) family, which mediates innate immune responses. Because inactivation of SARM1 prevents various forms of axonal degeneration, we tested whether it might protect against prion-induced neurotoxicity. Instead, we found that SARM1 deficiency exacerbates the progression of prion pathogenesis. This deleterious effect was not due to SARM1-dependent modulation of prion-induced neuroinflammation, since microglial activation, astrogliosis, and brain cytokine profiles were not altered by SARM1 deficiency...
March 6, 2019: Journal of Experimental Medicine
Charles Nicaise, Catherine Marneffe, Joanna Bouchat, Jacques Gilloteaux
Osmotic demyelination syndrome (ODS) is a disorder of the central myelin that is often associated with a precipitous rise of serum sodium. Remarkably, while the myelin and oligodendrocytes of specific brain areas degenerate during the disease, neighboring neurons and axons appear unspoiled, and neuroinflammation appears only once demyelination is well established. In addition to blood‒brain barrier breakdown and microglia activation, astrocyte death is among one of the earliest events during ODS pathology...
March 5, 2019: International Journal of Molecular Sciences
Aaron D Johnstone, Andrés de Léon, Nicolás Unsain, Julien Gibon, Philip A Barker
Development of the nervous system relies on a balance between axon and dendrite growth and subsequent pruning and degeneration. The developmental degeneration of dorsal root ganglion (DRG) sensory axons has been well studied in part because it can be readily modeled by removing the trophic support by nerve growth factor (NGF) in vitro . We have recently reported that axonal fragmentation induced by NGF withdrawal is dependent on Ca2+ , and here, we address the mechanism of Ca2+ entry required for developmental axon degeneration of mouse embryonic DRG neurons...
January 2019: ENeuro
Maria Jeziorska, Andrew Atkinson, Lewis Kass-Iliyya, Saad Javed, Christopher Kobylecki, David Gosal, Andrew Marshall, Monty Silverdale, Rayaz A Malik
Background: Previous studies have shown cutaneous small fiber pathology in patients with Parkinson's disease (PD). These studies have focused on nerve degeneration, but recent reports suggest that nerve regeneration may also be important in PD pathology. Objective: To establish the extent of intraepidermal nerve fiber (IENF) degeneration and regeneration and its relationship to clinical and neurological deficits in Parkinson's disease (PD). Methods: Twenty-three PD patients and 10 age-matched controls underwent skin biopsy and assessment of somatic and autonomic symptoms and deficits...
2019: Frontiers in Neurology
Yolandi van der Merwe, Anne E Faust, Ecem T Sakalli, Caroline C Westrick, George Hussey, Ian P Conner, Valeria L N Fu, Stephen F Badylak, Michael B Steketee
Injury to retinal ganglion cells (RGC), central nervous system neurons that relay visual information to the brain, often leads to RGC axon degeneration and permanently lost visual function. Herein this study shows matrix-bound nanovesicles (MBV), a distinct class of extracellular nanovesicle localized specifically to the extracellular matrix (ECM) of healthy tissues, can neuroprotect RGCs and preserve visual function after severe, intraocular pressure (IOP) induced ischemia in rat. Intravitreal MBV injections attenuated IOP-induced RGC axon degeneration and death, protected RGC axon connectivity to visual nuclei in the brain, and prevented loss in retinal function as shown by histology, anterograde axon tracing, manganese-enhanced magnetic resonance imaging, and electroretinography...
March 5, 2019: Scientific Reports
Jing Pan, Jia Yu, Lixin Sun, Chengsong Xie, Lisa Chang, Junbing Wu, Sarah Hawes, Sara Saez-Atienzar, Wang Zheng, Justin Kung, Jinhui Ding, Weidong Le, Shengdi Chen, Huaibin Cai
Aldehyde dehydrogenase 1A1 (ALDH1A1), a retinoic acid (RA) synthase, is selectively expressed by the nigrostriatal dopaminergic (nDA) neurons that preferentially degenerate in Parkinson's disease (PD). ALDH1A1-positive axons mainly project to the dorsal striatum. However, whether ALDH1A1 and its products regulate the activity of postsynaptic striatal neurons is unclear. Here we show that μ-type opioid receptor (MOR1) levels were severely decreased in the dorsal striatum of postnatal and adult Aldh1a1 knockout mice, whereas dietary supplement of RA restores its expression...
March 5, 2019: Scientific Reports
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