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axon degenerate

Albert Leung, Eric Yang, Michael Lim, Valerie Metzger-Smith, Rebecca Theilmann, David Song, Lisa Lin, Alice Tsai, Roland Lee
The occurrence of debilitating chronic persistent (24/7) headache after mild traumatic brain injury (MTBI) represents a central neuropathic pain state. Previous studies suggest that this chronic headache (HA) state can be attributed to altered supraspinal modulatory functional connectivity in both resting and evoked pain states. Abnormalities in the myelin sheaths along the supraspinal Superior Longitudinal Fasciculus (SLF) and Anterior Thalamic Radiation (ATR) are frequently associated with alteration in pain modulation related to functional connectivity deficit with the prefrontal cortex...
October 16, 2018: Molecular Pain
David J Simon, Trent A Watkins
PURPOSE OF REVIEW: The current review analyzes recent findings that suggest that axon degeneration is a druggable process in the treatment of neurodegenerative disorders and a subset of traumas. RECENT FINDINGS: Emerging evidence reveals that axon degeneration is an active and regulated process in the early progression of some neurodegenerative diseases and acute traumas, which is orchestrated through a combination of axon-intrinsic and somatically derived signaling events...
October 12, 2018: Current Opinion in Neurology
Éric Martineau, Adriana Di Polo, Christine Vande Velde, Richard Robitaille
Despite being an early event in ALS, it remains unclear whether the denervation of neuromuscular junctions (NMJ) is simply the first manifestation of a globally degenerating motor neuron. Using in vivo imaging of single axons and their NMJs over a three-month period, we identify that single motor-units are dismantled asynchronously in SOD1G37R mice. We reveal that weeks prior to complete axonal degeneration, the dismantling of axonal branches is accompanied by contemporaneous new axonal sprouting resulting in synapse formation onto nearby NMJs...
October 15, 2018: ELife
Sandra Kuehn, Wilhelm Meißner, Pia Grotegut, Carsten Theiss, H Burkhard Dick, Stephanie C Joachim
The glial protein S100B, which belongs to a calcium binding protein family, is up-regulated in neurological diseases, like multiple sclerosis or glaucoma. In previous studies, S100B immunization led to retinal ganglion cell (RGC) loss in an experimental autoimmune glaucoma (EAG) model. Now, the direct degenerative impact of S100B on the retina and optic nerve was evaluated. Therefore, 2 μl of S100B was intravitreally injected in two concentrations (0.2 and 0.5 μg/μl). At day 3, 14 and 21, retinal neurons, such as RGCs, amacrine and bipolar cells, as well as apoptotic mechanisms were analyzed...
2018: Frontiers in Cellular Neuroscience
Trygve Holmøy, Egil Røsjø, Henrik Zetterberg, Kaj Blennow, Jonas Christoffer Lindstrøm, Linn Hofsøy Steffensen, Margitta T Kampman
OBJECTIVES: The effect of vitamin D supplementation on the disease course of multiple sclerosis (MS) is not established. Neurofilament light chain (NFL) is a sensitive marker of axonal degeneration. The aim of this study was to establish whether high-dose vitamin D supplementation reduces serum levels of NFL. MATERIALS AND METHODS: We have performed a 96 weeks placebo-controlled randomized study of weekly supplementation with 20.000 IU vitamin D3 in 71 patients with relapsing remitting MS (RRMS)...
October 13, 2018: Acta Neurologica Scandinavica
Jonathan Gilley, Paul Mayer, Gang Yu, Michael P Coleman
NMNAT2 is an endogenous axon maintenance factor that preserves axon health by blocking Wallerian-like axon degeneration. Mice lacking NMNAT2 die at birth with severe axon defects in both the PNS and CNS so a complete absence of NMNAT2 in humans is likely to be similarly harmful, but probably rare. However, there is evidence of widespread natural variation in human NMNAT2 mRNA expression so it is important to establish whether reduced levels of NMNAT2 have consequences that impact health. Whilst mice that express reduced levels of NMNAT2, either those heterozygous for a silenced Nmnat2 allele, or compound heterozygous for one silenced and one partially silenced Nmnat2 allele, remain overtly normal into old age, we now report that Nmnat2 compound heterozygote mice present with early and age-dependent peripheral nerve axon defects...
October 9, 2018: Human Molecular Genetics
Aaron S Field, Alexey Samsonov, Andrew L Alexander, Pouria Mossahebi, Ian D Duncan
BACKGROUND: The feeding of irradiated food to healthy adult cats results in widespread, noninflammatory demyelination of the central nervous system (CNS); a return to a normal diet results in endogenous remyelination with functional recovery. This recently discovered, reversible disease might provide a compelling clinical neuroimaging model system for the development and testing of myelin-directed MRI methods as well as future remyelination therapies. PURPOSE: Identify the noninvasive imaging characteristics of this new disease model and determine whether it features measurable changes on conventional and quantitative MRI...
October 9, 2018: Journal of Magnetic Resonance Imaging: JMRI
Ruth Gallily, Zhannah Yekhtin
Multiple sclerosis (MS) is an autoimmune disease leading to the destruction of myelin with consequent axonal degeneration and severe physical debilitation. The disease can be treated with immunosuppressive drugs that alleviate the symptoms and retard disease aggravation. One such drug in clinical use is glatiramer acetate (Copaxone). The non-psychotropic immunosuppressive cannabinoid compound cannabidiol (CBD) has recently been shown to have beneficial effects on experimental autoimmune encephalomyelitis (EAE)...
October 5, 2018: Inflammopharmacology
Junda Hu, Yiji Tu, Zuoyou Ding, Zenggan Chen, A Lee Dellon, William C Lineaweaver, Feng Zhang
BACKGROUND: Diabetic rats are more sensitive to nerve entrapment. This study was conducted to evaluate nerve function and histological changes in diabetic rats after nerve compression and subsequent decompression. METHODS: A total of 35 Wistar rats were included. The experimental group was divided into diabetic sciatic nerve compression group (DSNC, n = 5) and diabetic sciatic nerve decompression group (DSND, n = 20). The DSNC model was created by wrapping a silicone tube circumferentially around the nerve for 4 weeks, and then the DSND group accepted nerve decompression and was followed up to 12 weeks...
October 3, 2018: Annals of Plastic Surgery
Emiliano Trias, Peter H King, Ying Si, Yuri Kwon, Valentina Varela, Sofía Ibarburu, Mariángeles Kovacs, Ivan C Moura, Joseph S Beckman, Olivier Hermine, Luis Barbeito
Neuroinflammation is a recognized pathogenic mechanism underlying motor neuron degeneration in amyotrophic lateral sclerosis (ALS), but the inflammatory mechanisms influencing peripheral motor axon degeneration remain largely unknown. A recent report showed a pathogenic role for c-Kit-expressing mast cells mediating inflammation and neuromuscular junction denervation in muscles from SOD1G93A rats. Here, we have explored whether mast cells infiltrate skeletal muscles in autopsied muscles from ALS patients. We report that degranulating mast cells were abundant in the quadriceps muscles from ALS subjects but not in controls...
October 4, 2018: JCI Insight
Konrad Mende, Michael A Tonkin
In severe carpal tunnel syndrome a continuum of neural changes takes place depending on the degree and duration of the compression, beginning with breakdown of the blood-nerve barrier, followed by endoneurial oedema and, subsequently, perineurial thickening and ischemia. Persisting chronic compression will eventually result in axonal degeneration. We report a case of longstanding carpal tunnel syndrome with amyloid deposits and the unusual intraoperative 'Austrian flag' sign.
September 2018: Journal of Hand Surgery Asian-Pacific Volume
Paula Rebelo, Marta Giacomello, Luca Scorrano
How neuromuscular junctions (NMJs) are lost in disease and aging is unclear. Recently in Cell Metabolism, Wang et al. (2018) discovered that endoplasmic reticulum-mitochondria tethering by Mitofusin 2 is required to organize a cleft between these two organelles, which, like a lorry, traffics down the axon to distribute calpastatin to terminals where it blocks NMJ degradation.
October 2, 2018: Cell Metabolism
Tana Pottorf, Alexis Mann, Shaneann Fross, Clayton Mansel, Bhupinder P S Vohra
Golgi fragmentation and loss of Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) are the early key features of many neurodegenerative disorders. We investigated the link between NMNAT2 loss, Golgi fragmentation and axon degeneration. Golgi fragmentation in the cultured dorsal root ganglion (DRG) neurons resulted in caspase dependent axon degeneration and neuronal cell death. NMNAT2 depletion in the DRG neurons caused Golgi fragmentation and caspase dependent axon degeneration. NMNAT2 depletion did not cause ATP loss in the axons...
September 29, 2018: Neurochemistry International
Bret A Moore, Christopher J Murphy, Annajane Marlar, Richard R Dubielzig, Leandro B C Teixeira, William T Ferrier, Steven R Hollingsworth
We describe a case series of photoreceptor dysplasia with secondary retinal degeneration in juvenile peregrine falcons. Six Peregrine Falcons ( Falco peregrinus) and three Peregrine Falcon × Prairie Falcon ( Falco mexicanus) hybrids had early-life visual deficits. Eight birds had visual defects shortly after hatching, and one bird had visual deficits first noticed at 5 mo of age. Complete ophthalmic examinations were performed in each animal. Eight of the animals had electroretinograms, and nine of the animals had their eyes examined histologically after euthanasia...
October 2, 2018: Journal of Wildlife Diseases
Scott Karney-Grobe, Alexandra Russo, Erin Frey, Jeffrey Milbrandt, Aaron DiAntonio
Peripheral nerve injury induces a robust proregenerative program that drives axon regeneration. While many regeneration-associated genes are known, the mechanisms by which injury activates them are less well-understood. To identify such mechanisms, we performed a loss-of-function pharmacological screen in cultured adult mouse sensory neurons for proteins required to activate this program. Well-characterized inhibitors were present as injury signaling was induced but were removed before axon outgrowth to identify molecules that block induction of the program...
October 1, 2018: Proceedings of the National Academy of Sciences of the United States of America
Dominic D Quintana, Xuefang Ren, Heng Hu, Elizabeth B Engler-Chiurazzi, Stephanie L Rellick, Sara E Lewis, Jessica M Povroznik, James W Simpkins, Mohammad Alvi
Chronic cerebrovascular hypoperfusion results in vascular dementia and increases predisposition to lacunar infarcts. However, there are no suitable animal models. In this study, we developed a novel model for chronic irreversible cerebral hypoperfusion in mice. Briefly, an ameroid constrictor was placed on the right carotid artery to gradually occlude the vessel, while a microcoil was placed on the left carotid artery to prevent compensation of the blood flow. This procedure resulted in a gradual hypoperfusion developing over a period of 34 days with no cerebral blood flow recovery...
September 28, 2018: Metabolic Brain Disease
Hamdino Attia, Medhat Taha, Ahmed Abdellatif
Cognitive decline due to aging is most probably the result of changes in the white matter in the central nervous system (CNS) and/or demyelination. Towards this end, we used electron microscopic analysis of the morphological changes in aging rats' optic nerves as an easily accessible part of the CNS. In the present study several age changes were observed were observed in aging rats (36 months) vs young adult rats (6 months), namely; degeneration of axons, decreased packing density, and morphological alterations of myelination, including the ballooning of some myelin sheaths, separation of myelin lamellae, and degenerative changes in the oligodendrocytes population...
September 27, 2018: International Journal of Neuroscience
Daniel M Virga, Jessica Capps, Bhupinder P S Vohra
Gut motility malfunction and pathological changes in the enteric nervous system (ENS) are observed in the early stages of Parkinson's disease (PD). In many cases disturbances in the autonomous functions such as gut motility precedes the observed loss of central motor functions in PD. However, the mechanism by which ENS degeneration occurs in PD is unknown. We show that parkinsonian mimetics rotenone and MPP+ induce neurite degeneration that precedes cell death in primary enteric neurons cultured in vitro. If the neuronal death signals originate from degenerating neurites, neuronal death should be prevented by inhibiting neurite degeneration...
September 27, 2018: Neurochemical Research
Hui-Wen Liu, Chadwick B Smith, Mark S Schmidt, Xiaolu A Cambronne, Michael S Cohen, Marie E Migaud, Charles Brenner, Richard H Goodman
Axon degeneration, a hallmark of chemotherapy-induced peripheral neuropathy (CIPN), is thought to be caused by a loss of the essential metabolite nicotinamide adenine dinucleotide (NAD+ ) via the prodegenerative protein SARM1. Some studies challenge this notion, however, and suggest that an aberrant increase in a direct precursor of NAD+ , nicotinamide mononucleotide (NMN), rather than loss of NAD+ , is responsible. In support of this idea, blocking NMN accumulation in neurons by expressing a bacterial NMN deamidase protected axons from degeneration...
October 16, 2018: Proceedings of the National Academy of Sciences of the United States of America
Fereshteh Alsahebfosoul, Hamidreza Jahanbani-Ardakani, Reza Ghavimi, Nahid Sedaghat, Masoud Etemadifar
INTRODUCTION: Multiple sclerosis is a chronic autoimmune demyelinating disorder of central nervous system with unknown origin. In MS disease, T cells are pointed to myelin antigens and it leads to myelin loss and axonal degeneration. Cytokines are important regulators of immune system and has critical roles in MS pathogenesis. Interleukin 36, a member of interleukin 1 family, has been shown having important roles in some autoimmune disorders due to its proinflammatory actions and its role in host immunity...
September 25, 2018: Journal of Immunoassay & Immunochemistry
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