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https://www.readbyqxmd.com/read/29779173/long-lasting-high-lysine-diet-aggravates-white-matter-injury-in-glutaryl-coa-dehydrogenase-deficient-gcdh-mice
#1
Silvia Olivera-Bravo, Bianca Seminotti, Eugenia Isasi, César A Ribeiro, Guilhian Leipnitz, Michael Woontner, Stephen I Goodman, Diogo Souza, Luis Barbeito, Moacir Wajner
Glutaric acidemia type I (GA-I) is a neurometabolic disease caused by deficient activity of glutaryl-CoA dehydrogenase (GCDH) that results in accumulation of metabolites derived from lysine (Lys), hydroxylysine, and tryptophan catabolism. GA-I patients typically develop encephalopatic crises with striatal degeneration and progressive white matter defects. However, late onset patients as well as Gcdh-/- mice only suffer diffuse myelinopathy, suggesting that neuronal death and white matter defects are different pathophysiological events...
May 19, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29778899/dopamine-loss-alters-the-hippocampus-nucleus-accumbens-synaptic-transmission-in-the-tg2576-mouse-model-of-alzheimer-s-disease
#2
Alberto Cordella, Paraskevi Krashia, Annalisa Nobili, Annabella Pignataro, Livia La Barbera, Maria Teresa Viscomi, Alessandro Valzania, Flavio Keller, Martine Ammassari-Teule, Nicola Biagio Mercuri, Nicola Berretta, Marcello D'Amelio
The functional loop involving the ventral tegmental area (VTA), dorsal hippocampus and nucleus accumbens (NAc) plays a pivotal role in the formation of spatial memory and persistent memory traces. In particular, the dopaminergic innervation from the VTA to the hippocampus is critical for hippocampal-related memory function and alterations in the midbrain dopaminergic system are frequently reported in Alzheimer's disease (AD), contributing to age-related decline in memory and non-cognitive functions. However, much less is known about the hippocampus-NAc connectivity in AD...
May 17, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29775216/neuroimmflammation-and-microglia-in-glaucoma-time-for-a-paradigm-shift
#3
REVIEW
Xin Wei, Kin-Sang Cho, Eric F Thee, Martine J Jager, Dong Feng Chen
Glaucoma is a complex neurodegenerative disease with many clinical subtypes. Some of its rare forms include pigmentary glaucoma, uveitic glaucoma and congenital glaucoma. While they all share common features of progressive retinal ganglion cell (RGC) loss, optic nerve damage and corresponding visual field loss, the exact mechanisms underlying glaucomatous neuron loss are not clear. This has largely hindered the development of a real cure for this disease. Elevated intraocular pressure (IOP) is a known major risk factor of glaucoma; however, progressive degeneration of RGCs and axons can also be found in patients with a normal IOP, i...
May 18, 2018: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29774773/mir-711-induced-down-regulation-of-angiopoietin-1-mediates-neuronal-cell-death
#4
Boris Sabirzhanov, Alan Faden, Taryn Aubrecht, Rebecca Henry, Ethan Glaser, Bogdan A Stoica
Angiopoietin-1 (Ang-1) is a well-known endothelial growth factor but its effects on neurons have yet to be elucidated. We show that Ang-1 is rapidly down-regulated in the injured brain after controlled cortical impact (CCI), a mouse experimental TBI model and in etoposide-induced neuronal apoptosis in vitro. Ang-1 treatment inhibits etoposide-induced up-regulation of pro-apoptotic Bcl-2 family members Noxa, Puma, Bim, and Bax; reduces markers of caspase-dependent (cytochrome c release/caspase activation) and caspase-independent (apoptosis-inducing factor release) pathways; and limits neuronal cell death...
May 18, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29774557/diabetes-induced-microvascular-complications-at-the-level-of-the-spinal-cord-a-contributing-factor-in-diabetic-neuropathic-pain
#5
N Ved, M E Da Vitoria Lobo, S M Bestall, C L Vidueira, N Beazley-Long, K Ballmer-Hofer, M Hirashima, D O Bates, L F Donaldson, R P Hulse
Abnormalities of neurovascular interactions within the central nervous system of diabetic patients is associated with the onset of many neurological disease states. However, to date, the link between the neurovascular network within the spinal cord and regulation of nociception has not been investigated despite neuropathic pain being common in diabetes. We hypothesised that hyperglycaemia-induced endothelial degeneration in the spinal cord, due to suppression of VEGF-A/VEGFR2 signalling, induces diabetic neuropathic pain...
May 17, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29774215/importance-of-functional-loss-of-fus-in-ftld-als
#6
REVIEW
Shinsuke Ishigaki, Gen Sobue
Fused in sarcoma (FUS) is an RNA binding protein that regulates RNA metabolism including alternative splicing, transcription, and RNA transportation. FUS is genetically and pathologically involved in frontotemporal lobar degeneration (FTLD)/amyotrophic lateral sclerosis (ALS). Multiple lines of evidence across diverse models suggest that functional loss of FUS can lead to neuronal dysfunction and/or neuronal cell death. Loss of FUS in the nucleus can impair alternative splicing and/or transcription, whereas dysfunction of FUS in the cytoplasm, especially in the dendritic spines of neurons, can cause mRNA destabilization...
2018: Frontiers in Molecular Biosciences
https://www.readbyqxmd.com/read/29773756/mir126-5p-down-regulation-facilitates-axon-degeneration-and-nmj-disruption-via-a-non-cell-autonomous-mechanism-in-als
#7
Roy Maimon, Ariel Ionescu, Avichai Bonnie, Sahar Sweetat, Shane Wald-Altman, Shani Inbar, Tal Gradus, Davide Trotti, Miguel Weil, Oded Behar, Eran Perlson
Axon degeneration and disruption of neuromuscular junctions (NMJs) are key events in Amyotrophic Lateral Sclerosis (ALS) pathology. Although the disease's etiology is not fully understood, it is thought to involve a non-cell-autonomous mechanism and alterations in RNA metabolism. Here, we identified reduced levels of miR-126-5p in pre-symptomatic ALS male mice models, and an increase in its targets: axon destabilizing type-3 Semaphorins and their co-receptor Neuropilins. Utilizing compartmentalized in vitro co-cultures, we demonstrated that myocytes expressing diverse ALS-causing mutations promote axon degeneration and NMJ dysfunction, which were inhibited by applying Neuropilin1 (NRP1) blocking antibody...
May 17, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29772521/myricetin-attenuates-neurodegeneration-and-cognitive-impairment-in-parkinsonism
#8
Vijayraja Dhanraj, Jeyaprakash Karuppaiah, Rengasamy Balakrishnan, Namasivayam Elangovan
Parkinson's disease (PD) is a progressive neurodegenerative disease due to dopaminergic neuron degeneration. It mostly affects the aged population, leads to memory decline and loss of motor coordination. The present study investigates the neuroprotective role of myricetin a flavonol isolated from the brown seaweed Turbinaria ornata in rotenone induced Drosophila model of PD. Rotenone administration led to dopaminergic neuronal degeneration, dopamine depletion, impaired muscular coordination, gait disturbances, memory decline oxidative stress and apoptosis...
June 1, 2018: Frontiers in Bioscience (Elite Edition)
https://www.readbyqxmd.com/read/29772357/modelling-the-dorsal-root-ganglia-using-human-pluripotent-stem-cells-a-platform-to-study-peripheral-neuropathies
#9
Serena Viventi, Mirella Dottori
Sensory neurons of the dorsal root ganglia (DRG) are the primary responders to stimuli inducing feelings of touch, pain, temperature, vibration, pressure and muscle tension. They consist of multiple subpopulations based on their morphology, molecular and functional properties. Our understanding of DRG sensory neurons has been predominantly driven by rodent studies and using transformed cell lines, whereas less is known about human sensory DRG neurons simply because of limited availability of human tissue. Although these previous studies have been fundamental for our understanding of the sensory system, it is imperative to profile human DRG subpopulations as it is becoming evident that human sensory neurons do not share the identical molecular and functional properties found in other species...
May 14, 2018: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/29771571/effect-of-weak-combined-static-and-extremely-low-frequency-alternating-magnetic-fields-on-spatial-memory-and-brain-amyloid-%C3%AE-in-two-animal-models-of-alzheimer-s-disease
#10
Natalia V Bobkova, Vadim V Novikov, Natalia I Medvinskaya, Irina Y Aleksandrova, Inna V Nesterova, Eugenii E Fesenko
Subchronic effect of a weak combined magnetic field (MF), produced by superimposing a constant component, 42 µT and an alternating MF of 0.08 µT, which was the sum of two frequencies of 4.38 and 4.88 Hz, was studied in olfactory bulbectomized (OBE) and transgenic Tg (APPswe, PSEN1) mice, which were used as animal models of sporadic and heritable Alzheimer's disease (AD) accordingly. Spatial memory was tested in a Morris water maze on the following day after completion of training trials with the hidden platform removed...
May 17, 2018: Electromagnetic Biology and Medicine
https://www.readbyqxmd.com/read/29771445/tirofiban-combined-with-rt-pa-intraarterial-thrombolysis-improves-the-recanalization-rate-of-acute-middle-cerebral-artery-occlusion-in-rabbits
#11
Y-J Yu, W Xiong
OBJECTIVE: To investigate the curative effect of tirofiban combined with recombinant tissue-plasminogen activator (rt-PA) selective intra-arterial thrombolysis on acute middle cerebral artery occlusion (MCAO). MATERIALS AND METHODS: A total of 60 adult male Japanese white rabbits weighing 2.5-3.0 kg were selected, and the acute cerebral infarction model was established via autologous thromboembolism of middle cerebral artery. Rabbits were randomly divided into 4 groups: tirofiban group (Ti group, 5 μg/kg, n=15), rt-PA group (rt-PA group, 2 mg/kg, n=15), tirofiban + rt-PA group (Ti + rt-PA group, 3 μg/kg Ti + 1 mg/kg rt-PA, n=15), and control group (Co group, n=15)...
May 2018: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/29770645/atoh1-regulation-in-the-cochlea-more-than-just-transcription
#12
REVIEW
Yen-Fu Cheng
More than 80% of all cases of deafness are related to the death or degeneration of cochlear hair cells and the associated spiral ganglion neurons, and a lack of regeneration of these cells leads to permanent hearing loss. Therefore, the regeneration of lost hair cells is an important goal for the treatment of deafness. Atoh1 is a basic helix-loop-helix (bHLH) transcription factor that is critical in both the development and regeneration of cochlear hair cells. Atoh1 is transcriptionally regulated by several signaling pathways, including Notch and Wnt signalings...
July 13, 2017: Journal of Zhejiang University. Science. B
https://www.readbyqxmd.com/read/29770442/current-concepts-in-the-neuropathogenesis-of-mucolipidosis-type-iv
#13
REVIEW
Lauren C Boudewyn, Steven U Walkley
Mucolipidosis type IV (MLIV) is an autosomal recessive, lysosomal storage disorder causing progressively severe intellectual disability, motor and speech deficits, retinal degeneration often culminating in blindness, and systemic disease causing a shortened lifespan. MLIV results from mutations in the gene MCOLN1 encoding the transient receptor potential channel mucolipin-1. It is an ultra-rare disease and is currently known to affect just over 100 diagnosed individuals. The last decade has provided a wealth of research focused on understanding the role of the enigmatic mucolipin-1 protein in cell and brain function and how its absence causes disease...
May 16, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29769718/ankrd16-prevents-neuron-loss-caused-by-an-editing-defective-trna-synthetase
#14
My-Nuong Vo, Markus Terrey, Jeong Woong Lee, Bappaditya Roy, James J Moresco, Litao Sun, Hongjun Fu, Qi Liu, Thomas G Weber, John R Yates, Kurt Fredrick, Paul Schimmel, Susan L Ackerman
Editing domains of aminoacyl tRNA synthetases correct tRNA charging errors to maintain translational fidelity. A mutation in the editing domain of alanyl tRNA synthetase (AlaRS) in Aars sti mutant mice results in an increase in the production of serine-mischarged tRNAAla and the degeneration of cerebellar Purkinje cells. Here, using positional cloning, we identified Ankrd16, a gene that acts epistatically with the Aars sti mutation to attenuate neurodegeneration. ANKRD16, a vertebrate-specific protein that contains ankyrin repeats, binds directly to the catalytic domain of AlaRS...
May 16, 2018: Nature
https://www.readbyqxmd.com/read/29769445/vegf-vegfr2-blockade-does-not-cause-retinal-atrophy-in-amd-relevant-models
#15
Da Long, Yogita Kanan, Jikui Shen, Sean F Hackett, Yuanyuan Liu, Zibran Hafiz, Mahmood Khan, Lili Lu, Peter A Campochiaro
Intraocular injections of VEGF-neutralizing proteins provide tremendous benefits in patients with choroidal neovascularization (NV) due to age-related macular degeneration (AMD), but during treatment some patients develop retinal atrophy. Suggesting that VEGF is a survival factor for retinal neurons, a clinical trial group attributed retinal atrophy to VEGF suppression and cautioned against frequent anti-VEGF injections. This recommendation may contribute to poor outcomes in clinical practice from insufficient treatment...
May 17, 2018: JCI Insight
https://www.readbyqxmd.com/read/29768876/protection-by-neostigmine-and-atropine-against-brain-and-liver-injury-induced-by-acute-malathion-exposure
#16
Omar M E Abdel-Salam, Eman R Youness, Reham Shehab ElNemr Esmail, Nadia A Mohammed, Yasser A Khadrawy, Amany A Sleem, Amany Mamdouh Abdulaziz
We examined the effect of treatment with neostigmine alone or with atropine on brain oxidative stress and on brain and liver tissue damage following acute malathion toxicity. Rats were intraperitoneally treated with malathion 150 mg/kg along with neostigmine (200 or 400 μg/kg) or neostigmine (200 μg/kg) + atropine (1 mg/kg) and euthanized 4 h later. Results indicated that compared with the saline group, malathion resulted in (i) higher brain malondialdehyde (MDA) and nitric oxide (46.4% and 86.2%); (ii) decreased brain reduced glutathione (GSH) (67...
January 1, 2018: Journal of Nanoscience and Nanotechnology
https://www.readbyqxmd.com/read/29767748/glial-activation-and-central-synapse-loss-but-not-motoneuron-degeneration-are-prevented-by-the-sigma-1-receptor-agonist-pre-084-in-the-smn2b-mouse-model-of-spinal-muscular-atrophy
#17
Clàudia Cerveró, Alba Blasco, Olga Tarabal, Anna Casanovas, Lídia Piedrafita, Xavier Navarro, Josep E Esquerda, Jordi Calderó
Spinal muscular atrophy (SMA) is characterized by the loss of α-motoneurons (MNs) with concomitant muscle denervation. MN excitability and vulnerability to disease are particularly regulated by cholinergic synaptic afferents (C-boutons), in which Sigma-1 receptor (Sig1R) is concentrated. Alterations in Sig1R have been associated with MN degeneration. Here, we investigated whether a chronic treatment with the Sig1R agonist PRE-084 was able to exert beneficial effects on SMA. We used a model of intermediate SMA, the Smn2B/- mouse, in which we performed a detailed characterization of the histopathological changes that occur throughout the disease...
May 14, 2018: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/29766664/tissue-engineered-nigrostriatal-pathway-for-treatment-of-parkinson-s-disease
#18
Laura A Struzyna, Kevin D Browne, Zachary D Brodnik, Justin C Burrell, James P Harris, H Isaac Chen, John A Wolf, Kate V Panzer, James Lim, John E Duda, Rodrigo A España, D Kacy Cullen
The classic motor deficits of Parkinson's disease are caused by degeneration of dopaminergic neurons in the substantia nigra pars compacta, resulting in the loss of their long-distance axonal projections that modulate the striatum. Current treatments only minimize the symptoms of this disconnection as there is no approach capable of replacing the nigrostriatal pathway. We are applying micro-tissue engineering techniques to create living, implantable constructs that mimic the architecture and function of the nigrostriatal pathway...
May 15, 2018: Journal of Tissue Engineering and Regenerative Medicine
https://www.readbyqxmd.com/read/29766029/seizure-suppressant-and-neuroprotective-effects-of-encapsulated-bdnf-producing-cells-in-a-rat-model-of-temporal-lobe-epilepsy
#19
Chiara Falcicchia, Giovanna Paolone, Dwaine F Emerich, Francesca Lovisari, William J Bell, Tracie Fradet, Lars U Wahlberg, Michele Simonato
Brain-derived neurotrophic factor (BDNF) may represent a therapeutic for chronic epilepsy, but evaluating its potential is complicated by difficulties in its delivery to the brain. Here, we describe the effects on epileptic seizures of encapsulated cell biodelivery (ECB) devices filled with genetically modified human cells engineered to release BDNF. These devices, implanted into the hippocampus of pilocarpine-treated rats, highly decreased the frequency of spontaneous seizures by more than 80%. These benefits were associated with improved cognitive performance, as epileptic rats treated with BDNF performed significantly better on a novel object recognition test...
June 15, 2018: Molecular Therapy. Methods & Clinical Development
https://www.readbyqxmd.com/read/29765300/detection-of-dna-double-strand-breaks-by-%C3%AE-h2ax-does-not-result-in-53bp1-recruitment-in-mouse-retinal-tissues
#20
Brigitte Müller, N M Ellinwood, Birgit Lorenz, Knut Stieger
Gene editing is an attractive potential treatment of inherited retinopathies. However, it often relies on endogenous DNA repair. Retinal DNA repair is incompletely characterized in humans and animal models. We investigated recruitment of the double stranded break (DSB) repair complex of γH2AX and 53bp1 in both developing and mature mouse neuroretinas. We evaluated the immunofluorescent retinal expression of these proteins during development (P07-P30) in normal and retinal degeneration models, as well as in potassium bromate induced DSB repair in normal adult (3 months) retinal explants...
2018: Frontiers in Neuroscience
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