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Neurodegeneration

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https://www.readbyqxmd.com/read/28822080/soluble-epoxide-hydrolase-inhibition-attenuates-mptp-induced-neurotoxicity-in-the-nigrostriatal-dopaminergic-system-involvement-of-%C3%AE-synuclein-aggregation-and-er-stress
#1
Hui-Ju Huang, Yi-Ting Wang, Hui-Ching Lin, Yi-Hsuan Lee, Anya Maan-Yuh Lin
Soluble epoxide hydrolase (sEH) is widely expressed in the mammalian brain and possesses dual enzymatic activities, including C-terminal epoxide hydrolase (C-EH) which degrades epoxyeicosatrienoic acid (EET), a beneficial arachidonic acid metabolite. In the present study, the neuroprotective effect of sEH inhibition on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using genetic and pharmacological approaches. MPTP (15 mg/kg) was intraperitoneally injected in sEH knockout (KO) mice and C57BL/6J mice as wild-type (WT) mice...
August 18, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28821675/synergistic-toxicity-of-polyglutamine-expanded-tbp-in-glia-and-neuronal-cells-therapeutic-implications-for-sca17
#2
Yang Yang, Su Yang, Jifeng Guo, Yiting Cui, Baisha Tang, Xiao-Jiang Li, Shihua Li
Spinocerebellar ataxia 17 (SCA17) is caused by polyglutamine (polyQ) repeat expansion in the TATA-binding protein (TBP) and is among a family of neurodegenerative diseases in which polyQ expansion leads to preferential neuronal loss in the brain. Although previous studies have demonstrated that expression of polyQ-expanded proteins in glial cells can cause neuronal injury via non-cell-autonomous mechanisms, these studies investigated animal models that overexpress transgenic mutant proteins. Since glial cells are particularly reactive to overexpressed mutant proteins, it is important to investigate the in vivo role of glial dysfunction in neurodegeneration when mutant polyQ proteins are endogenously expressed...
August 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28821658/opposite-synaptic-alterations-at-the-neuromuscular-junction-in-an-als-mouse-model-when-motor-units-matter
#3
Tremblay Elsa, Martineau Éric, Robitaille Richard
Denervation of the neuromuscular junction (NMJ) precedes the loss of motor neurons (MNs) in amyotrophic lateral sclerosis (ALS). ALS is characterized by a motor unit (MU) dependent vulnerability where MNs with fast-fatigable (FF) characteristics are lost first, followed by fast-fatigue resistant (FR) and slow (S) ones. However, changes of NMJ properties as a function of MU types remain debated. We hypothesized that NMJ synaptic functions would be altered precociously in a MU specific manner, prior to structural alterations of the NMJ...
August 11, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28820649/targets-of-neuroprotection-in-glaucoma
#4
Shaoqing He, Dorota L Stankowska, Dorette Z Ellis, Raghu R Krishnamoorthy, Thomas Yorio
Progressive neurodegeneration of the optic nerve and the loss of retinal ganglion cells is a hallmark of glaucoma, the leading cause of irreversible blindness worldwide, with primary open-angle glaucoma (POAG) being the most frequent form of glaucoma in the Western world. While some genetic mutations have been identified for some glaucomas, those associated with POAG are limited and for most POAG patients, the etiology is still unclear. Unfortunately, treatment of this neurodegenerative disease and other retinal degenerative diseases is lacking...
August 18, 2017: Journal of Ocular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/28820437/are-astrocytes-the-predominant-cell-type-for-activation-of-nrf2-in-aging-and-neurodegeneration
#5
REVIEW
Jeffrey R Liddell
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates hundreds of antioxidant genes, and is activated in response to oxidative stress. Given that many neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease and multiple sclerosis are characterised by oxidative stress, Nrf2 is commonly activated in these diseases. Evidence demonstrates that Nrf2 activity is repressed in neurons in vitro, and only cultured astrocytes respond strongly to Nrf2 inducers, leading to the interpretation that Nrf2 signalling is largely restricted to astrocytes...
August 18, 2017: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/28820328/lps-induced-inflammatory-response-triggers-cell-cycle-reactivation-in-murine-neuronal-cells-through-retinoblastoma-proteins-induction
#6
Barbara D'Angelo, Carlo Astarita, Silvia Boffo, Mina Massaro-Giordano, Carmelina Iannuzzi, Antonella Caporaso, Marcella Macaluso, Antonio Giordano
Cell cycle reactivation in adult neurons is an early hallmark of neurodegeneration. The lipopolysaccharide (LPS) is a well-known pro-inflammatory factor that provokes neuronal cell death via glial cells activation. The retinoblastoma (RB) family includes RB1/p105, retinoblastoma-like 1 (RBL1/p107), and retinoblastoma-like 2 (Rb2/p130). Several studies have indicated that RB proteins exhibit tumor suppressor activities, and play a central role in cell cycle regulation. In this study, we assessed LPS-mediated inflammatory effect on cell cycle reactivation and apoptosis of neuronally differentiated cells...
August 18, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28820282/mir505-3p-regulates-axonal-development-via-inhibiting-the-autophagy-pathway-by-targeting-atg12
#7
Kan Yang, Bin Yu, Cheng Cheng, Tianlin Cheng, Bo Yuan, Kai Li, Junhua Xiao, Zilong Qiu, Yuxun Zhou
In addition to the canonical role in protein homeostasis, autophagy has recently been found to be involved in axonal dystrophy and neurodegeneration. Whether autophagy may also be involved in neural development remains largely unclear. Here we report that Mir505-3p is a crucial regulator for axonal elongation and branching in vitro and in vivo, through modulating autophagy in neurons. We identify that the key target gene of Mir505-3p in neurons is Atg12, encoding ATG12 (autophagy related 12) which is an essential component of the autophagy machinery during the initiation and expansion steps of autophagosome formation...
August 18, 2017: Autophagy
https://www.readbyqxmd.com/read/28819888/paraquat-induced-movement-disorder-in-relation-to-oxidative-stress-mediated-neurodegeneration-in-the-brain-of-drosophila-melanogaster
#8
S Niveditha, S R Ramesh, T Shivanandappa
Exposure to pesticides like paraquat (PQ) is considered as a risk factor for Parkinson's disease (PD). PQ has been shown to induce PD-like phenotype in experimental animals. Drosophila, a valuable laboratory model organism, is widely used to study neurodegenerative disorders including PD. The acute (single dose) PQ model of PD in Drosophila is associated with high mortality as well as reversibility of locomotor deficits and, therefore, does not replicate the disease phenotype. We have investigated the relevance of the acute and multiple (sublethal) dose of PQ to induce PD-like symptoms in Drosophila and shown that multiple-dose of PQ induces irreversible locomotor impairment without significant mortality...
August 18, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28819795/leptin-regulation-of-synaptic-function-at-hippocampal-ta-ca1-and-sc-ca1-synapses-implications-for-health-and-disease
#9
Gemma McGregor, Jenni Harvey
Growing evidence indicates that the endocrine hormone leptin regulates hippocampal synaptic function in addition to its established role as a hypothalamic satiety signal. Indeed, numerous studies show that leptin facilitates the cellular events that underlie hippocampal learning and memory including activity-dependent synaptic plasticity and glutamate receptor trafficking, indicating that leptin may be a potential cognitive enhancer. Although there has been extensive investigation into the modulatory role of leptin at hippocampal Schaffer collateral (SC)-CA1 synapses, recent evidence indicates that leptin also potently regulates excitatory synaptic transmission at the anatomically distinct temporoammonic (TA) input to hippocampal CA1 neurons...
August 18, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28819076/-molecularly-targeted-therapy-of-spinocerebellar-ataxia-type-1-by-hmgb1
#10
Kyota Fujita, Hitoshi Okazawa
Spinocerebellar ataxia type 1 (SCA1) is an untreatable neurodegenerative disease. We reported a decrease in HMGB1 levels in the nucleus of cerebellar neurons in mouse SCA 1. The decrease in this DNA architectural protein leads to the impairment of DNA repair and transcription, the two essential nuclear functions, and eventually causes neurodegeneration. We have designed a gene therapy using AAV-HMGB1 and tested it using the mouse model. Based on the results of these proof of concept (POC) studies, we are now preparing GMP-level AAV vector and designing human clinical trials...
August 2017: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/28818478/mutations-in-ddhd1-encoding-a-phospholipase-a1-is-a-novel-cause-of-retinopathy-and-neurodegeneration-with-brain-iron-accumulation
#11
Rodolphe Dard, Claire Meyniel, Valérie Touitou, Giovanni Stevanin, Foudil Lamari, Alexandra Durr, Claire Ewenczyk, Fanny Mochel
Defects of phospholipids remodelling and synthesis are inborn errors of metabolism responsible for various clinical presentations including spastic paraplegia, retinopathy, optic atrophy, myo- and cardiomyopathies, and osteo-cutaneous manifestations. DDHD1 encodes a phospholipase A1, which is involved in the remodelling of phospholipids. We previously described a relatively pure hereditary spastic paraplegia (HSP) phenotype associated with mutations in DDHD1. Here we report a complex form of HSP associated with retinal dystrophy and a pattern of neurodegeneration with brain iron accumulation (NBIA) on brain MRI, due to a novel homozygous mutation in DDHD1...
August 14, 2017: European Journal of Medical Genetics
https://www.readbyqxmd.com/read/28818116/distinct-white-matter-microstructural-abnormalities-and-extracellular-water-increases-relate-to-cognitive-impairment-in-alzheimer-s-disease-with-and-without-cerebrovascular-disease
#12
Fang Ji, Ofer Pasternak, Siwei Liu, Yng Miin Loke, Boon Linn Choo, Saima Hilal, Xin Xu, Mohammad Kamran Ikram, Narayanaswamy Venketasubramanian, Christopher Li-Hsian Chen, Juan Zhou
BACKGROUND: Mixed vascular and neurodegenerative dementia, such as Alzheimer's disease (AD) with concomitant cerebrovascular disease, has emerged as the leading cause of age-related cognitive impairment. The brain white matter (WM) microstructural changes in neurodegeneration well-documented by diffusion tensor imaging (DTI) can originate from brain tissue or extracellular free water changes. The differential microstructural and free water changes in AD with and without cerebrovascular disease, especially in normal-appearing WM, remain largely unknown...
August 17, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28818091/non-canonical-soluble-amyloid-beta-aggregates-and-plaque-buffering-controversies-and-future-directions-for-target-discovery-in-alzheimer-s-disease
#13
REVIEW
David L Brody, Hao Jiang, Norelle Wildburger, Thomas J Esparza
The specific amyloid-beta (Aβ) species or other amyloid-precursor protein cleavage products that are most directly related to human neurodegeneration and clinical dementia of the Alzheimer's type have not yet been directly identified. Without a clear understanding of the most relevant species, it is difficult to determine whether therapeutic candidates successfully engaged the correct target(s). Here, we review some of the controversies regarding soluble Aβ aggregates (also termed oligomers, dimers, trimers, Aβ*56, amylospheroids, etc...
August 17, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28816559/the-role-of-the-lectin-like-oxldl-receptor-lox-1-in-traffic-generated-air-pollution-exposure-mediated-alteration-of-the-brain-microvasculature-in-apolipoprotein-apo-e-knockout-mice
#14
JoAnn Lucero, Usa Suwannasual, Lindsay M Herbert, Jacob D McDonald, Amie K Lund
Recent studies have shown a strong correlation between air pollution-exposure and detrimental outcomes in the central nervous system, including alterations in blood brain barrier (BBB) integrity, neuroinflammation, and neurodegeneration. However, the mechanisms mediating these pathologies have not yet been fully elucidated. We have previously reported that exposure to traffic-generated air pollution results in increased circulating oxidized low-density lipoprotein (oxLDL), associated with alterations in BBB integrity, in atherosclerotic Apolipoprotein E null (ApoE(-/-)) mice...
August 17, 2017: Inhalation Toxicology
https://www.readbyqxmd.com/read/28816551/1%C3%AE-25-dihydroxyvitamin-d3-up-regulates-il-34-expression-in-sh-sy5y-neural-cells
#15
Dong Zhang, Miaomiao Li, Yang Dong, Xinhui Zhang, Xingyun Liu, Zhangming Chen, Yongji Zhu, Huiming Wang, Xuwen Liu, Jialiang Zhu, Yujun Shen, Heinrich Korner, Songcheng Ying, Shengyun Fang, Yuxian Shen
Vitamin D supplementation is regarded as a novel approach to treat Alzheimer's disease, but the underlying mechanism remains elusive. The cytokine IL-34 provides strong neuroprotective and survival signals in brain injury and neurodegeneration and could be an immunological mediator for the vitamin D-induced protection. The aim of this study was to investigate whether human IL-34 is up-regulated in neuronal cells by the hormonally active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3]. We found that IL-34 was detectable in a variety of cell lines and its expression was strongly induced in SH-SY5Y neural cells in a dose- and time-dependent manner by 1α,25(OH)2D3 through the vitamin D receptor (VDR)...
January 1, 2017: Innate Immunity
https://www.readbyqxmd.com/read/28816110/reduced-beta-amyloid-sensitivity-for-platelet-monocyte-aggregates-in-edta-blood-of-alzheimer-patients
#16
Michaela Defrancesco, Josef Marksteiner, Christian Humpel
Alzheimer´s disease (AD) is a severe neurodegenerative brain disorder characterized by beta-amyloid plaques, Tau pathology, inflammation, neurodegeneration, and cerebrovascular dysfunction. Besides that, alterations in monocytes and platelets have been reported in the blood of Alzheimer patients. In the present study, we measured circulating levels of platelet-monocyte aggregates in EDTA blood of cognitively healthy participants and 40 AD patients, and examined their changes induced by stimulation with beta-amyloid peptides...
August 17, 2017: International Psychogeriatrics
https://www.readbyqxmd.com/read/28816001/plasma-and-cerebrospinal-fluid-tau-and-neurofilament-concentrations-in-rapidly-progressive-neurological-syndromes-a-neuropathology-based-cohort
#17
G G Kovacs, U Andreasson, V Liman, G Regelsberger, M I Lutz, K Danics, E Keller, H Zetterberg, K Blennow
BACKGROUND AND PURPOSE: Cerebrospinal fluid (CSF) tau and neurofilament light chain (NF-L) proteins have proved to be reliable biomarkers for neuronal damage; however, there is a strong need for blood-based tests. METHODS: The present study included 132 autopsy cases with rapidly progressive neurological syndromes, including Alzheimer disease (AD) (21), sporadic (65) and genetic (21) Creutzfeldt-Jakob disease (CJD), 25 cases with vascular, neoplastic and inflammatory alterations, and additionally 18 healthy control individuals...
August 16, 2017: European Journal of Neurology: the Official Journal of the European Federation of Neurological Societies
https://www.readbyqxmd.com/read/28815576/microrna-and-mesial-temporal-lobe-epilepsy-with-hippocampal-sclerosis-whole-mirnome-profiling-of-human-hippocampus
#18
Petra Bencurova, Jiri Baloun, Katerina Musilova, Lenka Radova, Boris Tichy, Martin Pail, Martin Zeman, Eva Brichtova, Marketa Hermanova, Sarka Pospisilova, Marek Mraz, Milan Brazdil
OBJECTIVE: Mesial temporal lobe epilepsy (mTLE) is a severe neurological disorder characterized by recurrent seizures. mTLE is frequently accompanied by neurodegeneration in the hippocampus resulting in hippocampal sclerosis (HS), the most common morphological correlate of drug resistance in mTLE patients. Incomplete knowledge of pathological changes in mTLE+HS complicates its therapy. The pathological mechanism underlying mTLE+HS may involve abnormal gene expression regulation, including posttranscriptional networks involving microRNAs (miRNAs)...
August 16, 2017: Epilepsia
https://www.readbyqxmd.com/read/28814543/loss-of-dual-leucine-zipper-kinase-signaling-is-protective-in-animal-models-of-neurodegenerative-disease
#19
Claire E Le Pichon, William J Meilandt, Sara Dominguez, Hilda Solanoy, Han Lin, Hai Ngu, Alvin Gogineni, Arundhati Sengupta Ghosh, Zhiyu Jiang, Seung-Hye Lee, Janice Maloney, Vineela D Gandham, Christine D Pozniak, Bei Wang, Sebum Lee, Michael Siu, Snahel Patel, Zora Modrusan, Xingrong Liu, York Rudhard, Miriam Baca, Amy Gustafson, Josh Kaminker, Richard A D Carano, Eric J Huang, Oded Foreman, Robby Weimer, Kimberly Scearce-Levie, Joseph W Lewcock
Hallmarks of chronic neurodegenerative disease include progressive synaptic loss and neuronal cell death, yet the cellular pathways that underlie these processes remain largely undefined. We provide evidence that dual leucine zipper kinase (DLK) is an essential regulator of the progressive neurodegeneration that occurs in amyotrophic lateral sclerosis and Alzheimer's disease. We demonstrate that DLK/c-Jun N-terminal kinase signaling was increased in mouse models and human patients with these disorders and that genetic deletion of DLK protected against axon degeneration, neuronal loss, and functional decline in vivo...
August 16, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28814227/mitochondrial-aconitase-in-neurodegenerative-disorders-role-of-a-metabolism-related-molecule-in-neurodegeneration
#20
Fariba Khodagholi, Fatemeh Shaerzadeh, Fateme Montazeri
Mitochondrial aconitase (Aco2), a member of the family of iron-sulfur [4Fe-4S]-containing dehydratases, is involved in cellular metabolism through the tricarboxylic acid cycle. Aco2 is highly susceptible to oxidative damage in a way that exposure to the reactive species and free radicals lead to release of iron from the central [4Fe-4S] cluster resulting in the production of the inactive form of Aco2. There is increasing evidence supporting a direct association between impaired energy metabolism and the incidence and progression of neurodegenerative disorders in neuronal cells...
August 16, 2017: Current Drug Targets
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