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https://www.readbyqxmd.com/read/28098243/vanillic-acid-attenuates-a%C3%AE-1-42-induced-oxidative-stress-and-cognitive-impairment-in-mice
#1
Faiz Ul Amin, Shahid Ali Shah, Myeong Ok Kim
Increasing evidence demonstrates that β-amyloid (Aβ) elicits oxidative stress, which contributes to the pathogenesis and disease progression of Alzheimer's disease (AD). The aims of the present study were to determine and explore the antioxidant nature and potential mechanism of vanillic acid (VA) in Aβ1-42-induced oxidative stress and neuroinflammation mediated cognitive impairment in mice. An intracerebroventricular (i.c.v.) injection of Aβ1-42 into the mouse brain triggered increased reactive oxygen species (ROS) levels, neuroinflammation, synaptic deficits, memory impairment, and neurodegeneration...
January 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28097205/impact-of-tau-and-amyloid-burden-on-glucose-metabolism-in-alzheimer-s-disease
#2
Gérard N Bischof, Frank Jessen, Klaus Fliessbach, Julian Dronse, Jochen Hammes, Bernd Neumaier, Oezguer Onur, Gereon R Fink, Juraj Kukolja, Alexander Drzezga, Thilo van Eimeren
In a multimodal PET imaging approach, we determined the differential contribution of neurofibrillary tangles (measured with [(18)F]AV-1451) and beta-amyloid burden (measured with [(11)C]PiB) on degree of neurodegeneration (i.e., glucose metabolism measured with [(18)F]FDG-PET) in patients with Alzheimer's disease. Across brain regions, we observed an interactive effect of beta-amyloid burden and tau deposition on glucose metabolism which was most pronounced in the parietal lobe. Elevated beta-amyloid burden was associated with a stronger influence of tau accumulation on glucose metabolism...
December 2016: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/28096265/prion-properties-of-sod1-in-amyotrophic-lateral-sclerosis-and-potential-therapy
#3
Caroline Sibilla, Anne Bertolotti
Amyotrophic lateral sclerosis (ALS) is a devastating and rapidly progressive neurodegenerative disease caused by the deterioration of motor neurons. The first symptoms of ALS always begin at a focal but variable site and consistently spread to neighboring regions, suggesting that neurodegeneration in ALS is an orderly and propagating process. Like other neurodegenerative diseases, misfolding of a specific protein is central to ALS. SOD1, the major constituent of the protein deposits in some familial and sporadic forms of ALS, propagates its misfolded conformation like prions, providing a plausible molecular basis for the focality and spreading of muscle weakness in ALS...
January 17, 2017: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/28096234/glutamate-oxaloacetate-transaminase-enables-anaplerotic-refilling-of-tca-cycle-intermediates-in-stroke-affected-brain
#4
Cameron Rink, Surya Gnyawali, Richard Stewart, Seth Teplitsky, Hallie Harris, Sashwati Roy, Chandan K Sen, Savita Khanna
Ischemic stroke results in excessive release of glutamate, which contributes to neuronal cell death. Here, we test the hypothesis that otherwise neurotoxic glutamate can be productively metabolized by glutamate oxaloacetate transaminase (GOT) to maintain cellular energetics and protect the brain from ischemic stroke injury. The GOT-dependent metabolism of glutamate was studied in primary neural cells and in stroke-affected C57-BL6 mice using magnetic resonance spectroscopy and GC-MS. Extracellular Glu sustained cell viability under hypoglycemic conditions and increased GOT-mediated metabolism in vitro Correction of stroke-induced hypoxia using supplemental oxygen in vivo lowered Glu levels as measured by (1)H magnetic resonance spectroscopy...
January 17, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28095363/curcumin-confers-neuroprotection-against-alcohol-induced-hippocampal-neurodegeneration-via-creb-bdnf-pathway-in-rats
#5
Majid Motaghinejad, Manijeh Motevalian, Sulail Fatima, Hajar Hashemi, Mina Gholami
BACKGROUND: Alcohol abuse causes severe damage to the brain neurons. Studies have reported the neuroprotective effects of curcumin against alcohol-induced neurodegeneration. However, the precise mechanism of action remains unclear. METHODS: Seventy rats were equally divided into 7 groups (10 rats per group). Group 1 received normal saline (0.7ml/rat) and group 2 received alcohol (2g/kg/day) for 21days. Groups 3, 4, 5 and 6 concurrently received alcohol (2g/kg/day) and curcumin (10, 20, 40 and 60mg/kg, respectively) for 21days...
January 14, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28094806/plant-toxin-%C3%AE-odap-activates-integrin-%C3%AE-1-and-focal-adhesion-a-critical-pathway-to-cause-neurolathyrism
#6
Rui-Yue Tan, Geng-Yan Xing, Guang-Ming Zhou, Feng-Min Li, Wen-Tao Hu, Fernand Lambein, Jun-Lan Xiong, Sheng-Xiang Zhang, Hai-Yan Kong, Hao Zhu, Zhi-Xiao Li, You-Cai Xiong
Neurolathyrism is a unique neurodegeneration disease caused by β-N-oxalyl-L-α, β- diaminopropionic (β-ODAP) present in grass pea seed (Lathyrus stativus L.) and its pathogenetic mechanism is unclear. This issue has become a critical restriction to take full advantage of drought-tolerant grass pea as an elite germplasm resource under climate change. We found that, in a human glioma cell line, β-ODAP treatment decreased mitochondrial membrane potential, leading to outside release and overfall of Ca(2+) from mitochondria to cellular matrix...
January 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28094792/identification-of-a-nuclear-respiratory-factor-1-recognition-motif-in-the-apolipoprotein-e-variant-apoe4-linked-to-alzheimer-s-disease
#7
Anne Urfer-Buchwalder, Roman Urfer
Alzheimer's disease affects tens of millions of people worldwide and its prevalence continues to rise. It is caused by a combination of a subject's heredity, environment, lifestyle, and medical condition. The most significant genetic risk factor for late onset Alzheimer's disease is a variant of the apolipoprotein E gene, APOE4. Here we show that the single nucleotide polymorphism rs429358 that defines APOE4 is located in a short sequence motif repeated several times within exon 4 of apolipoprotein E, reminiscent of the structure of transcriptional enhancers...
January 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28094300/sequestration-of-prmt1-and-nd1-l-mrna-into-als-linked-fus-mutant-r521c-positive-aggregates-contributes-to-neurite-degeneration-upon-oxidative-stress
#8
Mi-Hee Jun, Hyun-Hee Ryu, Yong-Woo Jun, Tongtong Liu, Yan Li, Chae-Seok Lim, Yong-Seok Lee, Bong-Kiun Kaang, Deok-Jin Jang, Jin-A Lee
Mutations in fused in sarcoma (FUS), a DNA/RNA binding protein, are associated with familial amyotrophic lateral sclerosis (ALS). However, little is known about how ALS-causing mutations alter protein-protein and protein-RNA complexes and contribute to neurodegeneration. In this study, we identified protein arginine methyltransferase 1 (PRMT1) as a protein that more avidly associates with ALS-linked FUS-R521C than with FUS-WT (wild type) or FUS-P525L using co-immunoprecipitation and LC-MS analysis. Abnormal association between FUS-R521C and PRMT1 requires RNA, but not methyltransferase activity...
January 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28093976/chemoinformatics-profiling-of-the-chromone-nucleus-as-a-mao-b-a2aar-dual-binding-scaffold
#9
Maykel Cruz-Monteagudo, Fernanda Borges, M Natália D S Cordeiroc, Aliuska Morales Helguerad, Eduardo Tejerab, Cesar Paz-Y-Miñob, Aminael Sánchez-Rodrígueze, Yunier Perera-Sardiñaf, Yunierkis Perez-Castillo
BACKGROUND: In the context of the current drug discovery efforts to find disease modifying therapies for Parkinson´s disease (PD) the current single target strategy has proved inefficient. Consequently, the search for multi-potent agents is attracting more and more attention due to the multiple pathogenetic factors implicated in PD. Multiple evidences points to the dual inhibition of the monoamine oxidase B (MAO-B), as well as adenosine A2A receptor (A2AAR) blockade, as a promising approach to prevent the neurodegeneration involved in PD...
January 16, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28093935/new-methods-for-monitoring-mitochondrial-biogenesis-and-mitophagy-in%C3%A2-vitro-and-in%C3%A2-vivo
#10
Jessica A Williams, Katrina Zhao, Shengkan Jin, Wen-Xing Ding
Removal of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. Increasing evidence implicates mitophagy in red blood cell differentiation, neurodegeneration, macrophage-mediated inflammation, ischemia, adipogenesis, drug-induced tissue injury, and cancer. Considerable progress has been made toward understanding the biochemical mechanisms involved in mitophagy regulation. However, few reliable assays to monitor and quantify mitophagy have been developed, particularly in vivo...
January 1, 2017: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/28093713/timing-of-future-remyelination-therapies-and-their-potential-to-stop-multiple-sclerosis-progression
#11
Burcu Zeydan, Moses Rodriguez, Orhun H Kantarci
Prior to the onset of demyelination in multiple sclerosis (MS), early oligodendrocyte injury, axonal degeneration and astroglial scarring occur. The irreversible progressive phase of MS begins when the axonal loss threshold is reached. Progressive disease onset has the highest impact on a poor prognosis in MS. Conversion to progressive disease is essentially an age-dependent process independent of disease duration and initial disease course. Although prevention of relapses has been the primary approach in the disease management, incomplete recovery from even the first relapse correlates with the long-term neurodegenerative phenotype of progressive MS onset...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28093710/role-of-oligodendrocyte-dysfunction-in-demyelination-remyelination-and-neurodegeneration-in-multiple-sclerosis
#12
Adriana Octaviana Dulamea
Oligodendrocytes (OLs) are the myelinating cells of the central nervous system (CNS) during development and throughout adulthood. They result from a complex and well controlled process of activation, proliferation, migration and differentiation of oligodendrocyte progenitor cells (OPCs) from the germinative niches of the CNS. In multiple sclerosis (MS), the complex pathological process produces dysfunction and apoptosis of OLs leading to demyelination and neurodegeneration. This review attempts to describe the patterns of demyelination in MS, the steps involved in oligodendrogenesis and myelination in healthy CNS, the different pathways leading to OLs and myelin loss in MS, as well as principles involved in restoration of myelin sheaths...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28093709/molecular-genetic-and-epigenetic-basis-of-multiple-sclerosis
#13
Zohreh Hojati
Multiple Sclerosis (MS) is a chronic immune-mediated disease of spinal cord and brain. The initial event in MS occurs when activated CD4(+) T cells in periphery exacerbates immune responses by stimulating immune cells such as B cells, CD8(+) cells, mast cells, granulocytes and monocytes. These proinflammatory cells pass blood brain barrier by secreting proinflammatory cytokines including TNF-α and INF-γ which activate adhesion factors. APCs (antigen-presenting cells) reactivate CD4(+) T cells after infiltrating the CNS and CD4(+) T cells produce cytokines and chemokines...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28093705/manipulation-of-oxygen-and-endoplasmic-reticulum-stress-factors-as-possible-interventions-for-treatment-of-multiple-sclerosis-evidence-for-and-against
#14
Paul Eggleton, Gary R Smerdon, Janet E Holley, Nicholas J Gutowski
Multiple sclerosis (MS) is normally considered a chronic inflammatory disease of the central nervous system (CNS), where T-cells breaching the blood brain barrier react against proteins of the axonal myelin sheaths, leading to focal plaques and demyelination in the brain and spinal cord. Many current therapies are immunosuppressive in nature and are designed to target the immune system at an early stage of the disease. But there is no cure and MS may evolve into a neurodegenerative disease, where immunomodulatory treatments appear less effective...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28093569/translational-evaluation-of-translocator-protein-as-a-marker-of-neuroinflammation-in-schizophrenia
#15
T Notter, J M Coughlin, T Gschwind, U Weber-Stadlbauer, Y Wang, M Kassiou, A C Vernon, D Benke, M G Pomper, A Sawa, U Meyer
Positron emission tomography (PET) imaging with radiotracers that target translocator protein 18 kDa (TSPO) has become a popular approach to assess putative neuroinflammatory processes and associated microglia activation in psychotic illnesses. It remains unclear, however, whether TSPO imaging can accurately capture low-grade inflammatory processes such as those present in schizophrenia and related disorders. Therefore, we evaluated the validity of TSPO as a disease-relevant marker of inflammation using a translational approach, which combined neurodevelopmental and neurodegenerative mouse models with PET imaging in patients with recent-onset schizophrenia and matched controls...
January 17, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28093491/early-microgliosis-precedes-neuronal-loss-and-behavioural-impairment-in-mice-with-a-frontotemporal-dementia-causing-chmp2b-mutation
#16
Emma L Clayton, Renzo Mancuso, Troels Tolstrup Nielsen, Sarah Mizielinska, Holly Holmes, Nicholas Powell, Frances Norona, Jytte Overgaard Larsen, Carmelo Milioto, Katherine M Wilson, Mark F Lythgoe, Sebastian Ourselin, Jörgen E Nielsen, Peter Johannsen, Ida Holm, John Collinge, A Frej, Peter L Oliver, Diego Gomez-Nicola, Adrian M Isaacs
Frontotemporal dementia (FTD)-causing mutations in the CHMP2B gene lead to the generation of mutant C-terminally truncated CHMP2B. We report that transgenic mice expressing endogenous levels of mutant CHMP2B developed late-onset brain volume loss associated with frank neuronal loss and FTD-like changes in social behaviour. These data are the first to show neurodegeneration in mice expressing mutant CHMP2B and indicate that our mouse model is able to recapitulate neurodegenerative changes observed in FTD. Neuroinflammation has been increasingly implicated in neurodegeneration, including FTD...
January 16, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28093241/new-isatin-derivative-inhibits-neurodegeneration-by-restoring-insulin-signaling-in-brain
#17
Meha Fatima Aftab, Shabbir Khan Afridi, Uzma Rasool Mughal, Aneela Karim, Darakhshan Jabeen Haleem, Nurul Kabir, Khalid M Khan, Rahman M Hafizur, Rizwana S Waraich
Diabetes is associated with neurodegeneration. Glycation ensues in diabetes and glycated proteins cause insulin resistance in brain resulting in amyloid plaques and NFTs. Also glycation enhances gliosis by promoting neuroinflammation. Currently there is no therapy available to target neurodegenration in brain therefore, development of new therapy that offers neuroprotection is critical. The objective of this study was to evaluate mechanistic effect of isatin derivative URM-II-81, an anti-glycation agent for improvement of insulin action in brain and inhibition of neurodegenration...
January 13, 2017: Journal of Chemical Neuroanatomy
https://www.readbyqxmd.com/read/28092684/biallelic-mutations-in-the-3-exonuclease-toe1-cause-pontocerebellar-hypoplasia-and-uncover-a-role-in-snrna-processing
#18
Rea M Lardelli, Ashleigh E Schaffer, Veerle R C Eggens, Maha S Zaki, Stephanie Grainger, Shashank Sathe, Eric L Van Nostrand, Zinayida Schlachetzki, Basak Rosti, Naiara Akizu, Eric Scott, Jennifer L Silhavy, Laura Dean Heckman, Rasim Ozgur Rosti, Esra Dikoglu, Anne Gregor, Alicia Guemez-Gamboa, Damir Musaev, Rohit Mande, Ari Widjaja, Tim L Shaw, Sebastian Markmiller, Isaac Marin-Valencia, Justin H Davies, Linda de Meirleir, Hulya Kayserili, Umut Altunoglu, Mary Louise Freckmann, Linda Warwick, David Chitayat, Susan Blaser, Ahmet Okay Çağlayan, Kaya Bilguvar, Huseyin Per, Christina Fagerberg, Henrik T Christesen, Maria Kibaek, Kimberly A Aldinger, David Manchester, Naomichi Matsumoto, Kazuhiro Muramatsu, Hirotomo Saitsu, Masaaki Shiina, Kazuhiro Ogata, Nicola Foulds, William B Dobyns, Neil C Chi, David Traver, Luigina Spaccini, Stefania Maria Bova, Stacey B Gabriel, Murat Gunel, Enza Maria Valente, Marie-Cecile Nassogne, Eric J Bennett, Gene W Yeo, Frank Baas, Jens Lykke-Andersen, Joseph G Gleeson
Deadenylases are best known for degrading the poly(A) tail during mRNA decay. The deadenylase family has expanded throughout evolution and, in mammals, consists of 12 Mg(2+)-dependent 3'-end RNases with substrate specificity that is mostly unknown. Pontocerebellar hypoplasia type 7 (PCH7) is a unique recessive syndrome characterized by neurodegeneration and ambiguous genitalia. We studied 12 human families with PCH7, uncovering biallelic, loss-of-function mutations in TOE1, which encodes an unconventional deadenylase...
January 16, 2017: Nature Genetics
https://www.readbyqxmd.com/read/28091722/hyperphosphorylated-tau-causes-reduced-hippocampal-ca1-excitability-by-relocating-the-axon-initial-segment
#19
Robert John Hatch, Yan Wei, Di Xia, Jürgen Götz
Hyperphosphorylated tau has a critical role in tauopathies such as Alzheimer's disease and frontotemporal dementia, impairing neuronal function and eventually leading to neurodegeneration. A critical role for tau is supported by studies in transgenic mouse models that express the P301L tau mutation found in cases of familial frontotemporal dementia, with the accumulation of hyperphosphorylated tau in the hippocampus causing reductions in hippocampal long-term potentiation and impairments in spatial learning and memory...
January 16, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28090391/neurotoxin-induced-catecholaminergic-loss-in-the-colonic-myenteric-plexus-of-rhesus-monkeys
#20
Jeanette M Shultz, Henry Resnikoff, Viktorya Bondarenko, Valerie Joers, Andres Mejia, Heather Simmons, Marina E Emborg
OBJECTIVE: Constipation is a common non-motor symptom of Parkinson's disease (PD). Although pathology of the enteric nervous system (ENS) has been associated with constipation in PD, the contribution of catecholaminergic neurodegeneration to this symptom is currently debated. The goal of this study was to assess the effects of the neurotoxin 6-hydroxydopamine (6-OHDA) on the colonic myenteric plexus and shed light on the role of catecholaminergic innervation in gastrointestinal (GI) function...
November 2016: Journal of Alzheimer's Disease and Parkinsonism
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