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https://www.readbyqxmd.com/read/28938120/prion-like-domains-program-ewing-s-sarcoma
#1
James Shorter
Prion-like domains have emerged as important drivers of neurodegenerative disease. Now, Boulay et al. establish that the translocated prion-like domain of the oncogenic EWS-FLI1 fusion protein enables phase-separation events, which inappropriately recruit chromatin-remodeling factors to elicit the aberrant transcriptional programs underlying Ewing's sarcoma.
September 21, 2017: Cell
https://www.readbyqxmd.com/read/28937955/military-blast-injury-and-chronic-neurodegeneration-research-presentations-from-the-2015-international-state-of-the-science-meeting
#2
Denes Agoston, Peethambaran Arun, Patrick Bellgowan, Steven Broglio, Robert Cantu, David Cook, Uade Olaghere da Silva, Dara Dickstein, Gregory Elder, Elizabeth Fudge, Sam Gandy, Jessica Gill, John F Glenn, Raj K Gupta, Sidney Hinds, Stuart Hoffman, Theresa Lattimore, Alexander Lin, Kun Ping Lu, Joseph Maroon, David Okonkwo, Daniel Perl, Meghan Robinson, Charles Rosen, Douglas Smith
Blast-related traumatic brain injury (TBI) is a signature injury of recent military conflicts, leading to increased Department of Defense (DoD) interest in its potential long-term effects, such as chronic traumatic encephalopathy (CTE). The DoD Blast Injury Research Program Coordinating Office convened the 2015 International State-of-the-Science Meeting to discuss the existing evidence regarding a causal relationship between TBI and CTE. Over the course of the meeting, experts across government, academia, and the sports community presented cutting edge research on the unique pathological characteristics of blast-related TBI, blast-related neurodegenerative mechanisms, risk factors for CTE, potential biomarkers for CTE, and treatment strategies for chronic neurodegeneration...
September 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28937953/the-biological-basis-of-chronic-traumatic-encephalopathy-following-blast-injury-a-literature-review
#3
Matt Aldag, Regina C Armstrong, Faris Bandak, Patrick S F Bellgowan, Timothy Bentley, Sean Biggerstaff, Katrina Caravelli, Joan Cmarik, Alicia Crowder, Thomas J DeGraba, Travis A Dittmer, Richard G Ellenbogen, Colin Greene, Raj K Gupta, Ramona Hicks, Stuart Hoffman, Robert C Latta, Michael J Leggieri, Donald Marion, Robert Mazzoli, Michael McCrea, John O'Donnell, Mark Packer, James B Petro, Todd E Rasmussen, Wendy Sammons-Jackson, Richard Shoge, Victoria Tepe, Ladd A Tremaine, James Zheng
The United States Department of Defense Blast Injury Research Program Coordinating Office organized the 2015 International State-of-the-Science meeting to explore links between blast-related head injury and the development of chronic traumatic encephalopathy (CTE). Before the meeting, the planning committee examined articles published between 2005 and October 2015 and prepared this literature review, which summarized broadly CTE research and addressed questions about the pathophysiological basis of CTE and its relationship to blast- and nonblast-related head injury...
September 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28937952/modeling-the-long-term-consequences-of-repeated-blast-induced-mild-traumatic-brain-injuries
#4
Denes V Agoston
Repeated mild traumatic brain injury (rmTBI) caused by playing collision sports or by exposure to blasts during military operations can lead to late onset, chronic diseases such as chronic traumatic encephalopathy (CTE), a progressive neurodegenerative condition that manifests in increasingly severe neuropsychiatric abnormalities years after the last injury. Currently, because of the heterogeneity of the clinical presentation, confirmation of a CTE diagnosis requires post-mortem examination of the brain. The hallmarks of CTE are abnormal accumulation of phosphorylated tau protein, TDP-43 immunoreactive neuronal cytoplasmic inclusions, and astroglial abnormalities, but the pathomechanism leading to these terminal findings remains unknown...
September 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28936802/significance-of-mitochondrial-protein-post-translational-modifications-in-pathophysiology-of-brain-injury
#5
Nina Klimova, Aaron Long, Tibor Kristian
Mitochondria are complex organelles that undergo constant fusion and fission in order to adapt to the ever-changing cellular environment. The fusion/fission proteins, localized in the inner and outer mitochondrial membrane, play critical roles under pathological conditions such as acute brain injury and neurodegenerative diseases. Post-translational modifications of these proteins tightly regulate their function and activity, ultimately impacting mitochondrial dynamics and their efficiency to generate ATP. The individual post-translational modifications that are known to affect mitochondrial dynamics include SUMOylation, ubiquitination, phosphorylation, S-nitrosylation, acetylation, O-linked N-acetyl-glucosamine glycosylation, ADP-ribosylation, and proteolytic cleavage...
September 21, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28936769/nlrp3-inflammasome-activation-in-a-transgenic-amyotrophic-lateral-sclerosis-model
#6
Agnese Gugliandolo, Sabrina Giacoppo, Placido Bramanti, Emanuela Mazzon
Amyotrophic lateral sclerosis (ALS) is a disabling progressive disease characterized by the degeneration of motor neurons, leading to muscle atrophy and paralysis. The majority of cases are sporadic, but also a familiar form of ALS exists, and some genes causative of the pathology were found. In particular, mutations in superoxide dismutase 1 (SOD1) were found in 20% of familiar cases. It is known that neuroinflammation plays a pivotal role in several neurodegenerative disorders, including ALS. Inflammasomes are protein complexes that induce inflammation in response to various stimuli, involved also in neuroinflammation...
September 21, 2017: Inflammation
https://www.readbyqxmd.com/read/28935914/neurodegenerative-disease-dlk-zips-across-neurodegeneration
#7
M Teresa Villanueva
No abstract text is available yet for this article.
September 22, 2017: Nature Reviews. Drug Discovery
https://www.readbyqxmd.com/read/28935901/a-brain-targeting-lipidated-peptide-for-neutralizing-rna-mediated-toxicity-in-polyglutamine-diseases
#8
Qian Zhang, Mengbi Yang, Kasper K Sørensen, Charlotte S Madsen, Josephine T Boesen, Ying An, Shao Hong Peng, Yuming Wei, Qianwen Wang, Knud J Jensen, Zhong Zuo, Ho Yin Edwin Chan, Jacky Chi Ki Ngo
Polyglutamine (PolyQ) diseases are progressive neurodegenerative disorders caused by both protein- and RNA-mediated toxicities. We previously showed that a peptidyl inhibitor, P3, which binds directly to expanded CAG RNA can inhibit RNA-induced nucleolar stress and suppress RNA-induced neurotoxicity. Here we report a N-acetylated and C-amidated derivative of P3, P3V8, that showed a more than 20-fold increase in its affinity for expanded CAG RNA. The P3V8 peptide also more potently alleviated expanded RNA-induced cytotoxicity in vitro, and suppressed polyQ neurodegeneration in Drosophila with no observed toxic effects...
September 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28935818/increased-mir-124-3p-in-microglial-exosomes-following-traumatic-brain-injury-inhibits-neuronal-inflammation-and-contributes-to-neurite-outgrowth-via-their-transfer-into-neurons
#9
Shan Huang, Xintong Ge, Jinwen Yu, Zhaoli Han, Zhenyu Yin, Ying Li, Fanglian Chen, Haichen Wang, Jianning Zhang, Ping Lei
Neuronal inflammation is the characteristic pathologic change of acute neurologic impairment and chronic traumatic encephalopathy after traumatic brain injury (TBI). Inhibiting the excessive inflammatory response is essential for improving the neurologic outcome. To clarify the regulatory mechanism of microglial exosomes on neuronal inflammation in TBI, we focused on studying the impact of microglial exosomal miRNAs on injured neurons in this research. We used a repetitive (r)TBI mouse model and harvested the injured brain extracts from the acute to the chronic phase of TBI to treat cultured BV2 microglia in vitro The microglial exosomes were collected for miRNA microarray analysis, which showed that the expression level of miR-124-3p increased most apparently in the miRNAs...
September 21, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28935338/soft-tissue-surgery-for-adults-with-nonfunctional-spastic-hands-following-central-nervous-system-lesions-a-retrospective-study
#10
Laure Gatin, Alexis Schnitzler, Fabien Calé, Guillaume Genêt, Philippe Denormandie, François Genêt
PURPOSE: Soft tissue surgery for upper extremity contractures can improve hygiene, pain, and appearance in adults with central nervous system lesions. The goal of such interventions is highly individual; thus, goal attainment scaling (GAS; a method of scoring the extent to which patient's individual goals are achieved [5 levels] in the course of intervention and using T score values) is pertinent to evaluate outcome. The objective of this study was to assess the effect of soft tissue surgery for upper extremity muscle contractures in patients with central nervous system lesions using GAS...
September 19, 2017: Journal of Hand Surgery
https://www.readbyqxmd.com/read/28935191/circadian-rhythm-and-autonomic-dysfunction-in-presymptomatic-and-early-huntington-s-disease
#11
Elena Bellosta Diago, Jesús Pérez Pérez, Sonia Santos Lasaosa, Alejandro Viloria Alebesque, Saül Martínez Horta, Jaime Kulisevsky, Javier López Del Val
INTRODUCTION: Sleep and circadian rhythm disturbances are common in patients with neurodegenerative diseases such as Huntington's disease (HD). The aim of this study was to evaluate variability in circadian blood pressure (BP) to determine the association between abnormal circadian BP and sleep quality in patients with HD. METHODS: Cross-sectional, multicenter study of 38 HD mutation carriers (23 premanifest and 15 early stage patients) who were compared to 38 age- and sex-matched controls...
September 15, 2017: Parkinsonism & related Disorders
https://www.readbyqxmd.com/read/28934963/metabolic-status-of-csf-distinguishes-rats-with-tauopathy-from-controls
#12
Radana Karlíková, Kateřina Mičová, Lukáš Najdekr, Alžběta Gardlo, Tomáš Adam, Petra Majerová, David Friedecký, Andrej Kováč
BACKGROUND: Tauopathies represent heterogeneous groups of neurodegenerative diseases that are characterised by abnormal deposition of the microtubule-associated protein tau. Alzheimer's disease is the most prevalent tauopathy, affecting more than 35 million people worldwide. In this study we investigated changes in metabolic pathways associated with tau-induced neurodegeneration. METHODS: Cerebrospinal fluid (CSF), plasma and brain tissue were collected from a transgenic rat model for tauopathies and from age-matched control animals...
September 21, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28934429/gene-expression-analysis-reveals-genes-common-to-cerebral-malaria-and-neurodegenerative-disorders
#13
Sandrine Cabantous, Ogobara Doumbo, Belco Poudiougou, Laurence Louis, Abdoulaye Barry, Aboubacar A Oumar, Abdoualye Traore, Sandrine Marquet, Alain Dessein
Cerebral malaria, a reversible encephalopathy affecting young children, is a medical emergency requiring urgent clinical assessment and treatment. We performed a whole-transcriptomic analysis of blood samples from Malian children with cerebral or uncomplicated malaria. We focused on transcripts from pathways for which dysfunction has been associated with neurodegenerative disorders. We found that SNCA, SIAH2, UBB, HSPA1A, TUBB2A, and PINK1 were upregulated (fold-increases, ≥2.6), whereas UBD and PSMC5 were downregulated (fold-decreases, ≤4...
September 15, 2017: Journal of Infectious Diseases
https://www.readbyqxmd.com/read/28934397/a-modifier-of-huntington-s-disease-onset-at-the-mlh1-locus
#14
Jong-Min Lee, Michael J Chao, Denise Harold, Kawther Abu Elneel, Tammy Gillis, Peter Holmans, Lesley Jones, Michael Orth, Richard H Myers, Seung Kwak, Vanessa C Wheeler, Marcy E MacDonald, James F Gusella
Huntington's disease (HD) is a dominantly inherited neurodegenerative disease caused by an expanded CAG repeat in HTT. Many clinical characteristics of HD such as age at motor onset are determined largely by the size of HTT CAG repeat. However, emerging evidence strongly supports a role for other genetic factors in modifying the disease pathogenesis driven by mutant huntingtin. A recent genome-wide association analysis to discover genetic modifiers of HD onset age provided initial evidence for modifier loci on chromosomes 8 and 15 and suggestive evidence for a locus on chromosome 3...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28934392/nceh-1-modulates-cholesterol-metabolism-and-protects-against-%C3%AE-synuclein-toxicity-in-a-c-elegans-model-of-parkinson-s-disease
#15
Siyuan Zhang, Samantha A Glukhova, Kim A Caldwell, Guy A Caldwell
Parkinson's disease (PD) is an aging-associated neurodegenerative disease affecting millions worldwide. Misfolding, oligomerization and accumulation of the human α-synuclein protein is a key pathological hallmark of PD and is associated with the progressive loss of dopaminergic neurons over the course of aging. Lifespan extension via the suppression of IGF-1/insulin-like signaling (IIS) offers a possibility to retard disease onset through induction of metabolic changes that provide neuroprotection. The nceh-1 gene of Caenorhabditis elegans encodes an ortholog of neutral cholesterol ester hydrolase 1 (NCEH-1), an IIS downstream protein that was identified in a screen as a modulator of α-synuclein accumulation in vivo...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28934390/protein-phosphatase-1-regulates-huntingtin-exon-1-aggregation-and-toxicity
#16
Joana Branco-Santos, Federico Herrera, Gonçalo M Poças, Yolanda Pires-Afonso, Flaviano Giorgini, Pedro M Domingos, Tiago F Outeiro
Huntington's disease is neurodegenerative disorder caused by a polyglutamine expansion in the N-terminal region of the huntingtin protein (N17). Here, we analysed the relative contribution of each phosphorylatable residue in the N17 region (T3, S13 and S16) towards huntingtin exon 1 (HTTex1) oligomerization, aggregation and toxicity in human cells and Drosophila neurons. We used bimolecular fluorescence complementation to show that expression of single phosphomimic mutations completely abolished HTTex1 aggregation in human cells...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28934387/mutations-in-tgm6-induce-the-unfolded-protein-response-in-sca35
#17
Debasmita Tripathy, Beatrice Vignoli, Nandini Ramesh, Maria Jose Polanco, Marie Coutelier, Christopher D Stephen, Marco Canossa, Marie-Lorraine Monin, Pascale Aeschlimann, Shannon Turberville, Daniel Aeschlimann, Jeremy D Schmahmann, Marios Hadjivassiliou, Alexandra Durr, Udai B Pandey, Maria Pennuto, Manuela Basso
Spinocerebellar ataxia type 35 (SCA35) is a rare autosomal-dominant neurodegenerative disease caused by mutations in the TGM6 gene, which codes for transglutaminase 6 (TG6). Mutations in TG6 induce cerebellar degeneration by an unknown mechanism. We identified seven patients bearing new mutations in TGM6. To gain insights into the molecular basis of mutant TG6-induced neurotoxicity, we analyzed all the seven new TG6 mutants and the five TG6 mutants previously linked to SCA35. We found that the wild-type (TG6-WT) protein mainly localized to the nucleus and perinuclear area, whereas five TG6 mutations showed nuclear depletion, increased accumulation in the perinuclear area, insolubility and loss of enzymatic function...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28934112/biological-mechanisms-by-which-antiproliferative-actions-of-resveratrol-are-minimized
#18
REVIEW
Yih Ho, Yu-Syuan Lin, Hsuan-Liang Liu, Ya-Jung Shih, Shin-Ying Lin, Ai Shih, Yu-Tang Chin, Yi-Ru Chen, Hung-Yun Lin, Paul J Davis
Preclinical and clinical studies have offered evidence for protective effects of various polyphenol-rich foods against cardiovascular diseases, neurodegenerative diseases, and cancers. Resveratrol is among the most widely studied polyphenols. However, the preventive and treatment effectiveness of resveratrol in cancer remain controversial because of certain limitations in existing studies. For example, studies of the activity of resveratrol against cancer cell lines in vitro have often been conducted at concentrations in the low μM to mM range, whereas dietary resveratrol or resveratrol-containing wine rarely achieve nM concentrations in the clinic...
September 21, 2017: Nutrients
https://www.readbyqxmd.com/read/28933978/the-glycosidase-treatment-of-gentianae-scabrae-radix-converts-trifloroside-into-deglucosyltrifloroside-with-an-enhancement-of-antioxidative-effects
#19
Eun-Ju Yang, Ju-Gyeong Lee, Kyung-Sik Song
Herbal medicines were subjected to enzyme reaction by using a commercial glycosidase AMG-300L, and were evaluated for enhancement of their antioxidative activities. The methanolic extract of Gentianae Scabrae Radix (GSR) showed the most dramatic changes after enzyme reaction, as seen in the high-performance liquid chromatography profiles and an increase in the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging effect. Trifloroside (1, TF) was identified as being significantly decreased by enzyme reaction, whereas deglucosyltrifloroside (2, DTF) increased...
September 21, 2017: Journal of Medicinal Food
https://www.readbyqxmd.com/read/28933786/pink1-interacts-with-%C3%AE-synuclein-and-abrogates-%C3%AE-synuclein-induced-neurotoxicity-by-activating-autophagy
#20
Jia Liu, Xue Wang, Yongquan Lu, Chunli Duan, Ge Gao, Lingling Lu, Hui Yang
Parkinson's disease (PD) is one of the most common neurodegenerative diseases, characterized by degeneration of dopaminergic neurons in the substantia nigra. α-synuclein (α-syn) and PTEN-induced putative kinase (PINK)1 are two critical proteins associated with the pathogenesis of PD. α-syn induces mitochondrial deficits and apoptosis, PINK1 was found to alleviate α-syn-induced toxicity, but the mechanistic details remain obscure. Here, we show that PINK1 interacts with α-syn mainly in the cytoplasm, where it initiates autophagy...
September 21, 2017: Cell Death & Disease
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