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https://www.readbyqxmd.com/read/29330884/synapsin-iii-is-a-key-component-of-%C3%AE-synuclein-fibrils-in-lewy-bodies-of-pd-brains
#1
Francesca Longhena, Gaia Faustini, Tatiana Varanita, Michela Zaltieri, Vanessa Porrini, Isabella Tessari, Pietro Luigi Poliani, Cristina Missale, Barbara Borroni, Alessandro Padovani, Luigi Bubacco, Marina Pizzi, PierFranco Spano, Arianna Bellucci
Lewy bodies (LB) and Lewy neurites (LN), which are primarily composed of α-synuclein (α-syn), are neuropathological hallmarks of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). We recently found that the neuronal phosphoprotein synapsin III (syn III) controls dopamine release via cooperation with α-syn and modulates α-syn aggregation. Here, we observed that LB and LN, in the substantia nigra of PD patients and hippocampus of one subject with DLB, displayed a marked immunopositivity for syn III...
January 13, 2018: Brain Pathology
https://www.readbyqxmd.com/read/29330047/an-intrinsically-disordered-domain-in-polaribacter-irgensii-kopri-22228-cspb-confers-extraordinary-freeze-tolerance
#2
Youn Hong Jung, Ji-Hyun Uh, Kyunghee Lee, Hana Im
Organisms living in extremely cold environments possess mechanisms to survive low temperatures. Among the known cold-induced genes, cold-shock proteins (Csps) are the most prominent. A csp-homologous gene, cspBPi, has been cloned from the Arctic bacterium Polaribacter irgensii KOPRI 22228, and overexpression of this gene greatly increased the freezing tolerance of its host. This protein consists of a unique N-terminal domain and a well conserved C-terminal cold shock domain. To elucidate the detailed mechanisms involved in the extraordinary freeze-tolerance conferred by CspBPi, we identified the responsible domain by mutational analysis...
January 9, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29327204/neuroprotective-effects-of-filgrastim-in-rotenone-induced-parkinson-s-disease-in-rats-insights-into-its-anti-inflammatory-neurotrophic-and-antiapoptotic-effects
#3
Mariama S Azmy, Esther T Menze, Reem N El-Naga, Mariane G Tadros
All current treatments of Parkinson's disease (PD) focus on enhancing the dopaminergic effects and providing symptomatic relief; however, they cannot delay the disease progression. Filgrastim, a recombinant methionyl granulocyte colony-stimulating factor, demonstrated neuroprotection in many neurodegenerative and neurological diseases. This study aimed to assess the neuroprotective effects of filgrastim in rotenone-induced rat model of PD and investigate the potential underlying mechanisms of filgrastim actions...
January 11, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29325612/genetics-of-parkinson-disease
#4
Aloysius Domingo, Christine Klein
An understanding of the genetic etiology of Parkinson disease (PD) has become imperative for the modern-day neurologist. Although genetic forms cause only a minority of PD, the disease mechanisms they elucidate advance the understanding of idiopathic cases. Moreover, recently identified susceptibility variants contribute to complex-etiology PD and broaden the contribution of genetics beyond familial and early-onset cases. Dominantly inherited monogenic forms mimic idiopathic PD and are caused by mutations or copy number variations of SNCA, LRRK2, and VPS35...
2018: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/29322595/identification-of-new-%C3%AE-synuclein-regulator-by-nontraditional-drug-development-pipeline
#5
Xi Chen, Sonja W Scholz
No abstract text is available yet for this article.
January 11, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29321620/lack-of-pink1-alters-glia-innate-immune-responses-and-enhances-inflammation-induced-nitric-oxide-mediated-neuron-death
#6
Liuke Sun, Ruifang Shen, Sandeep K Agnihotri, Yun Chen, Zhiwei Huang, Hansruedi Büeler
Neuroinflammation is involved in the pathogenesis of Parkinson's disease (PD) and other neurodegenerative disorders. We show that lack of PINK1- a mitochondrial kinase linked to recessive familial PD - leads to glia type-specific abnormalities of innate immunity. PINK1 loss enhances LPS/IFN-γ stimulated pro-inflammatory phenotypes of mixed astrocytes/microglia (increased iNOS, nitric oxide and COX-2, reduced IL-10) and pure astrocytes (increased iNOS, nitric oxide, TNF-α and IL-1β), while attenuating expression of both pro-inflammatory (TNF-α, IL-1β) and anti-inflammatory (IL-10) cytokines in microglia...
January 10, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29320696/using-a-fret-library-with-multiple-probe-pairs-to%C3%A2-drive-monte-carlo-simulations-of-%C3%AE-synuclein
#7
John J Ferrie, Conor M Haney, Jimin Yoon, Buyan Pan, Yi-Chih Lin, Zahra Fakhraai, Elizabeth Rhoades, Abhinav Nath, E James Petersson
We describe a strategy for experimentally-constraining computational simulations of intrinsically disordered proteins (IDPs), using α-synuclein, an IDP with a central role in Parkinson's disease pathology, as an example. Previously, data from single-molecule Förster Resonance Energy Transfer (FRET) experiments have been effectively utilized to generate experimentally constrained computational models of IDPs. However, the fluorophores required for single-molecule FRET experiments are not amenable to the study of short-range (<30 Å) interactions...
January 9, 2018: Biophysical Journal
https://www.readbyqxmd.com/read/29317336/astroglial-and-microglial-contributions-to-iron-metabolism-disturbance-in-parkinson-s-disease
#8
REVIEW
Ning Song, Jun Wang, Hong Jiang, Junxia Xie
Understandings of the disturbed iron metabolism in Parkinson's disease (PD) are largely from the perspectives of neurons. Neurodegenerative processes in PD trigger universal and conserved astroglial dysfunction and microglial activation. In this review, we start with astroglia and microglia in PD with an emphasis on their roles in spreading α-synuclein pathology, and then focus on their contributions in iron metabolism under normal conditions and the diseased state of PD. Elevated iron in the brain regions affects glial features, meanwhile, glial effects on neuronal iron metabolism are largely dependent on their releasing factors...
January 6, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29316776/phagocytic-roles-of-glial-cells-in-healthy-and-diseased-brains
#9
REVIEW
Yeon-Joo Jung, Won-Suk Chung
Glial cells are receiving much attention since they have been recognized as important regulators of many aspects of brain function and disease. Recent evidence has revealed that two different glial cells, astrocytes and microglia, control synapse elimination under normal and pathological conditions via phagocytosis. Astrocytes use the MEGF10 and MERTK phagocytic pathways, and microglia use the classical complement pathway to recognize and eliminate unwanted synapses. Notably, glial phagocytosis also contributes to the clearance of disease-specific protein aggregates, such as β-amyloid, huntingtin, and α-synuclein...
January 10, 2018: Biomolecules & Therapeutics
https://www.readbyqxmd.com/read/29315801/the-emerging-role-of-rab-gtpases-in-the-pathogenesis-of-parkinson-s-disease
#10
REVIEW
Yujing Gao, Gabrielle R Wilson, Sarah E M Stephenson, Kiymet Bozaoglu, Matthew J Farrer, Paul J Lockhart
The identification of pathogenic mutations in Ras analog in brain 39B (RAB39B) and Ras analog in brain 32 (RAB32) that cause Parkinson's disease (PD) has highlighted the emerging role of protein trafficking in disease pathogenesis. Ras analog in brain (Rab) Guanosine triphosphatase (GTPase) function as master regulators of membrane trafficking, including vesicle formation, movement along cytoskeletal networks, and membrane fusion. Recent studies have linked Rab GTPases with α-synuclein, Leucine-rich repeat kinase 2, and Vacuolar protein sorting 35, 3 key proteins in PD pathogenesis...
January 9, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29313531/fluorescence-spectroscopy-reveals-n-terminal-order-in-fibrillar-forms-of-%C3%AE-synuclein
#11
Conor M Haney, E James Petersson
The neuronal protein α-synuclein (αS) plays a key role in Parkinson's disease, forming inclusions termed Lewy bodies and Lewy neurites. Recent improvements in cryo-electron diffraction and solid state NMR (ssNMR) have led to the elucidation of the structures of peptides derived from the αS fibril core and full-length human αS in fibrils. Despite the valuable insight offered by these methods, there are still several questions about the structures' relevance to pathological aggregates. Herein, we present fluorescence data collected in vitro under the conditions which fibrils are typically assembled...
January 9, 2018: Chemical Communications: Chem Comm
https://www.readbyqxmd.com/read/29313342/a-microfluidic-diffusion-platform-for-characterizing-the-size-of-lipid-vesicles-and-the-thermodynamics-of-protein-lipid-interactions
#12
Hongze Gang, Celine Galvagnion, Georg Meisl, Thomas Müller, Alexander K Buell, Aviad Levin, Christopher M Dobson, Bo-Zhong Mu, Tuomas P J Knowles
Elucidation of the fundamental interactions of proteins with biological membranes under native conditions is crucial for understanding the molecular basis of their biological function and malfunction. Notably, the large surface to volume ratio of living cells provides a molecular landscape for significant interactions of cellular components with membranes modulating their function. However, such interactions can be challenging to probe using conventional biophysical methods due to the heterogeneity of the species and processes involved...
January 9, 2018: Analytical Chemistry
https://www.readbyqxmd.com/read/29311479/transcriptome-analysis-reveals-that-midnolin-regulates-mrna-expression-levels-of-multiple-parkinson-s-disease-causative-genes
#13
Yutaro Obara, Kuniaki Ishii
We recently found that 10.5% of sporadic Parkinson's disease (PD) patients lacked one copy of the midnolin (MIDN) gene. In addition, gene knock-down/out of MIDN caused down-regulation of parkin E3 ubiquitin ligase, indicating MIDN to be a novel PD-risk factor or causative gene. In this study, we performed RNA-sequencing and transcriptome analysis of Midn wild-type and knockout cells. Midn positively or negatively regulated the expression of a wide variety of genes, including causative familial PD genes, such as α-synuclein, parkin, and EIF4G1...
2018: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/29311330/gba1-deficiency-negatively-affects-physiological-%C3%AE-synuclein-tetramers-and-related-multimers
#14
Sangjune Kim, Seung Pil Yun, Saebom Lee, George Essien Umanah, Veera Venkata Ratnam Bandaru, Xiling Yin, Peter Rhee, Senthilkumar S Karuppagounder, Seung-Hwan Kwon, Hojae Lee, Xiaobo Mao, Donghoon Kim, Akhilesh Pandey, Gabsang Lee, Valina L Dawson, Ted M Dawson, Han Seok Ko
Accumulating evidence suggests that α-synuclein (α-syn) occurs physiologically as a helically folded tetramer that resists aggregation. However, the mechanisms underlying the regulation of formation of α-syn tetramers are still mostly unknown. Cellular membrane lipids are thought to play an important role in the regulation of α-syn tetramer formation. Since glucocerebrosidase 1 (GBA1) deficiency contributes to the aggregation of α-syn and leads to changes in neuronal glycosphingolipids (GSLs) including gangliosides, we hypothesized that GBA1 deficiency may affect the formation of α-syn tetramers...
January 8, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29310663/%C3%AE-synuclein-accumulation-and-gba-deficiency-due-to-l444p-gba-mutation-contributes-to-mptp-induced-parkinsonism
#15
Seung Pil Yun, Donghoon Kim, Sangjune Kim, SangMin Kim, Senthilkumar S Karuppagounder, Seung-Hwan Kwon, Saebom Lee, Tae-In Kam, Suhyun Lee, Sangwoo Ham, Jae Hong Park, Valina L Dawson, Ted M Dawson, Yunjong Lee, Han Seok Ko
BACKGROUND: Mutations in glucocerebrosidase (GBA) cause Gaucher disease (GD) and increase the risk of developing Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). Since both genetic and environmental factors contribute to the pathogenesis of sporadic PD, we investigated the susceptibility of nigrostriatal dopamine (DA) neurons in L444P GBA heterozygous knock-in (GBA +/L444P ) mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective dopaminergic mitochondrial neurotoxin...
January 8, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29309590/parkinson-s-disease-linked-dnajc13-mutation-aggravates-alpha-synuclein-induced-neurotoxicity-through-perturbation-of-endosomal-trafficking
#16
Shun Yoshida, Takafumi Hasegawa, Mari Suzuki, Naoto Sugeno, Junpei Kobayashi, Morio Ueyama, Mitsunori Fukuda, Akemi Ido-Fujibayashi, Kiyotoshi Sekiguchi, Michinori Ezura, Akio Kikuchi, Toru Baba, Atsushi Takeda, Hideki Mochizuki, Yoshitaka Nagai, Masashi Aoki
Mutations in DNAJC13 gene have been linked to familial form of Parkinson's disease (PD) with Lewy pathology. DNAJC13 is an endosome-related protein and believed to regulate endosomal membrane trafficking. However, the mechanistic link between DNAJC13 mutation and α-synuclein (αSYN) pathology toward neurodegeneration remains poorly understood. In this study, we showed that PD-linked N855S mutant DNAJC13 caused αSYN accumulation in the endosomal compartment, presumably due to defective cargo trafficking from the early endosome to the late and/or recycling endosome...
January 3, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29308725/the-role-of-the-prion-protein-in-the-internalization-of-%C3%AE-synuclein-amyloids
#17
Elena De Cecco, Giuseppe Legname
Synucleinopathies are a group of neurodegenerative diseases characterized by the accumulation of α-synuclein amyloids in several regions of the brain. α-Synuclein fibrils are able to spread via cell-to-cell transfer, and once inside the cells, they can template the misfolding and aggregation of the endogenous α-synuclein. Multiple mechanisms have been shown to participate in the process of propagation: endocytosis, tunneling nanotubes and micropinocytosis. Recently, we published a research showing that the cellular form of the prion protein (PrPC) acts as a receptor for α-synuclein amyloid fibrils, facilitating their internalization through and endocytic pathway...
January 8, 2018: Prion
https://www.readbyqxmd.com/read/29307058/serum-mortalin-correlated-with-%C3%AE-synuclein-as-serum-markers-in-parkinson-s-disease-a-pilot-study
#18
Amrendra Pratap Singh, Teena Bajaj, Divya Gupta, Sundararajan Baskar Singh, Avinash Chakrawarty, Vinay Goyal, Aparajit B Dey, Sharmistha Dey
Mortalin, a mitochondrial chaperone, plays a crucial role in reducing toxicity of Lewy bodies. Earlier studies had reported that Mortalin level gets downregulated in astrocytes and other brain tissue samples in Parkinson's disease (PD). This study aims to estimate the Mortalin concentration in serum and correlate with α-synuclein (α-Syn) in PD. The concentration of Mortalin and α-Syn in serum samples of 38 PD patients and 33 control group (CG) individuals was quantified by surface plasmon resonance. The receiver operating characteristic curves were plotted to develop it as blood-based protein marker...
January 6, 2018: Neuromolecular Medicine
https://www.readbyqxmd.com/read/29306403/serum-titers-of-autoantibodies-against-%C3%AE-synuclein-and-tau-in-child-and-adulthood
#19
Isabell Kuhn, Tobias Rogosch, Theresa I Schindler, Björn Tackenberg, Michael Zemlin, Rolf F Maier, Richard Dodel, Yannick Kronimus
Autoreactive antibodies against the proteins alpha-synuclein (α-syn) and tau are detectable in body fluids of both healthy and diseased elderly people. However, nothing is known about their presence or titers in children. To close this gap and to characterize their temporary expression levels, we used ELISA techniques to investigate the serum titers of α-syn and tau reactive autoantibodies in 37 and 32 adults and 37 and 31 children, respectively. Most serum samples from the children exhibited both antibody types and interestingly, the levels were similar to those observed in the adult serum samples...
February 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29305919/pathological-role-of-lipid-interaction-with-%C3%AE-synuclein-in-parkinson-s-disease
#20
REVIEW
Mari Suzuki, Kazunori Sango, Keiji Wada, Yoshitaka Nagai
Alpha-synuclein (αSyn) plays a central role in the pathogenesis of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In sporadic PD and DLB, normally harmless αSyn proteins without any mutations might gain toxic functions by unknown mechanisms. Thus, it is important to elucidate the factors promoting the toxic conversion of αSyn, towards understanding the pathogenesis of and developing disease-modifying therapies for PD and DLB. Accumulating biophysical and biochemical studies have demonstrated that αSyn interacts with lipid membrane, and the interaction influences αSyn oligomerization and aggregation...
January 3, 2018: Neurochemistry International
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