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Alpha synuclein

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https://www.readbyqxmd.com/read/29341898/induction-of-alpha-synuclein-pathology-in-the-enteric-nervous-system-of-the-rat-and-non-human-primate-results-in-gastrointestinal-dysmotility-and-transient-cns-pathology
#1
Fredric P Manfredsson, Kelvin C Luk, Matthew J Benskey, Aysegul Guezer, Joanna Garcia, Nathan C Kuhn, Ivette M Sandoval, Joseph R Patterson, Alana O'Mara, Reid Yonkers, Jeffrey H Kordower
Alpha-Synuclein (α-syn) is by far the most highly vetted pathogenic and therapeutic target in Parkinson's disease. Aggregated α-syn is present in sporadic Parkinson's disease, both in the central nervous system (CNS) and peripheral nervous system (PNS). The enteric division of the PNS is of particular interest because 1) gastric dysfunction is a key clinical manifestation of Parkinson's disease, and 2) Lewy pathology in myenteric and submucosal neurons of the enteric nervous system (ENS) has been referred to as stage zero in the Braak pathological staging of Parkinson's disease...
January 13, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29325612/genetics-of-parkinson-disease
#2
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/29309590/parkinson-s-disease-linked-dnajc13-mutation-aggravates-alpha-synuclein-induced-neurotoxicity-through-perturbation-of-endosomal-trafficking
#3
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/29306403/serum-titers-of-autoantibodies-against-%C3%AE-synuclein-and-tau-in-child-and-adulthood
#4
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
#5
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
https://www.readbyqxmd.com/read/29305061/a-refined-concept-%C3%AE-synuclein-dysregulation-disease
#6
REVIEW
Hideki Mochizuki, Chi-Jing Choong, Eliezer Masliah
α-synuclein (αSyn) still remains a mysterious protein even two decades after SNCA encoding it was identified as the first causative gene of familial Parkinson's disease (PD). Accumulation of αSyn causes α-synucleinopathies including PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Recent advances in therapeutic approaches offer new antibody-, vaccine-, antisense-oligonucleotide- and small molecule-based options to reduce αSyn protein levels and aggregates in patient's brain. Gathering research information of other neurological disease particularly Alzheimer's disease, recent disappointment of an experimental amyloid plaques busting antibody in clinical trials underscores the difficulty of treating people who show even mild dementia as damage in their brain may already be too extensive...
January 2, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29300342/snca-is-a-functionally-low-expressed-gene-in-lung-adenocarcinoma
#7
Yuanliang Yan, Zhijie Xu, Xiaofang Hu, Long Qian, Zhi Li, Yangying Zhou, Shuang Dai, Shuangshuang Zeng, Zhicheng Gong
There is increasing evidence for the contribution of synuclein alpha (SNCA) to the etiology of neurological disorders, such as Parkinson's disease (PD). However, little is known about the detailed role of SNCA in human cancers, especially lung cancers. Here, we evaluated the effects of SNCA on the occurrence and prognosis of lung adenocarcinoma (ADC). Comprehensive bioinformatics analyses of data obtained from the Oncomine platform, the human protein atlas (HPA) project and the cancer cell line encyclopedia (CCLE) demonstrated that SNCA expression was significantly reduced in both ADC tissues and cancer cells...
January 4, 2018: Genes
https://www.readbyqxmd.com/read/29297728/chronic-fatigue-and-immune-deficiency-syndrome-cfids-cellular-metabolism-and-ionizing-radiation-a-review-of-contemporary-scientific-literature-and-suggested-directions-for-future-research
#8
Andrej Rusin, Colin Seymour, Carmel Mothersill
PURPOSE: To investigate biochemical pathways known to be involved in radiation response and in CFIDS to determine if there might be common underlying mechanisms leading to symptoms experienced by those accidentally or deliberately exposed to radiation and those suffering from CFIDS. If such a link were established, to suggest testable hypotheses to investigate the mechanisms with the aim of identifying new therapeutic targets. CONCLUSIONS: Evidence for involvement of the alpha-synuclein, cytochrome c oxidiase, αB-crystallin, RNase L, and lactate dehydrogenase/STAT1 pathways is strong and suggests a common underlying mechanism involving mitochondrial dysfunction mediated by ROS and disruption of ATP production...
January 3, 2018: International Journal of Radiation Biology
https://www.readbyqxmd.com/read/29295991/network-connectivity-determines-cortical-thinning-in-early-parkinson-s-disease-progression
#9
Y Yau, Y Zeighami, T E Baker, K Larcher, U Vainik, M Dadar, V S Fonov, P Hagmann, A Griffa, B Mišić, D L Collins, A Dagher
Here we test the hypothesis that the neurodegenerative process in Parkinson's disease (PD) moves stereotypically along neural networks, possibly reflecting the spread of toxic alpha-synuclein molecules. PD patients (n = 105) and matched controls (n = 57) underwent T1-MRI at entry and 1 year later as part of the Parkinson's Progression Markers Initiative. Over this period, PD patients demonstrate significantly greater cortical thinning than controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex...
January 2, 2018: Nature Communications
https://www.readbyqxmd.com/read/29289693/manganese-induced-alpha-synuclein-overexpression-impairs-synaptic-vesicle-fusion-by-disrupting-the-rab3-cycle-in-primary-cultured-neurons
#10
Tong-Yu Wang, Zhuo Ma, Can Wang, Chang Liu, Dong-Ying Yan, Yu Deng, Wei Liu, Zhao-Fa Xu, Bin Xu
Overexposure to Manganese (Mn) has been known to disrupt neurotransmitter release in the brain. However, the underlying mechanisms of Mn exposure on neurotransmitter vesicle release are still unclear. The current study investigated whether Mn-induced alpha-synuclein protein overexpression could disrupt the Rab3 cycle leading to synaptic vesicle fusion dysfunction. After the neurons were exposed to Mn (100 μM) for 0, 6, 12, 24 h, [Ca2+]i, alpha-synuclein and Rab3A-GTP protein expression increased gradually...
December 28, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/29278715/accumulation-of-beta-synuclein-in-cortical-neurons-is-associated-with-autophagy-attenuation-in-the-brains-of-dementia-with-lewy-body-patients
#11
Tracey Evans, Wai Ling Kok, Katrina Cowan, Megan Hefford, Oleg Anichtchik
Dementia with Lewy bodies (DLB) is the second most prevalent neurodegenerative dementia, where an accumulation of aggregated fibrillar alpha-synuclein in neurons of limbic and forebrain regions of the brain leads to visual hallucination, cognitive impairment of a fluctuating nature and extrapyramidal motor disturbances. Beta-synuclein counteracts aggregation of alpha-synuclein in vitro and in animal models, however it is not clear whether this effect occurs in human Lewy body dementia (LBD) diseases. Here we examine expression of alpha-, beta-synuclein and autophagy markers in the frontal cortex (BA9) and occipital cortex (BA18-19) of patients with neuropathologically confirmed DLB/LBD and age-matched controls...
December 23, 2017: Brain Research
https://www.readbyqxmd.com/read/29276384/investigation-of-the-effects-of-carbon-based-nanomaterials-on-a53t-alpha-synuclein-aggregation-using-a-whole-cell-recombinant-biosensor
#12
Soheila Mohammadi, Maryam Nikkhah, Saman Hosseinkhani
The aggregation of alpha-synuclein (αS), natively unstructured presynaptic protein, is a crucial factor leading to the pathogenesis of Parkinson's disease (PD) and other related disorders. Recent studies have shown prefibrillar and oligomeric intermediates of αS as toxic to the cells. Herein, split-luciferase complementation assay is used to design a "signal-on" biosensor to monitor oligomerization of A53T αS inside the cells. Then, the effect of carbon-based nanomaterials, such as graphene quantum dots (GQDs) and graphene oxide quantum dots (GOQDs), on A53T αS oligomerization in vitro and in living cells is investigated...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/29248340/role-of-lrrk2-and-snca-in-autosomal-dominant-parkinson-s-disease-in-turkey
#13
Christoph Kessler, Burcu Atasu, Hasmet Hanagasi, Javier Simón-Sánchez, Ann-Kathrin Hauser, Meltem Pak, Basar Bilgic, Nihan Erginel-Unaltuna, Hakan Gurvit, Thomas Gasser, Ebba Lohmann
INTRODUCTION: Mutations in the LRRK2 and alpha-synuclein (SNCA) genes are well-established causes of autosomal dominant Parkinson's disease (PD). However, their frequency differs widely between ethnic groups. Only three studies have screened all coding regions of LRRK2 and SNCA in European samples so far. In Turkey, the role of LRRK2 in Parkinson's disease has been studied fragmentarily, and the incidence of SNCA copy number variations is unknown. The purpose of this study is to determine the frequency of LRRK2 and SNCA mutations in autosomal dominant PD in Turkey...
December 9, 2017: Parkinsonism & related Disorders
https://www.readbyqxmd.com/read/29246724/toxic-properties-of-microsome-associated-alpha-synuclein-species-in-mouse-primary-neurons
#14
Emanuela Colla, Giulia Panattoni, Alessio Ricci, Caterina Rizzi, Lucia Rota, Nicola Carucci, Verdiana Valvano, Francesco Gobbo, Simona Capsoni, Michael K Lee, Antonino Cattaneo
α-synuclein (αS) is a small protein that self-aggregates into α-helical oligomer species and subsequently into larger insoluble amyloid fibrils that accumulate in intraneuronal inclusions during the development of Parkinson's disease. Toxicity of αS oligomers and fibrils has been long debated and more recent data are suggesting that both species can induce neurodegeneration. However while most of these data are based on differences in structure between oligomer and aggregates, often preassembled in vitro, the in vivo situation might be more complex and subcellular locations where αS species accumulate, rather than their conformation, might contribute to enhanced toxicity...
December 12, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29236052/micrornas-in-parkinson-s-disease-from-pathogenesis-to-novel-diagnostic-and-therapeutic-approaches
#15
REVIEW
Loredana Leggio, Silvia Vivarelli, Francesca L'Episcopo, Cataldo Tirolo, Salvo Caniglia, Nunzio Testa, Bianca Marchetti, Nunzio Iraci
Parkinson's disease (PD) is the most prevalent central nervous system (CNS) movement disorder and the second most common neurodegenerative disease overall. PD is characterized by the progressive loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc) within the midbrain, accumulation of alpha-synuclein (α-SYN) in Lewy bodies and neurites and excessive neuroinflammation. The neurodegenerative processes typically begin decades before the appearance of clinical symptoms. Therefore, the diagnosis is achievable only when the majority of the relevant DAergic neurons have already died and for that reason available treatments are only palliative at best...
December 13, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29233723/the-different-faces-of-the-p-a53t-alpha-synuclein-mutation-a-screening-of-greek-patients-with-parkinsonism-and-or-dementia
#16
Marianthi Breza, Georgios Koutsis, Georgia Karadima, Constantin Potagas, Chrisoula Kartanou, Sokratis G Papageorgiou, George P Paraskevas, Elisabeth Kapaki, Leonidas Stefanis, Marios Panas
BACKGROUND: The p. A53T mutation in the alpha-synuclein (SNCA) gene is a rare cause of autosomal dominant Parkinson's disease (PD). Although generally rare, it is particularly common in the Greek population due to a founder effect. A53T-positive PD patients often develop dementia during disease course and may very rarely present with dementia. METHODS: We screened for the p. A53T SNCA mutation a total of 347 cases of Greek origin with parkinsonism and/or dementia, collected over 15 years at the Neurogenetics Unit, Eginition Hospital, University of Athens...
December 9, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/29228971/alpha-synuclein-oligomer-selective-antibodies-reduce-intracellular-accumulation-and-mitochondrial-impairment-in-alpha-synuclein-exposed-astrocytes
#17
Gabriel Gustafsson, Veronica Lindström, Jinar Rostami, Eva Nordström, Lars Lannfelt, Joakim Bergström, Martin Ingelsson, Anna Erlandsson
BACKGROUND: Due to its neurotoxic properties, oligomeric alpha-synuclein (α-syn) has been suggested as an attractive target for passive immunization against Parkinson's disease (PD). In mouse models of PD, antibody treatment has been shown to lower the levels of pathogenic α-syn species, including oligomers, although the mechanisms of action remain unknown. We have previously shown that astrocytes rapidly engulf α-syn oligomers that are intracellularly stored, rather than degraded, resulting in impaired mitochondria...
December 11, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29227247/stress-induced-cdk5-activity-enhances-cytoprotective-basal-autophagy-in-drosophila-melanogaster-by-phosphorylating-acinus-at-serine437
#18
Nilay Nandi, Lauren K Tyra, Drew Stenesen, Helmut Krämer
Cdk5 is a post-mitotic kinase with complex roles in maintaining neuronal health. The various mechanisms by which Cdk5 inhibits and promotes neurodegeneration are still poorly understood. Here, we show that in Drosophila melanogaster Cdk5 regulates basal autophagy, a key mechanism suppressing neurodegeneration. In a targeted screen, Cdk5 genetically interacted with Acinus (Acn), a primarily nuclear protein, which promotes starvation-independent, basal autophagy. Loss of Cdk5, or its required cofactor p35, reduces S437-Acn phosphorylation, whereas Cdk5 gain-of-function increases pS437-Acn levels...
December 11, 2017: ELife
https://www.readbyqxmd.com/read/29225795/multiple-system-atrophy-genetic-risks-and-alpha-synuclein-mutations
#19
REVIEW
Heather T Whittaker, Yichen Qui, Conceição Bettencourt, Henry Houlden
Multiple system atrophy (MSA) is one of the few neurodegenerative disorders where we have a significant understanding of the clinical and pathological manifestations but where the aetiology remains almost completely unknown. Research to overcome this hurdle is gaining momentum through international research collaboration and a series of genetic and molecular discoveries in the last few years, which have advanced our knowledge of this rare synucleinopathy. In MSA, the discovery of α-synuclein pathology and glial cytoplasmic inclusions remain the most significant findings...
2017: F1000Research
https://www.readbyqxmd.com/read/29218419/an-unexpected-improvement-in-spatial-learning-and-memory-ability-in-alpha-synuclein-a53t-transgenic-mice
#20
Qi Liu, YuYu Xu, WenPing Wan, ZeGang Ma
Growing evidence suggests, as Parkinson's disease (PD) progresses, that its non-motor symptoms appear prior to or in parallel with its motor deficits. Alpha-synuclein A53T transgenic mouse (A53T) is an essential tool to investigate the onsets and the extents of PD non-motor symptoms. Our aim is to investigate spatial learning and memory ability in A53T mice. In our rotarod tests, no motor coordination impairments were detected in mice of 3, 6, 9, and 12 months old. We then investigated their spatial learning and memory ability through Morris water maze in 3- and 9-month-old mice...
December 7, 2017: Journal of Neural Transmission
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