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https://www.readbyqxmd.com/read/29027056/curcumin-affords-neuroprotection-and-inhibits-%C3%AE-synuclein-aggregation-in-lipopolysaccharide-induced-parkinson-s-disease-model
#1
Neha Sharma, Bimla Nehru
Parkinson's disease (PD) pathology is characterized by the abnormal accumulation and aggregation of the pre-synaptic protein α-synuclein in the dopaminergic neurons as Lewy bodies (LBs). Curcumin, which plays a neuroprotective role in various animal models of PD, was found to directly modulate the aggregation of α-synuclein in in vitro as well as in in vivo studies. While curcumin has been shown to exhibit strong anti-oxidant and anti-inflammatory properties, there are a number of other possible mechanisms by which curcumin may alter α-synuclein aggregation which still remains obscure...
October 12, 2017: Inflammopharmacology
https://www.readbyqxmd.com/read/28759332/the-cellular-prion-protein-prp-c-as-neuronal-receptor-for-%C3%AE-synuclein
#2
Laura Urrea, Isidro Ferrer, Rosalina Gavín, José Antonio Del Río
The term 'prion-like' is used to define some misfolded protein species that propagate intercellularly, triggering protein aggregation in recipient cells. For cell binding, both direct plasma membrane interaction and membrane receptors have been described for particular amyloids. In this respect, emerging evidence demonstrates that several β-sheet enriched proteins can bind to the cellular prion protein (PrP(C)). Among other interactions, the physiological relevance of the binding between β-amyloid and PrP(C) has been a relevant focus of numerous studies...
July 4, 2017: Prion
https://www.readbyqxmd.com/read/28350199/a-novel-autophagy-modulator-6-bio-ameliorates-snca-%C3%AE-synuclein-toxicity
#3
S N Suresh, Aravinda K Chavalmane, Vidyadhara Dj, Haorei Yarreiphang, Shashank Rai, Abhik Paul, James P Clement, Phalguni Anand Alladi, Ravi Manjithaya
Parkinson disease (PD) is a life-threatening neurodegenerative movement disorder with unmet therapeutic intervention. We have identified a small molecule autophagy modulator, 6-Bio that shows clearance of toxic SNCA/α-synuclein (a protein implicated in synucleopathies) aggregates in yeast and mammalian cell lines. 6-Bio induces autophagy and dramatically enhances autolysosome formation resulting in SNCA degradation. Importantly, neuroprotective function of 6-Bio as envisaged by immunohistology and behavior analyses in a preclinical model of PD where it induces autophagy in dopaminergic (DAergic) neurons of mice midbrain to clear toxic protein aggregates suggesting that it could be a potential therapeutic candidate for protein conformational disorders...
July 3, 2017: Autophagy
https://www.readbyqxmd.com/read/28088342/nanoparticle-standards-for-immuno-based-quantitation-of-%C3%AE-synuclein-oligomers-in-diagnostics-of-parkinson-s-disease-and-other-synucleinopathies
#4
Yvonne Herrmann, Tuyen Bujnicki, Christian Zafiu, Andreas Kulawik, Katja Kühbach, Luriano Peters, Judith Fabig, Johannes Willbold, Oliver Bannach, Dieter Willbold
Parkinson's disease (PD) is a neurodegenerative disorder that is characterized by symptoms such as rigor, tremor and bradykinesia. A reliable and early diagnosis could improve the development of early therapeutic strategies before death of dopaminergic neurons leads to the first clinical symptoms. The sFIDA (surface-based fluorescence intensity distribution analysis) assay is a highly sensitive method to determine the concentration of α-synuclein (α-syn) oligomers which are presumably the major toxic isoform of α-syn and potentially the most direct biomarker for PD...
March 2017: Clinica Chimica Acta; International Journal of Clinical Chemistry
https://www.readbyqxmd.com/read/27334945/non-amyloid-pet-imaging-biomarkers-for-neurodegeneration-focus-on-tau-alpha-synuclein-and-neuroinflammation
#5
REVIEW
Ana M Catafau, Santiago Bullich
Clinical classifications of neurodegenerative disorders are often based on neuropathology. The term "proteinopathies" includes disorders that have in common abnormal proteins as a hallmark, e.g. amyloidoses, tauopathies, synucleopathies, ubiquitinopathies. Different proteins can also co-exist in the same disease. To further complicate the pathophysiology scenario, not only different proteins, but also cells are believed to play an active role in neurodegeneration, in particular those participating in neuroinflammatory processes in the brain, such as activated microglia and astrocytes...
2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/26931439/the-novel-isotopically-coded-short-range-photo-reactive-crosslinker-2-4-6-triazido-1-3-5-triazine-tata-for-studying-protein-structures
#6
Nicholas I Brodie, Evgeniy V Petrotchenko, Christoph H Borchers
Short-distance molecular-modeling constraints are advantageous for elucidating the structures of individual proteins and protein conformational changes. Commonly used amine-reactive crosslinks are relatively long (14Å), partly due to the length of the lysine side-chain, and are sparsely distributed throughout a protein. Short-distance non-specific crosslinkers can provide a larger number of tighter molecular-modeling constraints. Here we describe the use of a short-range homo-trifunctional isotopically-coded non-specific photo-reactive crosslinking reagent, 2,4,6-triazido-1,3,5-triazine (TATA)-(12)C3/(13)C3, for MS-based protein crosslinking studies...
February 27, 2016: Journal of Proteomics
https://www.readbyqxmd.com/read/26813776/autophagy-and-alpha-synuclein-relevance-to-parkinson-s-disease-and-related-synucleopathies
#7
REVIEW
Maria Xilouri, Oeystein Roed Brekk, Leonidas Stefanis
Evidence from human postmortem material, transgenic mice, and cellular/animal models of PD link alpha-synuclein accumulation to alterations in the autophagy lysosomal pathway. Conversely, alpha-synuclein mutations related to PD pathogenesis, as well as post-translational modifications of the wild-type protein, result in the generation of aberrant species that may impair further the function of the autophagy lysosomal pathway, thus generating a vicious cycle leading to neuronal death. Moreover, PD-linked mutations in lysosomal-related genes, such as glucocerebrosidase, have been also shown to contribute to alpha-synuclein accumulation and related toxicity, indicating that lysosomal dysfunction may, in part, account for the neurodegeneration observed in synucleinopathies...
February 2016: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/26068223/detection-of-disease-associated-%C3%AE-synuclein-by-enhanced-elisa-in-the-brain-of-transgenic-mice-overexpressing-human-a53t-mutated-%C3%AE-synuclein
#8
Dominique Bétemps, Jérémy Verchère, Anne-Laure Mougenot, Ingolf Lachmann, Eric Morignat, Emilie Antier, Latifa Lakhdar, Stéphane Legastelois, Thierry Baron
In addition to established methods like Western blot, new methods are needed to quickly and easily quantify disease-associated α-synuclein (αS(D)) in experimental models of synucleopathies. A transgenic mouse line (M83) over-expressing the human A53T αS and spontaneously developing a dramatic clinical phenotype between eight and 22 months of age, characterized by symptoms including weight loss, prostration, and severe motor impairment, was used in this study. For molecular analyses of αS(D) (disease-associated αS) in these mice, an ELISA was designed to specifically quantify αS(D) in sick mice...
May 30, 2015: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/25230221/ignored-avenues-in-alpha-synuclein-associated-proteopathy
#9
REVIEW
Rimpy K Chowhan, Shruti Mittal, Tanveer A Dar, Mohammad A Kamal, Laishram R Singh
Alpha-Synuclein (αSyn) is a 14 kDa pre-synaptic protein predominantly expressed in various regions of brain comprising neocortex, hippocampus, striatum, thalamus and cerebellum. αSyn aggregates have special neuropathologic relevance for comprehending Parkinson's disease (PD) and other synucleopathies due to the presence of αSyn aggregates in brain of patients suffering from these diseases. Direct relationship between PD and various single nuclear polymorphisms of αSyn further displays an inherent significance of mutated αSyn in increasing the risk for developing PD...
2014: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/25214445/down-regulating-%C3%AE-synuclein-for-treating-synucleopathies
#10
EDITORIAL
Mathieu Bourdenx, Benjamin Dehay, Erwan Bezard
No abstract text is available yet for this article.
October 2014: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/25159221/protease-resistant-sod1-aggregates-in-amyotrophic-lateral-sclerosis-demonstrated-by-paraffin-embedded-tissue-pet-blot
#11
Petra Steinacker, Christian Berner, Dietmar R Thal, Johannes Attems, Albert C Ludolph, Markus Otto
OBJECTIVES: The paraffin-embedded tissue (PET) blot technique followed by limited protease digestion has been established to detect protein aggregates in prion diseases, alpha-synucleopathies, and tauopathies. We analyzed whether the scope of the method can be extended to analyze aggregates in mouse and human tissue with amyotrophic lateral sclerosis (ALS) associated with superoxide dismutase 1 (SOD1) mutation. METHODS: Formalin-fixed and paraffin-embedded brain and spinal cord tissue from SOD1G93A mice was first analyzed for the expression of SOD1, aggregated SOD1, ubiquitin, and p62 by convential immunohistochemistry and then used to establish the PET blot technique, limited protease digest, and immunodetection of SOD1 aggregates...
August 28, 2014: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/23939303/mouse-models-of-cognitive-deficits-due-to-alpha-synuclein-pathology
#12
REVIEW
Iddo Magen, Marie-Françoise Chesselet
Synucleopathies are neurodegenerative disorders characterized by abnormal accumulation of alpha-synuclein, most often in neurons. Familial forms are due to mutations or multiplications of the gene encoding for alpha-synuclein but most synucleopathies occur sporadically. They include Parkinson's disease (PD) and dementia with Lewy Bodies (DLB), which are both linked to cognitive decline. In DLB, dementia dominates the symptoms whereas in PD, subtle cognitive deficits are frequent and may appear even before motor symptoms, but only a fraction of patients develop severe dementia-type cognitive deficits...
2011: Journal of Parkinson's Disease
https://www.readbyqxmd.com/read/22166404/vaccination-for-parkinson-s-disease
#13
REVIEW
A Schneeberger, M Mandler, F Mattner, W Schmidt
Idiopathic Parkinson's disease (PD) is, like other neurodegenerative diseases such as Alzheimer's disease (AD) considered a proteinopathy. Thus, a disease that is driven by the accumulation and aggregation of misfolded proteins, in case of PD α-synuclein (aSyn) is incriminated. Accordingly, removal of aSyn is assumed of having the potential to modify the course of the disease. Both active and passive aSyn targeting immunotherapy were found to modify disease in mice overexpressing human aSyn and recapitulating various aspects of synucleopathies...
January 2012: Parkinsonism & related Disorders
https://www.readbyqxmd.com/read/21342025/%C3%AE-synuclein-in-parkinson-disease-and-other-neurodegenerative-disorders
#14
REVIEW
Michael Eller, David R Williams
With the aging population in the Western hemisphere, neurodegenerative parkinsonism and dementia will become two of the great public health challenges of this century. A major pillar in the effort to treat these conditions will be the shift from symptomatic treatment to disease modifying therapy. This step will absolutely require cheap and reliable biomarkers; patients will need to be diagnosed before irreversible change has occurred. α-Synuclein (αS) is a recent candidate biomarker for Lewy body neurodegeneration...
March 2011: Clinical Chemistry and Laboratory Medicine: CCLM
https://www.readbyqxmd.com/read/21055449/inducible-dopaminergic-glutathione-depletion-in-an-%C3%AE-synuclein-transgenic-mouse-model-results-in-age-related-olfactory-dysfunction
#15
Y H Kim, S Lussier, A Rane, S W Choi, J K Andersen
Parkinson's disease (PD) involves both motor and non-motor disturbances. Non-motor features include alterations in sensory olfactory function which may constitute a viable biomarker for the disorder. It is not clear what causes olfactory dysfunction but it appears to coincide with the development of synucleopathy within the olfactory bulb (OB). Elevation in alpha-synuclein (a-syn) is indeed a risk factor for development of the sporadic disorder. The multifactorial nature of the idiopathic disease combined with variability in its presentation suggests that it is likely to be influenced by several factors and that in vivo models that explore the synergistic effect of alpha-synuclein elevation with other potential contributing factors are likely to be of importance in understanding the disease etiology...
January 13, 2011: Neuroscience
https://www.readbyqxmd.com/read/19664623/alpha-synuclein-immunopositive-aggregates-in-the-myenteric-plexus-of-the-aging-fischer-344-rat
#16
Robert J Phillips, Gary C Walter, Brittany E Ringer, Katherine M Higgs, Terry L Powley
Dystrophic axons and terminals are common in the myenteric plexus and smooth muscle of the gastrointestinal (GI) tract of aged rats. In young adult rats, alpha-synuclein in its normal state is abundant throughout the myenteric plexus, making this protein-which is prone to fibrillization-a candidate marker for axonopathies in the aged rat. To determine if aggregation of alpha-synuclein is involved in the formation of age-related enteric neuropathies, we sampled the stomach, small intestine and large intestine of adult, middle-aged, and aged virgin male Fischer 344 rats stained for alpha-synuclein in both its normal and pathological states...
November 2009: Experimental Neurology
https://www.readbyqxmd.com/read/19549071/functional-dissection-of-the-alpha-synuclein-promoter-transcriptional-regulation-by-zscan21-and-znf219
#17
COMPARATIVE STUDY
Richard Lee Clough, Georgia Dermentzaki, Leonidas Stefanis
Alpha-synuclein (SNCA) is an abundant neuronal protein involved in synaptic neurotransmission. SNCA expression levels have been strongly implicated in Parkinson's disease pathogenesis. We have previously demonstrated that in the PC12 cell line elements in intron 1 may mediate SNCA transcriptional regulation in response to neurotrophins. We have now identified transcription factor (TF) binding sites in intron 1 and the 5'-promoter of SNCA. A binding site for the TF zinc finger and SCAN domain containing (ZSCAN)21 in the 5'-region of intron 1 is required for intron 1 transcriptional activity...
September 2009: Journal of Neurochemistry
https://www.readbyqxmd.com/read/19342108/the-association-of-metal-ion-exposure-with-alpha-synuclein-like-immunoreactivity-in-the-central-nervous-system-of-fish-catostomus-commersoni
#18
Heather S Boudreau, Karmen M Krol, Joseph K Eibl, Linda D Williams, John P Rossiter, Vincent P Palace, Gregory M Ross
Alpha-synuclein protein aggregates are a major component of Lewy bodies, the intracytoplasmic inclusions found in dopaminergic neurons that are a defining characteristic of Parkinson's disease. Other "synucleopathies" include dementia with Lewy bodies and multisystem atrophy. In vitro, the formation of these deposits can be induced by a number of substances, including metal ions. Fish provide a useful model to study the long-term biological effects of metal ion exposure, but to date no studies have been reported concerning such exposures with respect to alpha-synuclein aggregation...
May 17, 2009: Aquatic Toxicology
https://www.readbyqxmd.com/read/18805302/-rem-sleep-behavior-disorders-and-their-characteristics-in-parkinson-s-disease
#19
REVIEW
V Cochen De Cock, I Arnulf
REM sleep behavior disorders (RBD) are vigorous, complex movements corresponding to enacted dreams. They may disturb sleep, and injure the patients or their bed partner. RBD are frequently associated with neurodegenerative diseases, especially synucleopathies. They can precede parkinsonism or dementia by five to 10 years. These presymptomatic RBDs are frequently associated with EEG slowing, reduced olfaction, mild visuospatial cognitive impairment, and decreased dopamine transport in functional brain imaging...
August 2008: Revue Neurologique
https://www.readbyqxmd.com/read/17512502/localization-of-parkinson-s-disease-associated-lrrk2-in-normal-and-pathological-human-brain
#20
Shinji Higashi, Saskia Biskup, Andrew B West, Daniel Trinkaus, Valina L Dawson, Richard L M Faull, Henry J Waldvogel, Heii Arai, Ted M Dawson, Darren J Moore, Piers C Emson
Mutations in the LRRK2 gene cause autosomal dominant, late-onset parkinsonism, which presents with pleomorphic pathology including alpha-synucleopathy. To promote our understanding of the biological role of LRRK2 in the brain we examined the distribution of LRRK2 mRNA and protein in postmortem human brain tissue from normal and neuropathological subjects. In situ hybridization and immunohistochemical analysis demonstrate the expression and localization of LRRK2 to various neuronal populations in brain regions implicated in Parkinson's disease (PD) including the cerebral cortex, caudate-putamen and substantia nigra pars compacta...
June 25, 2007: Brain Research
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