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https://www.readbyqxmd.com/read/29790977/alpha-synuclein-aggregates-in-labial-salivary-glands-of-idiopathic-rapid-eye-movement-sleep-behavior-disorder
#1
Alx Iranzo, Sergi Borrego, Isabel Vilaseca, Carles Martí, Mónica Serradell, Raquel Sánchez-Valle, Gabor G Kovacs, Francesc Valldeoriola, Carles Gaig, Joan Santamaria, Eduard Tolosa, Ellen Gelpi
Study Objectives : To assess whether biopsy of the labial minor salivary glands safely detects phosphorylated alpha-synuclein (pAS) deposits in idiopathic REM sleep behavior disorder (IRBD), a condition that precedes the cardinal manifestations of synuclein disorders associated with Lewy type pathology, namely Parkinson disease (PD) and dementia with Lewy bodies (DLB). Methods: In a prospective study, labial biopsy of the minor salivary glands was performed in 62 IRBD patients, 13 PD and 10 DLB patients who were initially diagnosed with IRBD, and in 33 controls...
May 22, 2018: Sleep
https://www.readbyqxmd.com/read/29785351/genetic-inactivation-of-alpha-synuclein-affects-embryonic-development-of-dopaminergic-neurons-of-the-substantia-nigra-but-not-the-ventral-tegmental-area-in-mouse-brain
#2
Tatiana V Tarasova, Olga A Lytkina, Valeria V Goloborshcheva, Larisa N Skuratovskaya, Alexandr I Antohin, Ruslan K Ovchinnikov, Michail S Kukharsky
Lesion of the dopaminergic neurons of the nigrostriatal system is a key feature of Parkinson's disease (PD). Alpha-synuclein is a protein that is a major component of Lewy bodies, histopathological hallmarks of PD, and is involved in regulation of dopamine (DA) neurotransmission. Previous studies of knockout mice have shown that inactivation of alpha-synuclein gene can lead to the reduction in number of DA neurons in the substantia nigra (SN). DA neurons of the SN are known to be the most affected in PD patients whereas DA neurons of neighboring ventral tegmental area (VTA) are much less susceptible to degeneration...
2018: PeerJ
https://www.readbyqxmd.com/read/29783988/tolerogenic-bone-marrow-derived-dendritic-cells-induce-neuroprotective-regulatory-t-cells-in-a-model-of-parkinson-s-disease
#3
Charles R Schutt, Howard E Gendelman, R Lee Mosley
BACKGROUND: Administration of granulocyte-macrophage colony-stimulating factor (GM-CSF) increases regulatory T cell (Treg) number and function with control of neuroinflammation and neuronal protection in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease (PD). Recently, we demonstrated in an early phase 1 clinical trial that GM-CSF also improves motor skills in PD patients. However, the mechanisms of Treg induction and its effects on neuroprotective responses remain unknown...
May 21, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29782835/multi-pronged-interactions-underlie-inhibition-of-%C3%AE-synuclein-aggregation-by-%C3%AE-synuclein
#4
Jonathan K Williams, Xue Yang, Tamr B Atieh, Michael P Olson, Sagar D Khare, Jean Baum
The intrinsically disordered protein β-synuclein is known to inhibit the aggregation of its intrinsically disordered homolog, α-synuclein, which is implicated in Parkinson's disease. While β-synuclein itself does not form fibrils at the cytoplasmic pH7.4, alteration of pH and other environmental perturbations are known to induce its fibrilization. However, the sequence and structural determinants of β-synuclein inhibition and self-aggregation are not well understood. We have utilized a series of domain-swapped chimeras of α-synuclein and β-synuclein to probe the relative contributions of the N-terminal, C-terminal and the central Non-Amyloid-β Component (NAC) domains to the inhibition of α-synuclein aggregation...
May 18, 2018: Journal of Molecular Biology
https://www.readbyqxmd.com/read/29780350/alpha-synuclein-from-early-synaptic-dysfunction-to-neurodegeneration
#5
REVIEW
Veronica Ghiglieri, Valeria Calabrese, Paolo Calabresi
Over the last two decades, many experimental and clinical studies have provided solid evidence that alpha-synuclein (α-syn), a small, natively unfolded protein, is closely related to Parkinson's disease (PD) pathology. To provide an overview on the different roles of this protein, here we propose a synopsis of seminal and recent studies that explored the many aspects of α-syn. Ranging from the physiological functions to its neurodegenerative potential, the relationship with the possible pathogenesis of PD will be discussed...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29780321/toll-like-receptor-2-signaling-and-current-approaches-for-therapeutic-modulation-in-synucleinopathies
#6
REVIEW
Ian F Caplan, Kathleen A Maguire-Zeiss
The innate immune response in the central nervous system (CNS) is implicated as both beneficial and detrimental to health. Integral to this process are microglia, the resident immune cells of the CNS. Microglia express a wide variety of pattern-recognition receptors, such as Toll-like receptors, that detect changes in the neural environment. The activation of microglia and the subsequent proinflammatory response has become increasingly relevant to synucleinopathies, including Parkinson's disease the second most prevalent neurodegenerative disease...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29775624/characterization-and-comparative-analysis-of-a-new-mouse-microglial-cell-model-for-studying-neuroinflammatory-mechanisms-during-neurotoxic-insults
#7
Souvarish Sarkar, Emir Malovic, Deeksha Sarda, Vivek Lawana, Dharmin Rokad, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, Anumantha G Kanthasamy
Microglia are the first responders of the central nervous system, acting as the key modulators of neuroinflammation observed during neurotoxic insults as well as in the pathophysiology of several neurodegenerative disorders including Alzheimer's (AD), Parkinson's (PD), and Huntington's diseases (HD). The number of publications on microglia has increased steadily throughout the past decade because of immense interests in the neuroinflammation that precedes the neurodegenerative process. To study microglial biology and its role in modulating neuroinflammation, immortalized microglial cell lines derived from mice, rats, and humans have been developed...
May 15, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29771508/comparison-of-kinetics-toxicity-oligomers-formation-and-membrane-binding-capacity-of-%C3%AE-synuclein-familial-mutations-at-a53-site-including-newly-discovered-a53v-mutation
#8
Ganesh M Mohite, Rakesh Kumar, Rajlaxmi Panigrahi, Ambuja Navalkar, Nitu Singh, Debalina Datta, Surabhi Mehra, Soumik Ray, Laxmikant G Gadhe, Subhadeep Das, Namrata Singh, Debdeep Chatterjee, Ashutosh Kumar, Samir K Maji
The involvement of α-synuclein (α-Syn) amyloid formation in Parkinson's disease (PD) pathogenesis is supported by the discovery of α-Syn gene (SNCA) mutations linked with familial PD, which are known to modulate the oligomerization and aggregation of α-Syn. Recently, the A53V mutation has been discovered, which leads to the late-onset PD. In the present study, we characterized for the first time the biophysical properties including the aggregation propensities, toxicity of aggregated species and membrane binding capability of A53V along with all familial mutations at A53 position...
May 17, 2018: Biochemistry
https://www.readbyqxmd.com/read/29770111/chronic-caffeine-treatment-protects-against-%C3%AE-synucleinopathy-by-reestablishing-autophagy-activity-in-the-mouse-striatum
#9
Yanan Luan, Xiangpeng Ren, Wu Zheng, Zhenhai Zeng, Yingzi Guo, Zhidong Hou, Wei Guo, Xingjun Chen, Fei Li, Jiang-Fan Chen
Despite converging epidemiological evidence for the inverse relationship of regular caffeine consumption and risk of developing Parkinson's disease (PD) with animal studies demonstrating protective effect of caffeine in various neurotoxin models of PD, whether caffeine can protect against mutant α-synuclein (α-Syn) A53T-induced neurotoxicity in intact animals has not been examined. Here, we determined the effect of chronic caffeine treatment using the α-Syn fibril model of PD by intra-striatal injection of preformed A53T α-Syn fibrils...
2018: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29769405/%C3%AE-synuclein-stimulation-of-monoamine-oxidase-b-and-legumain-protease-mediates-the-pathology-of-parkinson-s-disease
#10
Seong Su Kang, Eun Hee Ahn, Zhentao Zhang, Xia Liu, Fredric P Manfredsson, Ivette M Sandoval, Susov Dhakal, P Michael Iuvone, Xuebing Cao, Keqiang Ye
Dopaminergic neurodegeneration in Parkinson's disease (PD) is associated with abnormal dopamine metabolism by MAO-B (monoamine oxidase-B) and intracellular α-Synuclein (α-Syn) aggregates, called the Lewy body. However, the molecular relationship between α-Syn and MAO-B remains unclear. Here, we show that α-Syn directly binds to MAO-B and stimulates its enzymatic activity, which triggers AEP (asparagine endopeptidase; legumain) activation and subsequent α-Syn cleavage at N103, leading to dopaminergic neurodegeneration...
May 16, 2018: EMBO Journal
https://www.readbyqxmd.com/read/29762036/biochemical-profiling-of-the-brain-and-blood-metabolome-in-a-mouse-model-of-prodromal-parkinson-s-disease-reveal-distinct-metabolic-profiles
#11
Stewart F Graham, Nowlen L Rey, Ali Yilmaz, Praveen Kumar, Zachary Madaj, Michael Maddens, Ray O Bahado-Singh, Katelyn Becker, Emily Schulz, Lindsay K Meyerdirk, Jennifer A Steiner, Jiyan Ma, Patrik Brundin
Parkinson's disease is the second most common neurodegenerative disease. In the vast majority of cases the origin is not genetic and the cause is not well understood, although progressive accumulation of α-synuclein aggregates appears central to the pathogenesis. Currently, treatments that slow disease progression are lacking and there are no robust biomarkers that can facilitate development of such treatments, or act as aids in early diagnosis. Therefore, we have defined metabolomic changes in the brain and serum in an animal model of prodromal Parkinson's disease...
May 15, 2018: Journal of Proteome Research
https://www.readbyqxmd.com/read/29762014/selective-and-sensitive-pull-down-of-amyloid-fibrils-produced-in-vitro-and-in-vivo-by-the-use-of-pentameric-thiophene-coupled-resins
#12
Anna Beatriz Wreden, Luiza Fernandes, Mirian Kelley, Antônio Pereira-Neves, Caroline S Moreira, David R da Rocha, Fernando L Palhano
Protein aggregation is a hallmark of several degenerative diseases, including Alzheimer's disease, Parkinson's disease and familial amyloidosis (Finnish type) (FAF). A method to isolate and detect amyloids is desired for the diagnosis of amyloid diseases. Here, we report the synthesis of pentameric thiophene amyloid ligand (p-FTAA) linked to agarose resin for selective purification of amyloid aggregates produced in vitro and in vivo. Using amyloid fibrils produced in vitro from alpha-synuclein, gelsolin and Aβ1-40 and gelsolin amyloid aggregates extracted from tissue homogenates of a mouse model of FAF, we observed that p-FTAA resin was able to pull down amyloid aggregates...
May 15, 2018: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29760292/-targeting-transcellular-transport-of-%C3%AE-synuclein-for-developing-disease-modifying-therapies-for-synucleinopathy
#13
Takafumi Hasegawa
Parkinson's disease (PD) is the second most common neurodegenerative disorder and it is characterized by progressive physical disability along with a variety of non-motor symptoms. Drugs that replenish dopamine can partly alleviate the motor symptoms; however, they do not cure the disease itself. Therefore, there is an urgent need for disease modifying therapies that would delay or prevent neurodegeneration. Increasing evidence suggests that α-synuclein, a key molecule in PD, is secreted into the extracellular environment and can be transported from cell-to-cell, thereby affecting the physiological state of the neighboring cells in a prion-like manner...
May 2018: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/29760287/-multi-organ-distribution-of-alpha-synuclein-pathology-in-dementia-with-lewy-bodies
#14
Koichi Wakabayashi, Yasuo Miki
In Parkinson's disease and dementia with Lewy bodies, neuronal α-synuclein aggregates (Lewy bodies and Lewy neurites) are distributed throughout the nervous system, including the brain, spinal cord, sympathetic ganglia, enteric nervous system, cardiac and pelvic plexuses, submandibular gland, adrenal medulla, and skin. Lewy bodies also occur in 10-20% of neurologically asymptomatic individuals older than 60 years. These cases are called incidental Lewy body disease (ILBD). In ILBD, Lewy bodies can be found in the brain, spinal cord, sympathetic ganglia, visceral autonomic nervous system and skin...
May 2018: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/29759483/induction-of-the-immunoproteasome-subunit-lmp7-links-proteostasis-and-immunity-in-%C3%AE-synuclein-aggregation-disorders
#15
Scott Ugras, Malcolm J Daniels, Hossein Fazelinia, Neal S Gould, Anastasia K Yocum, Kelvin C Luk, Esteban Luna, Hua Ding, Chris McKennan, Steven Seeholzer, Dan Martinez, Perry Evans, Daniel Brown, John E Duda, Harry Ischiropoulos
Accumulation of aggregated α-synuclein into Lewy bodies is thought to contribute to the onset and progression of dopaminergic neuron degeneration in Parkinson's disease (PD) and related disorders. Although protein aggregation is associated with perturbation of proteostasis, how α-synuclein aggregation affects the brain proteome and signaling remains uncertain. In a mouse model of α-synuclein aggregation, 6% of 6215 proteins and 1.6% of 8183 phosphopeptides changed in abundance, indicating conservation of proteostasis and phosphorylation signaling...
May 11, 2018: EBioMedicine
https://www.readbyqxmd.com/read/29756231/susceptibility-mri-captures-nigral-pathology-in-patients-with-parkinsonian-syndromes
#16
Mechelle M Lewis, Guangwei Du, Jennifer Baccon, Amanda M Snyder, Ben Murie, Felicia Cooper, Christy Stetter, Lan Kong, Christopher Sica, Richard B Mailman, James R Connor, Xuemei Huang
BACKGROUND: Parkinsonisms are neurodegenerative disorders characterized pathologically by α-synuclein-positive (e.g., PD, diffuse Lewy body disease, and MSA) and/or tau-positive (e.g., PSP, cortical basal degeneration) pathology. Using R2* and quantitative susceptibility mapping, susceptibility changes have been reported in the midbrain of living parkinsonian patients, although the exact underlying pathology of these alterations is unknown. OBJECTIVE: The current study investigated the pathological correlates of these susceptibility MRI measures...
May 14, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29755356/anti-parkinson-potential-of-silymarin-mechanistic-insight-and-therapeutic-standing
#17
REVIEW
Hammad Ullah, Haroon Khan
Parkinson's disease (PD) involves aggregation of α-synuclein and progressive loss of dopaminergic neurons. Pathogenesis of PD may also be related to one's genetic background. PD is most common among geriatric population and approximately 1-2% of population suffers over age 65 years. Currently no successful therapies are in practice for the management of PD and available therapies tend to decrease the symptoms of PD only. Furthermore, these are associated with diverse range of adverse effects profile. The neuroprotective effects of polyphenols are widely studied and documented...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29755341/plasma-biomarkers-differentiate-parkinson-s-disease-from-atypical-parkinsonism-syndromes
#18
Chin-Hsien Lin, Shieh-Yueh Yang, Herng-Er Horng, Che-Chuan Yang, Jen-Jie Chieh, Hsin-Hsien Chen, Bing-Hsien Liu, Ming-Jang Chiu
Objective: Parkinson's disease (PD) has significant clinical overlaps with atypical parkinsonism syndromes (APS), which have a poorer treatment response and a more aggressive course than PD. We aimed to identify plasma biomarkers to differentiate PD from APS. Methods: Plasma samples ( n = 204) were obtained from healthy controls and from patients with PD, dementia with Lewy bodies (DLB), multiple system atrophy, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), or frontotemporal dementia (FTD) with parkinsonism (FTD-P) or without parkinsonism...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29755323/environmental-enrichment-prevents-transcriptional-disturbances-induced-by-alpha-synuclein-overexpression
#19
Zinah Wassouf, Thomas Hentrich, Sebastian Samer, Carola Rotermund, Philipp J Kahle, Ingrid Ehrlich, Olaf Riess, Nicolas Casadei, Julia M Schulze-Hentrich
Onset and progression of neurodegenerative disorders, including synucleinopathies such as Parkinson's disease, have been associated with various environmental factors. A highly compelling association from a therapeutic point of view has been found between a physically active lifestyle and a significantly reduced risk for Parkinson's disease. Mimicking such conditions in animal models by promoting physical activity, social interactions, and novel surroundings yields in a so-called enriched environment known to enhance adult neurogenesis, increase synaptic plasticity, and decelerate neuronal loss...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29755317/microglial-phagocytosis-and-its-regulation-a-therapeutic-target-in-parkinson-s-disease
#20
REVIEW
Elzbieta Janda, Laura Boi, Anna R Carta
The role of phagocytosis in the neuroprotective function of microglia has been appreciated for a long time, but only more recently a dysregulation of this process has been recognized in Parkinson's disease (PD). Indeed, microglia play several critical roles in central nervous system (CNS), such as clearance of dying neurons and pathogens as well as immunomodulation, and to fulfill these complex tasks they engage distinct phenotypes. Regulation of phenotypic plasticity and phagocytosis in microglia can be impaired by defects in molecular machinery regulating critical homeostatic mechanisms, including autophagy...
2018: Frontiers in Molecular Neuroscience
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