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parkinson's disease and autophagy

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https://www.readbyqxmd.com/read/29676481/high-mobility-group-box-1-in-parkinson-s-disease-from-pathogenesis-to-therapeutic-approaches
#1
REVIEW
Efthalia Angelopoulou, Christina Piperi, Athanasios G Papavassiliou
Parkinson's disease (PD) presents the second most common neurodegenerative disorder with largely unknown pathogenesis and inefficient therapeutic management. Accumulating data indicate that neuroinflammation, autophagy impairment, α-synuclein aggregation and mitochondrial dysfunction may contribute to PD onset; however the molecular mechanisms underlying these pathophysiological processes are still under elucidation. Interestingly, recent evidence has indicated that High-mobility group box 1 (HMGB1), a DNA-binding protein that can be actively secreted by inflammatory cells and passively released by necrotic cells may play a key role in PD pathogenesis...
April 20, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29676231/combating-neurodegenerative-diseases-with-the-plant-alkaloid-berberine-molecular-mechanisms-and-therapeutic-potential
#2
Dahua Fan, Liping Liu, Zhengzhi Wu, Meiqun Cao
Neurodegenerative diseases are among the most serious health problems affecting millions of people worldwide. Such diseases are characterized by a progressive degeneration and / or death of neurons in the central nervous system. Currently, there are no therapeutic approaches to cure or even halt the progression of neurodegenerative diseases. During the last two decades, much attention has been paid to the neuroprotective and anti-neurodegenerative activities of compounds isolated from natural products with high efficacy and low toxicity...
April 19, 2018: Current Neuropharmacology
https://www.readbyqxmd.com/read/29673238/association-of-exercise-induced-autophagy-upregulation-and-apoptosis-suppression-with-neuroprotection-against-pharmacologically-induced-parkinson-s-disease
#3
Yong Chul Jang, Dong Joo Hwang, Jung Hoon Koo, Hyun Seob Um, Nam Hee Lee, Dong Cheol Yeom, Youngil Lee, Joon Yong Cho
PURPOSE: We investigated whether treadmill exercise (TE)-induced neuroprotection was associated with enhanced autophagy and reduced apoptosis in a mouse model of pharmacologically induced Parkinson's disease (PD). METHODS: PD was induced via the administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). C57BL/6 male mice were randomly assigned to the following three groups: control (C57BL, n=10), MPTP with probenecid (MPTP/C, n=10), and MPTP/ C plus exercise (MPTP-TE, n=10)...
March 30, 2018: Journal of Exercise Nutrition & Biochemistry
https://www.readbyqxmd.com/read/29649621/astrocyte-specific-dj-1-overexpression-protects-against-rotenone-induced-neurotoxicity-in-a-rat-model-of-parkinson-s-disease
#4
Briana R De Miranda, Emily M Rocha, Qing Bai, Amina El Ayadi, David Hinkle, Edward A Burton, J Timothy Greenamyre
DJ-1 is a redox-sensitive protein with several putative functions important in mitochondrial physiology, protein transcription, proteasome regulation, and chaperone activity. High levels of DJ-1 immunoreactivity are reported in astrocytes surrounding pathology associated with idiopathic Parkinson's disease, possibly reflecting the glial response to oxidative damage. Previous studies showed that astrocytic over-expression of DJ-1 in vitro prevented oxidative stress and mitochondrial dysfunction in primary neurons...
April 9, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29628303/overexpression-of-tfeb-drives-a-pleiotropic-neurotrophic-effect-and-prevents-parkinson-s-disease-related-neurodegeneration
#5
Albert Torra, Annabelle Parent, Thais Cuadros, Beatriz Rodríguez-Galván, Esther Ruiz-Bronchal, Andrea Ballabio, Analía Bortolozzi, Miquel Vila, Jordi Bové
The possible implication of transcription factor EB (TFEB) as a therapeutic target in Parkinson's disease has gained momentum since it was discovered that TFEB controls lysosomal biogenesis and autophagy and that its activation might counteract lysosomal impairment and protein aggregation. However, the majority of putative direct targets of TFEB described to date is linked to a range of biological processes that are not related to the lysosomal-autophagic system. Here, we assessed the effect of overexpressing TFEB with an adeno-associated viral vector in mouse substantia nigra dopaminergic neurons...
February 27, 2018: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/29627340/deregulation-of-autophagy-and-vesicle-trafficking-in-parkinson-s-disease
#6
REVIEW
Patricia Sheehan, Zhenyu Yue
Parkinson's disease (PD) is a common neurodegenerative disease characterized pathologically by the selective loss of dopaminergic neurons in the substantia nigra and the intracellular accumulation of α-synuclein in the Lewy bodies. While the pathogenic mechanisms of PD are poorly understood, many lines of evidence point to a role of altered autophagy and membrane trafficking in the development of the disease. Emerging studies show that connections between the deregulation of autophagy and synaptic vesicle (SV) trafficking may contribute to PD...
April 5, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29626647/multiple-pathways-for-mitophagy-a-neurodegenerative-conundrum-for-parkinson-s-disease
#7
REVIEW
Charleen T Chu
It has been nearly a decade since the first landmark studies implicating familial recessive Parkinson's disease genes in the regulation of selective mitochondrial autophagy. The PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase Parkin (encoded by the PARK2 gene) act together to mark depolarized mitochondria for degradation. There is now an extensive body of literature detailing key mediators and steps in this pathway, based mostly on work in transformed cell lines. However, the degree to which PINK1-triggered mitophagy contributes to mitochondrial quality control in the mammalian brain, and the extent to which its disruption contributes to Parkinson's disease pathogenesis remain uncertain...
April 4, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29621594/rock-inhibition-in-models-of-neurodegeneration-and-its-potential-for-clinical-translation
#8
REVIEW
Jan Christoph Koch, Lars Tatenhorst, Anna-Elisa Roser, Kim-Ann Saal, Lars Tönges, Paul Lingor
Neurodegenerative disorders like Parkinson's disease, Alzheimer's disease, or amyotrophic lateral sclerosis are affecting a rapidly increasing population worldwide. While common pathomechanisms such as protein aggregation, axonal degeneration, dysfunction of protein clearing and an altered immune response have been characterized, no disease-modifying therapies have been developed so far. Interestingly, a significant involvement of the Rho kinase (ROCK) signaling pathway has been described in all of these mechanisms making it a promising target for new therapeutic approaches...
April 2, 2018: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/29608948/mir-181b-regulates-autophagy-in-a-model-of-parkinson-s-disease-by-targeting-the-pten-akt-mtor-signaling-pathway
#9
Wei Li, Yongmei Jiang, Yuan Wang, Shaonan Yang, Xinran Bi, Xudong Pan, Aijun Ma, Wei Li
OBJECTIVE: Parkinson's disease (PD) is the second most common neurodegenerative disease. Recent studies have shown that dysregulation of microRNA plays an important role in PD, and defects in autophagy are also critically associated with mechanisms underlying PD. We aim to investigate the effect of miR-181b on autophagy, particularly the involvement of miR-181b in the regulation of the phosphatase and tensin homolog (PTEN)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway and neuronal autophagy in a 1-methyl-4- phenylpyridinium iodide(MPP+ )-induced cellular model of Parkinson's disease...
March 30, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29599708/distinct-mechanisms-of-pathogenic-dj-1-mutations-in-mitochondrial-quality-control
#10
Daniela Strobbe, Alexis A Robinson, Kirsten Harvey, Lara Rossi, Caterina Ferraina, Valerio de Biase, Carlo Rodolfo, Robert J Harvey, Michelangelo Campanella
The deglycase and chaperone protein DJ-1 is pivotal for cellular oxidative stress responses and mitochondrial quality control. Mutations in PARK7 , encoding DJ-1, are associated with early-onset familial Parkinson's disease and lead to pathological oxidative stress and/or disrupted protein degradation by the proteasome. The aim of this study was to gain insights into the pathogenic mechanisms of selected DJ-1 missense mutations, by characterizing protein-protein interactions, core parameters of mitochondrial function, quality control regulation via autophagy, and cellular death following dopamine accumulation...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29593482/aminochrome-induces-irreversible-mitochondrial-dysfunction-by-inducing-autophagy-dysfunction-in-parkinson-s-disease
#11
Juan Segura-Aguilar, Sandro Huenchuguala
No abstract text is available yet for this article.
2018: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29579719/copper-accumulation-in-senescent-cells-interplay-between-copper-transporters-and-impaired-autophagy
#12
Shashank Masaldan, Sharnel A S Clatworthy, Cristina Gamell, Zoe M Smith, Paul S Francis, Delphine Denoyer, Peter M Meggyesy, Sharon La Fontaine, Michael A Cater
Cellular senescence is characterized by irreversible growth arrest incurred through either replicative exhaustion or by pro-oncogenic cellular stressors (radioactivity, oxidative stress, oncogenic activation). The enrichment of senescent cells in tissues with age has been associated with tissue dyshomeostasis and age-related pathologies including cancers, neurodegenerative disorders (e.g. Alzheimer's, Parkinson's, etc.) and metabolic disorders (e.g. diabetes). We identified copper accumulation as being a universal feature of senescent cells [mouse embryonic fibroblasts (MEF), human prostate epithelial cells and human diploid fibroblasts] in vitro...
March 17, 2018: Redox Biology
https://www.readbyqxmd.com/read/29579237/acid-ceramidase-inhibition-ameliorates-%C3%AE-synuclein-accumulation-upon-loss-of-gba1-function
#13
Myung Jong Kim, Sohee Jeon, Lena F Burbulla, Dimitri Krainc
GBA1 encodes the lysosomal enzyme β-glucocerebrosidase (GCase) which converts glucosylceramide into ceramide and glucose. Mutations in GBA1 lead to Gaucher's disease and are a major risk factor for Parkinson's disease (PD) and Dementia with Lewy bodies (DLB), synucleinopathies characterized by accumulation of intracellular α-synuclein. In this study, we examined whether decreased ceramide that is observed in GCase-deficient cells contributes to α-synuclein accumulation. We demonstrated that deficiency of GCase leads to a reduction of C18-ceramide species and altered intracellular localization of Rab8a, a small GTPase implicated in secretory autophagy, that contributed to impaired secretion of α-synuclein and accumulation of intracellular α-synuclein...
March 22, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29570846/neuroprotective-effects-of-creatine-in-the-cmvmjd135-mouse-model-of-spinocerebellar-ataxia-type-3
#14
Sara Duarte-Silva, Andreia Neves-Carvalho, Carina Soares-Cunha, Joana M Silva, Andreia Teixeira-Castro, Rita Vieira, Anabela Silva-Fernandes, Patrícia Maciel
BACKGROUND AND OBJECTIVE: Mitochondrial dysfunction has been implicated in several neurodegenerative diseases. Creatine administration increases concentration of the energy buffer phosphocreatine, exerting protective effects in the brain. We evaluate whether a creatine-enriched diet would be beneficial for a mouse model of spinocerebellar ataxia type 3, a genetically defined neurodegenerative disease for which no treatment is available. METHODS: We performed 2 independent preclinical trials using the CMVMJD135 mouse model (treating 2 groups of animals with different disease severity) and wild-type mice, to which 2% creatine was provided for 19 (preclinical trial 1) or 29 (preclinical trial 2) weeks, starting at a presymptomatic age...
March 23, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29561612/a-small-molecule-activator-of-unc-51-like-kinase-1-ulk1-that-induces-cytoprotective-autophagy-for-parkinson-s-disease-treatment
#15
Liang Ouyang, Lan Zhang, Shouyue Zhang, Dahong Yao, Yuqian Zhao, Guan Wang, Leilei Fu, Peng Lei, Bo Liu
UNC-51-like kinase 1 (ULK1), the yeast Atg1 ortholog, is the sole serine-threonine kinase and initiating enzyme in autophagy, which may be regarded as a target in Parkinson's disease (PD). Herein, we discovered a small molecule 33i (BL-918) as a potent activator of ULK1 by structure-based drug design. Subsequently, some key amino acid residues (Arg18, Lys50, Asn86 and Tyr89) were found to be crucial to the binding pocket between ULK1 and 33i by site-directed mutagenesis. Moreover, we found that 33i induced autophagy via the ULK complex in SH-SY5Y cells...
March 21, 2018: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29559387/endurance-exercise-mediates-neuroprotection-against-mptp-mediated-parkinson-s-disease-via-enhanced-neurogenesis-antioxidant-capacity-and-autophagy
#16
Yongchul Jang, Insu Kwon, Wankeun Song, Ludmila M Cosio-Lima, Youngil Lee
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunction. Growing evidence has demonstrated that endurance exercise (EE) confers neuroprotection against PD; However, the exact molecular mechanisms responsible for exercise-induced protection of dopaminergic neurons in PD remain unclear. Since oxidative stress plays a key role in the degenerative process of PD. We investigated whether EE-induced neuroprotection is associated with enhanced antioxidative capacity and autophagy, using a mouse model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration...
March 17, 2018: Neuroscience
https://www.readbyqxmd.com/read/29551576/hmgb1-promotes-the-starvation-induced-autophagic-degradation-of-%C3%AE-synuclein-in-sh-sy5y-cells-atg-5-dependently
#17
Yi Guan, Yiping Li, Gang Zhao, Yunqian Li
Impaired autophagic clearance of aggregated α-synuclein is considered as one of key mechanisms underlining Parkinson disease (PD). High-mobility group protein B1 (HMGB1) has recently been demonstrated to mediate persistent neuroinflammation and consequent progressive neurodegeneration by promoting multiple inflammatory and neurotoxic factors. In this study, we examined the influence of the overexpression of wild-type (WT) and mutant-type (MT, A53T and A30P) α-synuclein on the autophagy in neuroblastoma SH-SY5Y cells under starvation, and then investigated the regulation of endogenous HMGB1 on the α-synuclein degradation and on the starvation-induced autophagy in the α-synuclein-overexpressed SH-SY5Y cells...
March 15, 2018: Life Sciences
https://www.readbyqxmd.com/read/29548988/axonal-autophagy-mini-review-for-autophagy-in-the-cns
#18
REVIEW
Andrea K H Stavoe, Erika L F Holzbaur
Neurons are long-lived and highly polarized cells that depend on autophagy to maintain cellular homeostasis. The robust, constitutive biogenesis of autophagosomes in the distal axon occurs via a conserved pathway that is required to maintain functional synapses and prevent axon degeneration. Autophagosomes are formed de novo at the axon terminal in a stepwise assembly process, engulfing mitochondrial fragments, aggregated proteins, and bulk cytosol in what appears to be a nonselective uptake mechanism. Following formation, autophagosomes fuse with late endosomes/lysosomes and then are rapidly and efficiently transported along the axon toward the soma, driven by the microtubule motor cytoplasmic dynein...
March 13, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29547474/exfoliation-syndrome-a-disease-of-autophagy-and-loxl1-proteopathy
#19
Audrey M Bernstein, Robert Ritch, J Mario Wolosin
Exfoliation syndrome (XFS) is an age-related disease involving the deposition of aggregated fibrillar material (XFM) at extracellular matrices in tissues that synthesize elastic fibers. Its main morbidity is in the eye, where XFM accumulations form on the surface of the ciliary body, iris and lens. Exfoliation glaucoma (XFG) occurs in a high proportion of persons with XFS and can be a rapidly progressing disease. Worldwide, XFG accounts for about 25% of open-angle glaucoma cases. XFS and XFG show a sharp age-dependence, similarly to the many age-related diseases classified as aggregopathies...
March 15, 2018: Journal of Glaucoma
https://www.readbyqxmd.com/read/29529025/parallel-roles-of-transcription-factors-dfoxo-and-fer2-in-the-development-and-maintenance-of-dopaminergic-neurons
#20
Damla Tas, Luca Stickley, Federico Miozzo, Rafael Koch, Nicolas Loncle, Virginie Sabado, Bettina Gnägi, Emi Nagoshi
Forkhead box (FOXO) proteins are evolutionarily conserved, stress-responsive transcription factors (TFs) that can promote or counteract cell death. Mutations in FOXO genes are implicated in numerous pathologies, including age-dependent neurodegenerative disorders, such as Parkinson's disease (PD). However, the complex regulation and downstream mechanisms of FOXOs present a challenge in understanding their roles in the pathogenesis of PD. Here, we investigate the involvement of FOXO in the death of dopaminergic (DA) neurons, the key pathological feature of PD, in Drosophila...
March 12, 2018: PLoS Genetics
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