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parkinson's disease and autophagy

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https://www.readbyqxmd.com/read/28542792/on-the-complexity-of-clinical-and-molecular-bases-of-neurodegeneration-with-brain-iron-accumulation
#1
REVIEW
Cristina Tello, Alejandra Darling, Vincenzo Lupo, Belén Pérez-Dueñas, Carmen Espinós
Neurodegeneration with brain iron accumulation (NBIA) are a group of inherited heterogeneous neurodegenerative rare disorders. These patients present with dystonia, spasticity, parkinsonism and neuropsychiatric disturbances, along with brain MRI evidence of iron accumulation. In sum, they are devastating disorders and to date, there is no specific treatment. Ten NBIA genes are accepted: PANK2, PLA2G6, C19orf12, COASY, FA2H, ATP13A2, WDR45, FTL, CP, and DCAF17, and. Nonetheless, a relevant percentage of patients remain without genetic diagnosis, suggesting that other novel NBIA genes remain to be discovered...
May 23, 2017: Clinical Genetics
https://www.readbyqxmd.com/read/28540642/plasma-and-white-blood-cells-show-different-mirna-expression-profiles-in-parkinson-s-disease
#2
Christine Schwienbacher, Luisa Foco, Anne Picard, Eloina Corradi, Alice Serafin, Jörg Panzer, Stefano Zanigni, Hagen Blankenburg, Maurizio F Facheris, Giulia Giannini, Marika Falla, Pietro Cortelli, Peter P Pramstaller, Andrew A Hicks
Parkinson's disease (PD) diagnosis is based on the assessment of motor symptoms, which manifest when more than 50% of dopaminergic neurons are degenerated. To date, no validated biomarkers are available for the diagnosis of PD. The aims of the present study are to evaluate whether plasma and white blood cells (WBCs) are interchangeable biomarker sources and to identify circulating plasma-based microRNA (miRNA) biomarkers for an early detection of PD. We profiled plasma miRNA levels in 99 L-dopa-treated PD patients from two independent data collections, in ten drug-naïve PD patients, and in unaffected controls matched by sex and age...
May 24, 2017: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/28504708/receptor-oligomerization-guides-pathway-choice-between-proteasomal-and-autophagic-degradation
#3
Kefeng Lu, Fabian den Brave, Stefan Jentsch
Abnormal or aggregated proteins have a strong cytotoxic potential and are causative for human disorders such as Alzheimer's, Parkinson's, Huntington's disease and amyotrophic lateral sclerosis. If not restored by molecular chaperones, abnormal proteins are typically degraded by proteasomes or eliminated by selective autophagy. The discovery that both pathways are initiated by substrate ubiquitylation but utilize different ubiquitin receptors incited a debate over how pathway choice is achieved. Here, we demonstrate in yeast that pathway choice is made after substrate ubiquitylation by competing ubiquitin receptors harbouring either proteasome- or autophagy-related protein 8 (Atg8/LC3)-binding modules...
May 15, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28504367/neuroprotective-natural-products-for-the-treatment-of-parkinson-s-disease-by-targeting-the-autophagy-lysosome-pathway-a-systematic-review
#4
REVIEW
Zi-Ying Wang, Jing-Yi Liu, Chuan-Bin Yang, Sandeep Malampati, Ying-Yu Huang, Mei-Xiang Li, Min Li, Ju-Xian Song
The autophagy-lysosome pathway (ALP) is a primary means by which damaged organelles and long-lived proteins are removed from cells and their components recycled. Impairment of the ALP has been found to be linked to the pathogenesis of Parkinson's disease (PD), a chronic neurodegenerative disorder characterized by the accumulation of protein aggregates and loss of dopaminergic neurons in the midbrain. In recent years, some active compounds derived from plants have been found to regulate the ALP and to exert neuroprotective effects in experimental models of PD, raising the possibility that autophagy enhancement may be an effective therapeutic strategy in PD treatment...
May 15, 2017: Phytotherapy Research: PTR
https://www.readbyqxmd.com/read/28498401/luteolin-induced-apoptosis-through-activation-of-endoplasmic-reticulum-stress-sensors-in-pheochromocytoma-cells
#5
Kisang Kwon, Young-Sook Kwon, Seung-Whan Kim, Kweon Yu, Kyung-Ho Lee, O-Yu Kwon
Luteolin [2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4-chromenone] is an active flavonoid compound from Lonicera japonica (Caprifoliaceae). Luteolin inhibits tumor cell proliferation, inflammatory and oxidative stress better, when compared with other flavonoids. In the present study, it was demonstrated that luteolin induces typical apoptosis in PC12 cells (derived from a pheochromocytoma of the rat adrenal medulla) accompanied by DNA fragmentation and formation of apoptotic bodies. In addition, luteolin regulates expression of the endoplasmic reticulum (ER) chaperone binding immunoglobulin protein, activating ER stress sensors (eukaryotic initiation factor 2α phosphorylation and X‑box binding protein 1 mRNA splicing) and induced autophagy...
May 12, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28476637/the-critical-role-of-nramp1-in-degrading-%C3%AE-synuclein-oligomers-in-microglia-under-iron-overload-condition
#6
Kuo-Chen Wu, Horng-Huei Liou, Yu-Han Kao, Chih-Yu Lee, Chun-Jung Lin
Oligomeric α-synuclein is a key mediator in the pathogenesis of Parkinson's disease (PD) and is mainly cleared by autophagy-lysosomal pathway, whose dysfunction results in the accumulation and cell-to-cell transmission of α-synuclein. In this study, concomitant with the accumulation of iron and oligomeric α-synuclein, higher expression of a lysosomal iron transporter, natural resistance-associated macrophage protein-1 (Nramp1), was observed in microglia in post-mortem striatum of sporadic PD patients. Using Nramp1-deficient macrophage (RAW264...
May 2, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28469644/the-emerging-role-of-autophagic-lysosomal-dysfunction-in-gaucher-disease-and-parkinson-s-disease
#7
REVIEW
Kerri J Kinghorn, Amir M Asghari, Jorge Iván Castillo-Quan
Gaucher disease (GD), the commonest lysosomal storage disorder, results from the lack or functional deficiency of glucocerebrosidase (GCase) secondary to mutations in the GBA1 gene. There is an established association between GBA1 mutations and Parkinson's disease (PD), and indeed GBA1 mutations are now considered to be the greatest genetic risk factor for PD. Impaired lysosomal-autophagic degradation of cellular proteins, including α-synuclein (α-syn), is implicated in the pathogenesis of PD, and there is increasing evidence for this also in GD and GBA1-PD...
March 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28459042/autophagy-regulating-micrornas-and-cancer
#8
REVIEW
Devrim Gozuacik, Yunus Akkoc, Deniz Gulfem Ozturk, Muhammed Kocak
Macroautophagy (autophagy herein) is a cellular stress response and a survival pathway that is responsible for the degradation of long-lived proteins, protein aggregates, as well as damaged organelles in order to maintain cellular homeostasis. Consequently, abnormalities of autophagy are associated with a number of diseases, including Alzheimers's disease, Parkinson's disease, and cancer. According to the current view, autophagy seems to serve as a tumor suppressor in the early phases of cancer formation, yet in later phases, autophagy may support and/or facilitate tumor growth, spread, and contribute to treatment resistance...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28454606/therapeutic-implication-of-autophagy-in-neurodegenerative-diseases
#9
Md Ataur Rahman, Hyewhon Rhim
Autophagy, a catabolic process to maintain intracellular homeostasis, has been recently focus in numerous human disease conditions, such as aging, cancer, development, immunity, longevity, and neurodegeneration. However, sustaining autophagy is essential for cell survival and dysregulate autophagy is anticipated to speed up neurodegeneration progression; although, the actual molecular mechanism is not yet fully understood. In contrast, emerging evidence suggests that basal autophagy is necessary for removal of misfolded aggregation proteins and damaged cellular organelles through lysosomal mediated degradation...
April 29, 2017: BMB Reports
https://www.readbyqxmd.com/read/28450057/environmental-neurotoxicant-manganese-regulates-exosome-mediated-extracellular-mirnas-in-cell-culture-model-of-parkinson-s-disease-relevance-to-%C3%AE-synuclein-misfolding-in-metal-neurotoxicity
#10
Dilshan S Harischandra, Shivani Ghaisas, Dharmin Rokad, Mostafa Zamanian, Huajun Jin, Vellareddy Anantharam, Michael Kimber, Arthi Kanthasamy, Anumantha Kanthasamy
Many chronic neurodegenerative disorders share a common pathogenic mechanism involving the aggregation and deposition of misfolded proteins. Recently, it was shown that these aggregated proteins could be transferred from one cell to another via extracellular nanovesicles called exosomes. Initially thought to be a means of cellular waste removal, exosomes have since been discovered to actively participate in cell-to-cell communication. Importantly, various inflammatory and signaling molecules, as well as small RNAs are selectively packaged in these vesicles...
April 24, 2017: Neurotoxicology
https://www.readbyqxmd.com/read/28431223/pink1-based-screen-shines-light-on-autophagy-enhancers-for-parkinson-s-disease
#11
Dominik Haddad, Ken Nakamura
In this issue of Cell Chemical Biology, Zhang et al. (2017) report a zebrafish model of Parkinson's disease (PD), incorporating the PD-protein PINK1 and rotenone, a toxin linked to PD. Using it as a drug-screening platform, they identify trifluoperazine and other piperazine phenothiazines as protective compounds that enhance autophagy independent of PINK1.
April 20, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28428740/protein-quality-control-by-molecular-chaperones-in-neurodegeneration
#12
REVIEW
Aaron Ciechanover, Yong Tae Kwon
Protein homeostasis (proteostasis) requires the timely degradation of misfolded proteins and their aggregates by protein quality control (PQC), of which molecular chaperones are an essential component. Compared with other cell types, PQC in neurons is particularly challenging because they have a unique cellular structure with long extensions. Making it worse, neurons are postmitotic, i.e., cannot dilute toxic substances by division, and, thus, are highly sensitive to misfolded proteins, especially as they age...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28400718/rab-gtpases-the-key-players-in-the-molecular-pathway-of-parkinson-s-disease
#13
REVIEW
Meng-Meng Shi, Chang-He Shi, Yu-Ming Xu
Parkinson's disease (PD) is a progressive movement disorder with multiple non-motor symptoms. Although family genetic mutations only account for a small proportion of the cases, these mutations have provided several lines of evidence for the pathogenesis of PD, such as mitochondrial dysfunction, protein misfolding and aggregation, and the impaired autophagy-lysosome system. Recently, vesicle trafficking defect has emerged as a potential pathogenesis underlying this disease. Rab GTPases, serving as the core regulators of cellular membrane dynamics, may play an important role in the molecular pathway of PD through the complex interplay with numerous factors and PD-related genes...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28390981/neurochemical-effects-of-the-r-form-of-%C3%AE-lipoic-acid-and-its-neuroprotective-mechanism-in-cellular-models-of-parkinson-s-disease
#14
Hong Zhao, Xingcheng Zhao, Lijuan Liu, Hongxu Zhang, Mingwen Xuan, Zhaohui Guo, Hongcai Wang, Chang Liu
OBJECTIVE: Parkinson's disease (PD) is a common neurodegenerative disease. This study aimed to investigate the effects of the R form of α-lipoic acid (RLA) in cellular models of PD induced by 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). METHODS: Cell viability and apoptosis were detected using CCK8 and Annexin V-FITC assays, respectively. Intracellular reactive oxygen species (ROS) were detected by fluorescence staining. ELISA assays were performed to detect the levels of dopamine and α-synuclein...
April 6, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28368777/pink1-and-becn1-relocalize-at-mitochondria-associated-membranes-during-mitophagy-and-promote-er-mitochondria-tethering-and-autophagosome-formation
#15
Vania Gelmetti, Priscilla De Rosa, Liliana Torosantucci, Elettra Sara Marini, Alessandra Romagnoli, Martina Di Rienzo, Giuseppe Arena, Domenico Vignone, Gian Maria Fimia, Enza Maria Valente
Mitophagy is a highly specialized process to remove dysfunctional or superfluous mitochondria through the macroautophagy/autophagy pathway, aimed at protecting cells from the damage of disordered mitochondrial metabolism and apoptosis induction. PINK1, a neuroprotective protein mutated in autosomal recessive Parkinson disease, has been implicated in the activation of mitophagy by selectively accumulating on depolarized mitochondria, and promoting PARK2/Parkin translocation to them. While these steps have been characterized in depth, less is known about the process and site of autophagosome formation upon mitophagic stimuli...
April 3, 2017: Autophagy
https://www.readbyqxmd.com/read/28366621/rescue-of-pink1-deficiency-by-stress-dependent-activation-of-autophagy
#16
Yuxi Zhang, David T Nguyen, Ellen M Olzomer, Gin P Poon, Nicholas J Cole, Anita Puvanendran, Brigitte R Phillips, Daniel Hesselson
Stimulating autophagy is a promising therapeutic strategy for slowing the progression of neurodegenerative disease. Neurons are insensitive to current approaches based on mTOR inhibition for activating autophagy, and instead may rely on the Parkinson's disease-associated proteins PINK1 and PARKIN to activate the autophagy-lysosomal pathway in response to mitochondrial damage. We developed a multifactorial zebrafish drug-screening platform combining Pink1 deficiency with an environmental toxin to compromise mitochondrial function and trigger dopaminergic neuron loss...
April 20, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28365714/microrna-181a-regulates-apoptosis-and-autophagy-process-in-parkinson-s-disease-by-inhibiting-p38-mitogen-activated-protein-kinase-mapk-c-jun-n-terminal-kinases-jnk-signaling-pathways
#17
Ying Liu, Yanfeng Song, Xiaotun Zhu
BACKGROUND microRNA (miR)-181a has been reported to be downregulated in Parkinson's disease (PD), but the regulatory mechanism of miR-181a on neuron apoptosis and autophagy is still poorly understood. We aimed to investigate the neuroprotective effects of miR-181a on PD in vitro. MATERIAL AND METHODS Human SK-N-SH neuroblastoma cells were incubated with different concentrations of 1-methyl-4-phenylpyridinium ion (MPP+) to induce the PD model. The expression of miR-181a was then analyzed. After transfection with miR-181a mimic or scramble following MPP+ treatment, the expression of autophagy protein markers (LC3II, LC3I, and Beclin 1) and p38 mitogen-activated protein kinase (MAPK)/c-Jun N-terminal kinases (JNK) signaling proteins (p-p38, p38, p-JNK, and JNK) and cell apoptosis were detected...
April 2, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28361482/induction-of-pink1-parkin-mediated-mitophagy
#18
Shigeto Sato, Norihiko Furuya
PINK1/Parkin mitophagy is a key mechanism to contribute mitochondrial quality control, and the defects are thought to be a cause of those Parkinson's disease onsets. Upon loss of mitochondrial membrane potential, PINK1 and Parkin are activated to promote the proteasomal degradation of mitochondrial outer membrane proteins and selective elimination of damaged mitochondria by autophagy. In this chapter, we describe the methods for induction of PINK1/Parkin-mediated mitophagy in tissue culture cell lines.
March 31, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28357809/neuroprotective-effects-of-temsirolimus-in-animal-models-of-parkinson-s-disease
#19
Rosalba Siracusa, Irene Paterniti, Marika Cordaro, Rosalia Crupi, Giuseppe Bruschetta, Michela Campolo, Salvatore Cuzzocrea, Emanuela Esposito
Parkinson's disease (PD) is a disorder caused by degeneration of dopaminergic neurons. At the moment, there is no cure. Recent studies have shown that autophagy may have a protective function against the advance of a number of neurodegenerative diseases. Temsirolimus is an analogue of rapamycin that induces autophagy by inhibiting mammalian target of rapamycin complex 1. For this purpose, in the present study we investigated the neuroprotective effects of temsirolimus (5 mg/kg intraperitoneal) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced (MPTP) neurotoxicity in in vivo model of PD...
March 29, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28353287/mechanisms-of-mutant-lrrk2-neurodegeneration
#20
Mark R Cookson
LRRK2 mutations are associated with the loss of neurons, that is to say toxicity, in patients and in experimental model systems. However, the mechanisms by which mutations can be linked to neurodegeneration are not fully defined. Here I will argue that mechanism in this context encompasses a variety of levels of information. Mutations or alterations in gene expression at a genetic level are one set of mechanisms that are reflected at the biochemical level likely in enhanced or persistent function of LRRK2. By impacting cellular pathways, prominently including changes in autophagy but also microtubule function, mitochondria and protein synthesis, in neurons and immune cells, the LRRK2 brain is primed for neurodegeneration in an age-dependent manner...
2017: Advances in Neurobiology
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