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parkinson's disease and endoplasmic reticulum stress

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https://www.readbyqxmd.com/read/29771174/signaling-and-induction-of-chaperone-mediated-autophagy-by-the-endoplasmic-reticulum-under-stress-conditions
#1
Wenming Li, Qian Yang, Zixu Mao
Chaperone-mediated autophagy (CMA), a form of selective autophagy, maintains cellular proteostasis in response to diverse stress conditions. Whether and how endoplasmic reticulum (ER) stress triggers CMA remains elusive. In our recent study, we demonstrate that various types of ER stress activate the CMA pathway via an EIF2AK3/PERK-MAP2K4/MKK4-MAPK14/p38-dependent manner. We term this process ERICA for ER stress-induced chaperone-mediated autophagy. This pathway is activated in response to stress associated with Parkinson disease and is required for the viability of the SNc dopaminergic neurons in an animal model of Parkinson disease...
May 17, 2018: Autophagy
https://www.readbyqxmd.com/read/29749529/%C3%AE-%C3%A2-synuclein-induces-apoptosis-of-astrocytes-by-causing-dysfunction-of-the-endoplasmic-reticulum%C3%A2-golgi-compartment
#2
Mei Liu, Lixia Qin, Lili Wang, Jieqiong Tan, Hainan Zhang, Jianguang Tang, Xiangmin Shen, Liming Tan, Chunyu Wang
Although previous work has demonstrated that the overexpression of wild‑type or mutant α‑synuclein (α‑syn) can induce cell death via a number of different mechanisms, including oxidative stress, dysfunction of the ubiquitin‑proteasome degradation system, mitochondrial damage and endoplasmic reticulum (ER) stress, research interest has primarily focused on neurons. However, there is accumulating evidence that suggests that astrocytes may be involved in the earliest changes, as well as the progression of Parkinson's disease (PD), though the role of α‑syn in astrocytes has not been widely studied...
May 9, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29731707/the-neuroprotection-of-low-dose-morphine-in-cellular-and-animal-models-of-parkinson-s-disease-through-ameliorating-endoplasmic-reticulum-er-stress-and-activating-autophagy
#3
Bing Wang, Cun-Jin Su, Teng-Teng Liu, Yan Zhou, Yu Feng, Ya Huang, Xu Liu, Zhi-Hong Wang, Li-Hua Chen, Wei-Feng Luo, Tong Liu
Parkinson's disease (PD) is a common neurodegenerative disease characterized the progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc). Brain endogenous morphine biosynthesis was reported to be impaired in PD patients and exogenous morphine attenuated 6-hydroxydopamine (6-OHDA)-induced cell death in vitro . However, the mechanisms underlying neuroprotection of morphine in PD are still unclear. In the present study, we investigated the neuroprotective effects of low-dose morphine in cellular and animal models of PD and the possible underlying mechanisms...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29725038/-poly-phenol-digested-metabolites-modulate-alpha-synuclein-toxicity-by-regulating-proteostasis
#4
Diana Macedo, Carolina Jardim, Inês Figueira, A Filipa Almeida, Gordon J McDougall, Derek Stewart, Jose E Yuste, Francisco A Tomás-Barberán, Sandra Tenreiro, Tiago F Outeiro, Cláudia N Santos
Parkinson's disease (PD) is an age-related neurodegenerative disease associated with the misfolding and aggregation of alpha-synuclein (aSyn). The molecular underpinnings of PD are still obscure, but nutrition may play an important role in the prevention, onset, and disease progression. Dietary (poly)phenols revert and prevent age-related cognitive decline and neurodegeneration in model systems. However, only limited attempts were made to evaluate the impact of digestion on the bioactivities of (poly)phenols and determine their mechanisms of action...
May 3, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29719505/cellular-and-molecular-basis-of-neurodegeneration-in-parkinson-disease
#5
REVIEW
Xian-Si Zeng, Wen-Shuo Geng, Jin-Jing Jia, Lei Chen, Peng-Peng Zhang
It has been 200 years since Parkinson disease (PD) was described by Dr. Parkinson in 1817. The disease is the second most common neurodegenerative disease characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Although the pathogenesis of PD is still unknown, the research findings from scientists are conducive to understand the pathological mechanisms. It is well accepted that both genetic and environmental factors contribute to the onset of PD. In this review, we summarize the mutations of main seven genes (α-synuclein, LRRK2, PINK1, Parkin, DJ-1, VPS35 and GBA1) linked to PD, discuss the potential mechanisms for the loss of dopaminergic neurons (dopamine metabolism, mitochondrial dysfunction, endoplasmic reticulum stress, impaired autophagy, and deregulation of immunity) in PD, and expect the development direction for treatment of PD...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29650257/neuropeptide-y-mitigates-er-stress-induced-neuronal-cell-death-by-activating-the-pi3k-xbp1-pathway
#6
Do Yeon Lee, Seung Hyun Hong, Bokyung Kim, Dong-Seok Lee, Kweon Yu, Kyu-Sun Lee
The unfolded protein response (UPR) is an evolutionarily conserved adaptive reaction that increases cell survival under endoplasmic reticulum (ER) stress conditions. ER stress-associated neuronal cell death pathways play roles in the pathogenesis of neurodegenerative diseases, including Alzheimer's, Parkinson's, and Huntington's disease. Neuropeptide Y (NPY) has an important role in neuroprotection against neurodegenerative diseases. In this study, we investigated whether NPY has a protective role in ER stress-induced neuronal cell death in SK-N-SH human neuroblastoma cells...
April 6, 2018: European Journal of Cell Biology
https://www.readbyqxmd.com/read/29623030/on-the-role-of-store-operated-calcium-entry-in-acute-and-chronic-neurodegenerative-diseases
#7
REVIEW
Agnese Secondo, Giacinto Bagetta, Diana Amantea
In both excitable and non-excitable cells, calcium (Ca2+ ) signals are maintained by a highly integrated process involving store-operated Ca2+ entry (SOCE), namely the opening of plasma membrane (PM) Ca2+ channels following the release of Ca2+ from intracellular stores. Upon depletion of Ca2+ store, the stromal interaction molecule (STIM) senses Ca2+ level reduction and migrates from endoplasmic reticulum (ER)-like sites to the PM where it activates the channel proteins Orai and/or the transient receptor potential channels (TRPC) prompting Ca2+ refilling...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29588162/aminochrome-decreases-ngf-gdnf-and-induces-neuroinflammation-in-organotypic-midbrain-slice-cultures
#8
Fillipe M de Araújo, Rafael S Ferreira, Cleide S Souza, Cleonice Creusa Dos Santos, Tácio L R S Rodrigues, Juliana Helena C E Silva, Juciano Gasparotto, Daniel Pens Gelain, Ramon S El-Bachá, Maria de Fátima D Costa, José Claudio M Fonseca, Juan Segura-Aguilar, Silvia L Costa, Victor Diogenes A Silva
Recent evidence shows that aminochrome induces glial activation related to neuroinflammation. This dopamine derived molecule induces formation and stabilization of alpha-synuclein oligomers, mitochondria dysfunction, oxidative stress, dysfunction of proteasomal and lysosomal systems, endoplasmic reticulum stress and disruption of the microtubule network, but until now there has been no evidence of effects on production of cytokines and neurotrophic factors, that are mechanisms involved in neuronal loss in Parkinson's disease (PD)...
March 24, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29545770/centrality-of-early-synaptopathy-in-parkinson-s-disease
#9
REVIEW
Paola Imbriani, Tommaso Schirinzi, Maria Meringolo, Nicola B Mercuri, Antonio Pisani
Significant advances have been made in the understanding of the numerous mechanisms involved in Parkinson's disease (PD) pathogenesis. The identification of PD pathogenic mutations and the use of different animal models have contributed to better elucidate the processes underlying the disease. Here, we report a brief survey of some relevant cellular mechanisms, including autophagic-lysosomal dysfunction, endoplasmic reticulum stress, and mitochondrial impairment, with the main aim to focus on their potential convergent roles in determining early alterations at the synaptic level, mainly consisting in a decrease in dopamine release at nigrostriatal terminals and loss of synaptic plasticity at corticostriatal synapses...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29499217/myxobacterial-natural-products-an-under-valued-source-of-products-for-drug-discovery-for-neurological-disorders
#10
Mona Dehhaghi, Fatemeh Mohammadipanah, Gilles J Guillemin
Age-related disorders impose noticeable financial and emotional burdens on society. This impact is becoming more prevalent with the increasing incidence of neurodegenerative diseases and is causing critical concerns for treatment of patients worldwide. Parkinson's disease, Alzheimer's disease, multiple sclerosis and motor neuron disease are the most prevalent and the most expensive to treat neurodegenerative diseases globally. Therefore, exploring effective therapies to overcome these disorders is a necessity...
May 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29497039/er-mitochondria-signaling-in-parkinson-s-disease
#11
REVIEW
Patricia Gómez-Suaga, José M Bravo-San Pedro, Rosa A González-Polo, José M Fuentes, Mireia Niso-Santano
Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular processes. Alterations in ER-mitochondria signaling have pleiotropic effects on a variety of intracellular events resulting in mitochondrial damage, Ca2+ dyshomeostasis, ER stress and defects in lipid metabolism and autophagy. Intriguingly, many of these cellular processes are perturbed in neurodegenerative diseases...
March 1, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29496607/a-novel-modelling-mechanism-of-pael-receptor-and-gabarapl2-interaction-involved-in-parkinson-s-disease
#12
Priyanka Dutta, Leila Dargahi, Kara E O'Connell, Ashini Bolia, Banu Ozkan, Andreas W Sailer, Kumlesh K Dev
Parkin associated endothelin like receptor (PAELR) is G-protein coupled and ubiquitinated by parkin, promoting its degradation. In autosomal recessive Parkinson's disease, mutations in parkin lead to PAELR aggregation in the endoplasmic reticulum (ER), ER stress, neurotoxicity and cell death. We have identified previously that the protein kinase C interacting protein (PICK1) interacts with and regulates the expression and cell toxicity of PAELR. Here, we experimentally identify and provide in-silico modelling of a novel interaction between PAELR and GABARAPL2 (γ-aminobutyrate type A receptor associated protein like 2), which is an autophagosome-specific Ub-like protein implicated in vesicle trafficking and autophagy...
April 23, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29487216/identification-of-a-highly-neurotoxic-%C3%AE-synuclein-species-inducing-mitochondrial-damage-and-mitophagy-in-parkinson-s-disease
#13
Diego Grassi, Shannon Howard, Minghai Zhou, Natalia Diaz-Perez, Nicolai T Urban, Debbie Guerrero-Given, Naomi Kamasawa, Laura A Volpicelli-Daley, Philip LoGrasso, Corinne Ida Lasmézas
Exposure of cultured primary neurons to preformed α-synuclein fibrils (PFFs) leads to the recruitment of endogenous α-synuclein and its templated conversion into fibrillar phosphorylated α-synuclein (pα-synF) aggregates resembling those involved in Parkinson's disease (PD) pathogenesis. Pα-synF was described previously as inclusions morphologically similar to Lewy bodies and Lewy neurites in PD patients. We discovered the existence of a conformationally distinct, nonfibrillar, phosphorylated α-syn species that we named "pα-syn*...
March 13, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29408665/selenium-and-zinc-two-key-players-against-cadmium-induced-neuronal-toxicity
#14
Jacopo J V Branca, Gabriele Morucci, Mario Maresca, Barbara Tenci, Roberta Cascella, Ferdinando Paternostro, Carla Ghelardini, Massimo Gulisano, Lorenzo Di Cesare Mannelli, Alessandra Pacini
Cadmium (Cd), a worldwide occupational pollutant, is an extremely toxic heavy metal, capable of damaging several organs, including the brain. Its toxicity has been related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. The neurotoxic potential of Cd has been attributed to the changes induced in the brain enzyme network involved in counteracting oxidative stress. On the other hand, it is also known that trace elements, such as zinc (Zn) and selenium (Se), required for optimal brain functions, appears to have beneficial effects on the prevention of Cd intoxication...
April 2018: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/29400127/glucocerebrosidase-and-parkinson-disease-molecular-clinical-and-therapeutic-implications
#15
Roberta Balestrino, Anthony H V Schapira
Parkinson disease (PD) is a complex neurodegenerative disease characterised by multiple motor and non-motor symptoms. In the last 20 years, more than 20 genes have been identified as causes of parkinsonism. Following the observation of higher risk of PD in patients affected by Gaucher disease, a lysosomal disorder caused by mutations in the glucocerebrosidase (GBA) gene, it was discovered that mutations in this gene constitute the single largest risk factor for development of idiopathic PD. Patients with PD and GBA mutations are clinically indistinguishable from patients with idiopathic PD, although some characteristics emerge depending on the specific mutation, such as slightly earlier onset...
February 1, 2018: Neuroscientist: a Review Journal Bringing Neurobiology, Neurology and Psychiatry
https://www.readbyqxmd.com/read/29355603/targeting-perk-signaling-with-the-small-molecule-gsk2606414-prevents-neurodegeneration-in-a-model-of-parkinson-s-disease
#16
Gabriela Mercado, Valentina Castillo, Paulina Soto, Nélida López, Jeffrey M Axten, Sergio P Sardi, Jeroen J M Hoozemans, Claudio Hetz
Parkinson's disease (PD) is the second most common neurodegenerative disorder, leading to the progressive decline of motor control due to the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Accumulating evidence suggest that altered proteostasis is a salient feature of PD, highlighting perturbations to the endoplasmic reticulum (ER), the main compartment involved in protein folding and secretion. PERK is a central ER stress sensor that enforces adaptive programs to recover homeostasis through a block of protein translation and the induction of the transcription factor ATF4...
April 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29331484/novel-biomolecular-information-in-rotenone-induced-cellular-model-of-parkinson-s-disease
#17
D Lin, Y Liang, D Zheng, Y Chen, X Jing, M Lei, Z Zeng, T Zhou, X Wu, S Peng, K Huang, L Yang, S Xiao, J Liu, E Tao
In order to uncover the remarkable pathogenic genes or molecular pathological process in Parkinson's disease (PD), we employed a microarray analysis upon the cellular PD model induced by rotenone. Compared to the control group, 2174 genes were screened out to be expressed differently in the rotenone-induced group by certain criterion. GO analysis and the pathways analysis showed the significant enrichment of genes that were associated with the biological process of cell cycle, apoptotic process, organelle fusion, mitochondrial lesion, endoplasmic reticulum stress and so on...
March 20, 2018: Gene
https://www.readbyqxmd.com/read/29330040/yod1-attenuates-neurogenic-proteotoxicity-through-its-deubiquitinating-activity
#18
Kunikazu Tanji, Fumiaki Mori, Yasuo Miki, Jun Utsumi, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi
Ubiquitination, a fundamental post-translational modification of intracellular proteins, is enzymatically reversed by deubiquitinase enzymes (deubiquitinases). >90 deubiquitinases have been identified. One of these enzymes, YOD1, possesses deubiquitinase activity and is similar to ovarian tumor domain-containing protein 1, which is associated with regulation of the endoplasmic reticulum (ER)-associated degradation pathway. Indeed, YOD1 is reported to be involved in the ER stress response induced by mislocalization of unfolded proteins in mammalian cells...
April 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29303785/mechanisms-of-disordered-neurodegenerative-function-concepts-and-facts-about-the-different-roles-of-the-protein-kinase-rna-like-endoplasmic-reticulum-kinase-perk
#19
Yasmeen M Taalab, Nour Ibrahim, Ahmed Maher, Mubashir Hassan, Wael Mohamed, Ahmed A Moustafa, Mohamed Salama, Dina Johar, Larry Bernstein
Neurodegenerative diseases, such as Alzheimer's disease, Huntington's disease, Parkinson's disease, prion disease, and amyotrophic lateral sclerosis, are a dissimilar group of disorders that share a hallmark feature of accumulation of abnormal intraneuronal or extraneuronal misfolded/unfolded protein and are classified as protein misfolding disorders. Cellular and endoplasmic reticulum (ER) stress activates multiple signaling cascades of the unfolded protein response (UPR). Consequently, translational and transcriptional alterations in target gene expression occur in response directed toward restoring the ER capacity of proteostasis and reestablishing the cellular homeostasis...
January 5, 2018: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/29234100/a-bi-fluorescence-complementation-system-to-detect-associations-between-the-endoplasmic-reticulum-and-mitochondria
#20
Mark Harmon, Philip Larkman, Giles Hardingham, Mandy Jackson, Paul Skehel
Close contacts between the endoplasmic reticulum membrane and the mitochondrial outer membrane facilitate efficient transfer of lipids between the organelles and coordinate Ca2+ signalling and stress responses. Changes to this coupling is associated with a number of metabolic disorders and neurodegenerative diseases including Alzheimer's, Parkinson's and motor neuron disease. The distance between the two membranes at regions of close apposition is below the resolution of conventional light microscopy, which makes analysis of these interactions challenging...
December 12, 2017: Scientific Reports
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